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Faye, Therese, Dag Anders Brede, Thor Langsrud, Ingolf F. Nes, and Helge Holo. "An Antimicrobial Peptide Is Produced by Extracellular Processing of a Protein from Propionibacterium jensenii." Journal of Bacteriology 184, no. 13 (July 1, 2002): 3649–56. http://dx.doi.org/10.1128/jb.184.13.3649-3656.2002.
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ABSTRACT A protease-activated antimicrobial peptide (PAMP) and its inactive precursor were purified from the culture supernatant of Propionibacterium jensenii LMG 3032 and characterized at the molecular level. PAMP is a 64-amino-acid cationic peptide of 6,383 Da with physicochemical features similar to those of bacteriocins from gram-positive bacteria. This peptide displayed bactericidal activity against several propionibacteria and lactobacilli. DNA sequencing indicated that the PAMP-encoding gene (pamA) is translated as a proprotein of 198 amino acids with an N-terminal signal peptide of 27 amino acids and that PAMP constitutes the C-terminal part of this precursor. The amino acid sequence of pro-PAMP showed no similarity to those of other known proteins. By using activity tests and mass spectrometry, we showed that PAMP was formed upon protease treatment of the precursor protein. The propionibacteria produced the PAMP precursor constitutively during growth up to a level of ∼4 mg/liter, but the producing bacteria were unable to activate the precursor. The requirement for an external protease represents a novel strategy for generating antimicrobial peptides.
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Brede, Dag Anders, Therese Faye, Melanie Patricia Stierli, Gottfried Dasen, Anita Theiler, Ingolf F. Nes, Leo Meile, and Helge Holo. "Heterologous Production of Antimicrobial Peptides in Propionibacterium freudenreichii." Applied and Environmental Microbiology 71, no. 12 (December 2005): 8077–84. http://dx.doi.org/10.1128/aem.71.12.8077-8084.2005.
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ABSTRACT Heterologous bacteriocin production in Propionibacterium freudenreichii is described. We developed an efficient system for DNA shuttling between Escherichia coli and P. freudenreichii using vector pAMT1. It is based on the P. freudenreichii rolling-circle replicating plasmid pLME108 and carries the cml(A)/cmx(A) chloramphenicol resistance marker. Introduction of the propionicin T1 structural gene (pctA) into pAMT1 under the control of the constitutive promoter (P4) yielded bacteriocin in amounts equal to those of the wild-type producer Propionibacterium thoenii 419. The P. freudenreichii clone showed propionicin T1 activity in coculture, killing 90% of sensitive bacteria within 48 h. The pamA gene from P. thoenii 419 encoding the protease-activated antimicrobial peptide (PAMP) was cloned and expressed in P. freudenreichii, resulting in secretion of the pro-PAMP protein. Like in the wild type, PAMP activation was dependent on externally added protease. Secretion of the antimicrobial peptide was obtained from a clone in which the pamA signal peptide and PAMP were fused in frame. The promoter region of pamA was identified by fusion of putative promoter fragments to the coding sequence of the pctA gene. The P4 and Ppamp promoters directed constitutive gene expression, and activity of both promoters was enhanced by elements upstream of the promoter core region.
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Veetil, Aneesh T., Junyi Zou, Katharine W. Henderson, Maulik S. Jani, Shabana M. Shaik, Sangram S. Sisodia, Melina E. Hale, and Yamuna Krishnan. "DNA-based fluorescent probes of NOS2 activity in live brains." Proceedings of the National Academy of Sciences 117, no. 26 (June 17, 2020): 14694–702. http://dx.doi.org/10.1073/pnas.2003034117.
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Innate immune cells destroy pathogens within a transient organelle called the phagosome. When pathogen-associated molecular patterns (PAMPs) displayed on the pathogen are recognized by Toll-like receptors (TLRs) on the host cell, it activates inducible nitric oxide synthase (NOS2) which instantly fills the phagosome with nitric oxide (NO) to clear the pathogen. Selected pathogens avoid activating NOS2 by concealing key PAMPs from their cognate TLRs. Thus, the ability to map NOS2 activity triggered by PAMPs can reveal critical mechanisms underlying pathogen susceptibility. Here, we describe DNA-based probes that ratiometrically report phagosomal and endosomal NO, and can be molecularly programmed to display precise stoichiometries of any desired PAMP. By mapping phagosomal NO produced in microglia of live zebrafish brains, we found that single-stranded RNA of bacterial origin acts as a PAMP and activates NOS2 by engaging TLR-7. This technology can be applied to study PAMP−TLR interactions in diverse organisms.
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Lloyd, Simon R., Henk-jan Schoonbeek, Martin Trick, Cyril Zipfel, and Christopher J. Ridout. "Methods to Study PAMP-Triggered Immunity in Brassica Species." Molecular Plant-Microbe Interactions® 27, no. 3 (March 2014): 286–95. http://dx.doi.org/10.1094/mpmi-05-13-0154-fi.
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The first layer of active defense in plants is based on the perception of pathogen-associated molecular patterns (PAMPs) leading to PAMP-triggered immunity (PTI). PTI is increasingly being investigated in crop plants, where it may have potential to provide durable disease resistance in the field. Limiting this work, however, is an absence of reliable bioassays to investigate PAMP responses in some species. Here, we present a series of methods to investigate PTI in Brassica napus. The assays allow measuring early responses such as the oxidative burst, mitogen-activated protein kinase phosphorylation, and PAMP-induced marker gene expression. Illumina-based RNA sequencing analysis produced a genome-wide survey of transcriptional changes upon PAMP treatment seen in both the A and C genomes of the allotetraploid B. napus. Later responses characterized include callose deposition and lignification at the cell wall, seedling growth inhibition, and PAMP-induced resistance to Pseudomonas syringae and Botrytis cinerea. Furthermore, using these assays, we demonstrated substantial variation in PAMP responses within a collection of diverse B. napus cultivars. The assays reported here could have widespread application in B. napus breeding and mapping programs to improve selection for broad-spectrum disease resistance.
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Yan, Yu, Dan Yao, and Xiaoyu Li. "Immunological Mechanism and Clinical Application of PAMP Adjuvants." Recent Patents on Anti-Cancer Drug Discovery 16, no. 1 (May 25, 2021): 30–43. http://dx.doi.org/10.2174/1574892816666210201114712.
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Background: The host innate immune system can recognize Pathogen-Associated Molecular Patterns (PAMPs) through Pattern Recognition Receptors (PRRs), thereby initiating innate immune responses and subsequent adaptive immune responses. PAMPs can be developed as a vaccine adjuvant for modulating and optimizing antigen-specific immune responses, especially in combating viral infections and tumor therapy. Although several PAMP adjuvants have been successfully developed they are still lacking in general, and many of them are in the preclinical exploration stage. Objective: This review summarizes the research progress and development direction of PAMP adjuvants, focusing on their immune mechanisms and clinical applications. Methods: PubMed, Scopus, and Google Scholar were screened for this information. We highlight the immune mechanisms and clinical applications of PAMP adjuvants. Results: Because of the differences in receptor positions, specific immune cells targets, and signaling pathways, the detailed molecular mechanism and pharmacokinetic properties of one agonist cannot be fully generalized to another agonist, and each PAMP should be studied separately. In addition, combination therapy and effective integration of different adjuvants can increase the additional efficacy of innate and adaptive immune responses. Conclusion: The mechanisms by which PAMPs exert adjuvant functions are diverse. With continuous discovery in the future, constant adjustments should be made to build new understandings. At present, the goal of therapeutic vaccination is to induce T cells that can specifically recognize and eliminate tumor cells and establish long-term immune memory. Following immune checkpoint modulation therapy, cancer treatment vaccines may be an option worthy of clinical testing.
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Yan, Qing, Conner J. Rogan, and Jeffrey C. Anderson. "Development of a Pseudomonas syringae–Arabidopsis Suspension Cell Infection System for Investigating Host Metabolite-Dependent Regulation of Type III Secretion and Pattern-Triggered Immunity." Molecular Plant-Microbe Interactions® 32, no. 5 (May 2019): 527–39. http://dx.doi.org/10.1094/mpmi-10-18-0295-fi.
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The importance of pattern-triggered immunity (PTI) in plant defense has been clearly established through genetic studies of mutants lacking functional pattern recognition receptors (PRRs) and signaling components downstream of PRR activation. Despite extensive knowledge of PRR-mediated signaling responses to pathogen-associated molecular patterns (PAMPs), little is known about which of these responses, if any, are directly responsible for limiting bacterial growth. In this work, we established a protocol for coculturing the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and Arabidopsis suspension cells. The system closely mirrors infection processes that occur in leaves, with bacteria relying on the type III secretion system (T3SS) for maximal growth and PAMP-induced plant defenses effectively limiting bacterial growth. To demonstrate the utility of this system, we investigated the molecular basis of PAMP-induced growth inhibition and discovered that T3SS-associated genes are inhibited when DC3000 is cocultured with PAMP-treated plant suspension cells. To determine the underlying mechanism of decreased T3SS gene expression, we performed metabolomics and biochemical analyses of suspension cell exudates and identified 14 metabolites that significantly increased or decreased following PAMP treatment. Citric acid, a known inducer of T3SS gene expression in DC3000, was among several organic acids decreased in exudates from PAMP-treated plant cells. Exogenous addition of citric acid increased T3SS gene expression and partially recovered growth of DC3000 in the presence of PAMP-treated cells, indicating that a portion of PAMP-induced defense in this system is decreased extracellular release of this metabolite. We envision that the well-defined infection conditions of this coculture system will be valuable for quantitative studies of type III effector delivery by P. syringae. Furthermore, this system provides a unique ‘top-down’ approach to unravel the molecular basis of PTI against P. syringae.
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Segers, Patrick, H. Alex Leather, Pascal Verdonck, Yuan-Yuan Sun, and Patrick F. Wouters. "Preload-adjusted maximal power of right ventricle: contribution of end-systolic P-V relation intercept." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 4 (October 1, 2002): H1681—H1687. http://dx.doi.org/10.1152/ajpheart.00340.2002.
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To assess whether preload-adjusted maximal power (PAMP), which is calculated asW˙max/V[Formula: see text] (whereW˙max is maximal power and Ved is end-diastolic volume with β = 2) is an index of right ventricular (RV) contractility, we measured RV pressure (P) and volume (V) and pulmonary artery pressure and flow in 10 dogs at baseline and after inotropic stimulation. PAMP was derived from steady-state data, whereas the slope ( E es) and intercept (Vd) of the end-systolic P-V relationship were derived from data obtained during vena caval occlusion. Inotropic stimulation increased E es (from 0.96 ± 0.25 to 1.62 ± 0.28 mmHg/ml; P < 0.001) and Vd (from −3.0 ± 17.2 to 12.4 ± 10.8 ml; P < 0.05) but not PAMP (from 0.24 ± 0.10 to 0.36 ± 0.22 mW/ml2; P = 0.09). We found a strong relationship between the optimal β-factor for preload adjustment and Vd. A corrected PAMP, PAMPc= W˙max/(Ved − Vd)2, which incorporated the Vddependency, was sensitive to the inotropic changes (from 0.23 ± 0.12 to 0.54 ± 0.17 mW/ml2; P < 0.001) with a good correlation with E es( r = 0.88; P < 0.001).
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Furukawa, Takehito, Hiroaki Inagaki, Ryota Takai, Hiroyuki Hirai, and Fang-Sik Che. "Two Distinct EF-Tu Epitopes Induce Immune Responses in Rice and Arabidopsis." Molecular Plant-Microbe Interactions® 27, no. 2 (February 2014): 113–24. http://dx.doi.org/10.1094/mpmi-10-13-0304-r.
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Plants sense potential pathogens by recognizing conserved pathogen-associated molecular patterns (PAMPs) that cause PAMP-triggered immunity (PTI). We previously reported that rice recognizes flagellin from the rice-incompatible N1141 strain of Acidovorax avenae and subsequently induces immune responses. Cell extracts isolated from flagellin-deficient N1141 (Δfla1141) still induced PTI responses, suggesting that Δfla1141 possesses an additional PAMP distinct from flagellin. Here, we show that elongation factor Tu (EF-Tu), one of the most abundant bacterial proteins, acts as a PAMP in rice and causes several PTI responses. In Brassicaceae species, EF-Tu and an N-acetylated peptide comprising the first 18 amino acids of the N-terminus, termed elf18, are fully active as inducers of PTI responses. By contrast, elf18 did not cause any immune responses in rice, whereas an EF-Tu middle region comprising Lys176 to Gly225, termed EFa50, is fully active as a PAMP in rice. In the leaves of rice plants, EF-Tu induced H2O2 generation and callose deposition, and also triggered resistance to coinfection with pathogenic bacteria. Taken together, these data demonstrate that rice recognizes EFa50, which is distinct from elf18, and that this epitope induces PTI responses.
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Kanazawa, H., H. Kamoi, T. Kawaguchi, S. Shoji, T. Fujii, S. Kudoh, K. Hirata, and J. Yoshikawa. "PAMP is a novel inhibitor of the tachykinin release in the airway of guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (June 1, 1997): L1066—L1069. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1066.
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Proadrenomedullin NH2-terminal 20 peptide (PAMP), a newly identified hypotensive peptide, may play physiological roles in airway and cardiovascular controls. This study was designed to determine the mechanism responsible for the bronchoprotective effects of PAMP on capsaicin-induced bron-choconstriction in anesthetized guinea pigs. PAMP (10(-8)-10(-6) M) significantly inhibited capsaicin-induced bronchoconstriction in a dose-dependent manner. The bronchoprotective effect of PAMP (10(-6) M) was as large as that of isoproterenol (10(-7) M) and lasted > 10 min. The concentration of immunoreactive substance P (SP) in bronchoalveolar lavage fluid after administration of capsaicin (4 x 10(-6) M) was 120 +/- 10 fmol/ml. PAMP significantly inhibited the release of immunoreactive SP in a dose-dependent manner (60 +/- 6 fmol/ml for (10(-6) M PAMP, P < 0.01; 84 +/- 6 fmol/ml for 10(-7) M PAMP, P < 0.01; and 95 +/- 6 fmol/ml for 10(-8) M PAMP, P < 0.05). PAMP (10(-6) M) did not significantly affect exogenous neurokinin A (NKA) or NKA + SP-induced bronchoconstriction, whereas isoproterenol (10(-7) M) significantly inhibited exogenous tachykinin-induced bronchoconstriction. These findings suggest that the bronchoprotective effects of PAMP are mainly due to inhibition of the release of tachykinins at airway C-fiber endings.
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Champion, H. C., W. A. Murphy, D. H. Coy, and P. J. Kadowitz. "Proadrenomedullin NH2-terminal 20 peptide has direct vasodilator activity in the cat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (April 1, 1997): R1047—R1054. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1047.
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The mechanism by which proadrenomedullin NH2-terminal 20 peptide (PAMP) decreases vascular resistance was investigated in the hindlimb vascular bed in the cat. Injections of PAMP, a shortened form of the peptide PAMP-(12-20), and adrenomedullin (ADM) into the hindlimb perfusion circuit elicit dose-related decreases in perfusion pressure. The order of potency was ADM > PAMP > PAMP-(12-20), and the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37) had no effect on vasodilator responses to PAMP or ADM. Vasodilator responses to PAMP were increased in duration by the adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase inhibitor Rolipram, whereas inhibitors of nitric oxide synthase and guanosine 3',5'-cyclic monophosphate phosphodiesterase had no effect. Vasodilator responses to PAMP were not altered by treatment with alpha-receptor or adrenergic nerve terminal blocking agents and were similar in innervated and denervated hindlimb preparations. Responses to PAMP were similar when vasoconstrictor tone was increased by stimulation of the sympathetic nerves or infusion of phenylephrine and were not altered by the passage of time. These data suggest that PAMP dilates the hindlimb vascular bed by a direct cAMP-dependent mechanism and that inhibition of norepinephrine release plays little if any role in mediating responses to the peptide in the regional vascular bed of the cat.
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Martínez, Alfredo, José Antonio Bengoechea, and Frank Cuttitta. "Molecular Evolution of Proadrenomedullin N-Terminal 20 Peptide (PAMP): Evidence for Gene Co-Option." Endocrinology 147, no. 7 (July 1, 2006): 3457–61. http://dx.doi.org/10.1210/en.2006-0105.
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Posttranslational processing of proadrenomedullin generates two biologically active peptides, adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP). Sequence comparison of homologous proadrenomedullin genes in vertebrate evolution shows a high degree of stability in the reading frame for AM, whereas PAMP sequence changes rapidly. Here we investigate the functional significance of PAMP phylogenetic variation studying two of PAMP’s better characterized physiological activities, angiogenic potential and antimicrobial capability, with synthetic peptides carrying the predicted sequence for human, mouse, chicken, and fish PAMP. All tested peptides induced angiogenesis when compared with untreated controls, but chicken and fish PAMP, which lack terminal amidation, were apparently less angiogenic than their human and mouse homologs. Confirming the role of amidation in angiogenesis, Gly-extended and free acid variants of human PAMP produced responses similar to the natural nonamidated peptides. In contrast, antimicrobial activity was restricted to human PAMP, indicating that this function may have been acquired at a late time during the evolution of PAMP. Interestingly, free acid human PAMP retained antimicrobial activity whereas the Gly-extended form did not. This fact may reflect the need for maintaining a tightly defined structural conformation in the pore-forming mechanism proposed for these antimicrobial agents. The evolution of PAMP provides an example of an angiogenic peptide that developed antimicrobial capabilities without losing its original function.
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Kaymaz, Cihangir, Ozgur Yasar Akbal, Aykun Hakgor, Hacer Ceren Tokgoz, Ibrahim Halil Tanboga, Tugba Aktemur, Sevim Turkday, et al. "Reappraisal of the reliability of Doppler echocardiographic estimations for mean pulmonary artery pressure in patients with pulmonary hypertension: a study from a tertiary centre comparing four formulae." Pulmonary Circulation 8, no. 2 (February 26, 2018): 204589401876227. http://dx.doi.org/10.1177/2045894018762270.
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Different Doppler echocardiography (DE) models have been proposed for estimation of mean pulmonary arterial pressures (PAMP) from tricuspid regurgitation (TR) jet velocity. We aimed to compare four TR-derived DE models in predicting the PAMP measured by right heart catheterization (RHC) in different groups of precapillary pulmonary hypertension (PH). A total of 287 patients with hemodynamically pre-capillary PH were enrolled (mean age = 51 ± 17.4 years, 59.9% female). All patients underwent DE before RHC (< 3 h) and four formulae (F) were used for TR-derived PAMP estimation (PAMP-DE). These were as follows: F1 = Chemla (0.61 × systolic pulmonary artery pressure [PASP] + 2); F2 = Friedberg (0.69 × PASP − 0.22), F3 = Aduen (0.70 × PASP); and F4 = Bech-Hanssen (0.65 × PASP − 1.2). The PASP and PAMP (mmHg) measured by RHC were 89.1 ± 30.4 and 55.8 ± 20.8, respectively. In the overall PH group, DE estimates for PASP (r = 0.59, P = 0.001) and PAMP (r = 0.56, P = 0.001 for all) showed significant correlations with corresponding RHC measures. Concordance was noted between Chemla and Bech-Hanssen, and Aduen and Bech-Hanssen. The Bland–Altman plot showed that Chemla and Bech-Hanssen overestimated and Friedberg and Aduen underestimated PAMP-RHC measures. Paired-t test showed significant systematic biases for Aduen and Bech-Hanssen while Passing-Bablok non-parametric analysis revealed significant systematic biases all four PAMP-DE estimates. There was poor agreement between PAMP-RHC measures and PAMP-DE deciles (Kappa values were 0.112, 0.097, 0.095, and 0.121, respectively). This study showed a poor agreement between PAMP-DE estimates by four TR-derived formulae and PAMP-RHC in patients with PH, regardless of the etiology. However, these results can not be fully extrapolated to a normal population and did not address the reliability of DE estimates for PH screening procedures.
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Larráyoz, Ignacio M., and Alfredo Martínez. "Proadrenomedullin N-Terminal 20 Peptide Increases Kinesin's Velocity Both in Vitro and in Vivo." Endocrinology 153, no. 4 (February 14, 2012): 1734–42. http://dx.doi.org/10.1210/en.2011-1685.
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Intracellular cargo transport relies on microtubules and motor proteins such as kinesins and dyneins. Currently we have ample knowledge of the mechanisms by which motor proteins propel themselves along the microtubules, but little is known about intracellular factors that regulate motor speed. Here we show that proadrenomedullin N-terminal 20 peptide (PAMP) increases kinesin velocity and ATP consumption in a dose-dependent manner, using a variety of human kinesins. Structure-activity studies found that the terminal amide of PAMP is required for modulating kinesin activity and that the smallest peptide fragment retaining this role is PAMP(12–20). On the other hand, peptide fragments as small as PAMP(18–20) maintained the ability of delaying tubulin polymerization, another function previously described for PAMP, indicating that these two activities depend on different regions of the molecule. To demonstrate that these observations are also relevant in vivo, hippocampal neurons were isolated from mice lacking the gene coding for PAMP and from wild type littermates. Intravital stains followed by time-lapse microscopy analysis revealed that mitochondrial speed inside neurons lacking PAMP was significantly slower than in cells expressing the peptide. External addition of synthetic PAMP reversed this phenotype in PAMP-null neurons. Besides the obvious implications for better understanding cell biology, these results may be also relevant for the rapidly evolving discipline of nanotechnology because PAMP may be used as an accelerator of nanodevices based on microtubules and motor proteins.
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Akers, Kevin S., Taylor Schlotman, Lee C. Mangum, Gerardo Garcia, Amanda Wagner, Benjamin Seiler, Mark Cartwright, Sami Rifai, Donald Ingber, and Michael Super. "653. Diagnosis of Burn Sepsis Using the FcMBL ELISA: A Pilot Study in Critically Ill Burn Patients." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S300. http://dx.doi.org/10.1093/ofid/ofz360.721.
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Abstract Background Infection is the leading cause of death among burn survivors, with sepsis associated with more extensive burns. Conventional diagnostic criteria are insensitive in this population. We examined a novel diagnostic ELISA based on Mannose-Binding Lectin (MBL) linked to an immunoglobulin Fc domain, which measures the concentration of Pathogen-Associated Molecular Patterns (PAMPs) across a broad range of bacterial and fungal organisms, for diagnosis and antimicrobial management of sepsis in burn patients. Methods We prospectively enrolled burn patients with ≥15% Total Body Surface Area (TBSA) burns into groups of noninfected, sepsis, or incipient infection, and healthy volunteers. Sepsis was defined by clinical actions responsive to sepsis. The FcMBL ELISA was performed daily using fresh whole blood. Burn subjects were sampled daily until completing antimicrobials, for 14 days if noninfected, and once for healthy controls. Differences in median PAMP concentrations between groups were assessed with the Kruskal–Wallis test, including multiple comparisons between categories. Results 14 burn patients (3 noninfected, of whom 1 died prior to sampling, 4 Sepsis, 7 Incipient) were enrolled. The median (25–75% CI) PAMP concentration was 0.53 (0.12–1.34) ng/mL in healthy controls, 3.725 (2.53–5.94) ng/mL in noninfected, 2.22 (1.42–4.62) ng/mL in incipient, and 1.59 (0.83–2.29) ng/mL in sepsis groups. PAMP concentrations in sepsis were different (P = 0.0057) from noninfected, but incipient did not differ from noninfected (P = 0.2025). The dynamic range was lower in healthy controls (2.69 ng/mL) than incipient (4.57 ng/mL), sepsis (4.70 ng/mL), or noninfected (5.90 ng/mL). PAMP elevations correlated with clinical deterioration from infection, and were not associated with OR visits for debridement and grafting. 7 of 11 infected patients had declining PAMP levels at completion of antimicrobial therapy. 2 subjects had PAMP elevations associated with Aspergillus molds in their burn wounds. Conclusion The FcMBL ELISA assay may be useful for diagnosis of infection in burn patients, and may facilitate earlier discontinuation of antimicrobials. This assay may also have a novel utility for early diagnosis of Invasive Fungal Infection. Disclosures All authors: No reported disclosures.
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Ali, Gul Shad, and A. S. N. Reddy. "PAMP-triggered immunity." Plant Signaling & Behavior 3, no. 6 (June 2008): 423–26. http://dx.doi.org/10.4161/psb.3.6.5472.
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Dempsey, Laurie A. "Retroviral PAMP sensor." Nature Immunology 16, no. 8 (July 21, 2015): 801. http://dx.doi.org/10.1038/ni.3240.
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Leavy, Olive. "New PAMP discovered." Nature Reviews Immunology 15, no. 7 (June 25, 2015): 403. http://dx.doi.org/10.1038/nri3880.
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Champion, Hunter C., Trinity J. Bivalacqua, Robert L. Pierce, William A. Murphy, David H. Coy, Albert L. Hyman, and Philip J. Kadowitz. "Responses to human CGRP, ADM, and PAMP in human thymic arteries." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (February 1, 2003): R531—R537. http://dx.doi.org/10.1152/ajpregu.00337.2002.
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Responses to human CGRP, adrenomedullin (ADM), and proadrenomedullin NH2-terminal 20 peptide (PAMP) were studied in small human thymic arteries. CGRP, ADM, and PAMP produced concentration-dependent vasodilator responses in arteries preconstricted with the thromboxane mimic U-46619. Responses to ADM and PAMP were attenuated, whereas responses to CGRP were not altered by endothelial denudation. Inhibitors of nitric oxide synthase and guanylyl cyclase attenuated responses to ADM and PAMP but not to CGRP. The CGRP1 receptor antagonist CGRP(8–37) attenuated responses to CGRP and ADM but not to PAMP. Responses to CGRP were reduced by SQ-22536 and Rp-cAMPS, inhibitors of adenylyl cyclase and PKA. These data suggest that responses to CGRP and ADM are mediated by CGRP(8–37)-sensitive receptors and that the endothelial ADM receptor induces vasodilation by a nitric oxide-guanylyl cyclase mechanism, whereas a smooth muscle CGRP receptor signals by a cAMP-dependent mechanism. A different endothelial receptor recognizes PAMP and signals by a nitric oxide-dependent mechanism.
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Sackett, Dan L., Laurent Ozbun, Enrique Zudaire, Lisa Wessner, John M. Chirgwin, Frank Cuttitta, and Alfredo Martínez. "Intracellular Proadrenomedullin-Derived Peptides Decorate the Microtubules and Contribute to Cytoskeleton Function." Endocrinology 149, no. 6 (March 6, 2008): 2888–98. http://dx.doi.org/10.1210/en.2007-1763.
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Adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) are secretory hormones, but it is not unusual to find them in intracellular compartments. Using yeast-2 hybrid technology, we found interactions between AM and several microtubule-associated proteins (MAPs), and between PAMP and tubulin. Expression of fluorescent-tagged AM and PAMP as well as immunofluorescence for the native peptides showed a complete decoration of the microtubules and colocalization with other MAPs. PAMP, but not AM, bound to tubulin in vitro and destabilized tubulin polymerization. Down-regulation of the gene coding for both AM and PAMP through small interfering RNA technology resulted in morphological changes, microtubule stabilization, increase in posttranslational modifications of tubulin such as acetylation and detyrosination, reduction in cell motility, and partial arrest at the G2 phase of the cell cycle, when compared with cells transfected with the same vector carrying a scrambled sequence. These results show that PAMP is a novel MAP, whereas AM may be exerting more subtle effects in regulating cytoskeleton function.
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Kato, Hiroaki, Kiyoshi Onai, Akira Abe, Motoki Shimizu, Hiroki Takagi, Chika Tateda, Hiroe Utsushi, et al. "Lumi-Map, a Real-Time Luciferase Bioluminescence Screen of Mutants Combined with MutMap, Reveals Arabidopsis Genes Involved in PAMP-Triggered Immunity." Molecular Plant-Microbe Interactions® 33, no. 12 (December 2020): 1366–80. http://dx.doi.org/10.1094/mpmi-05-20-0118-ta.
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Plants recognize pathogen-associated molecular patterns (PAMPs) to activate PAMP-triggered immunity (PTI). However, our knowledge of PTI signaling remains limited. In this report, we introduce Lumi-Map, a high-throughput platform for identifying causative single-nucleotide polymorphisms (SNPs) for studying PTI signaling components. In Lumi-Map, a transgenic reporter plant line is produced that contains a firefly luciferase (LUC) gene driven by a defense gene promoter, which generates luminescence upon PAMP treatment. The line is mutagenized and the mutants with altered luminescence patterns are screened by a high-throughput real-time bioluminescence monitoring system. Selected mutants are subjected to MutMap analysis, a whole-genome sequencing-based method of rapid mutation identification, to identify the causative SNP responsible for the luminescence pattern change. We generated nine transgenic Arabidopsis reporter lines expressing the LUC gene fused to multiple promoter sequences of defense-related genes. These lines generate luminescence upon activation of FLAGELLIN-SENSING 2 (FLS2) by flg22, a PAMP derived from bacterial flagellin. We selected the WRKY29-promoter reporter line to identify mutants in the signaling pathway downstream of FLS2. After screening 24,000 ethylmethanesulfonate-induced mutants of the reporter line, we isolated 22 mutants with altered WRKY29 expression upon flg22 treatment (abbreviated as awf mutants). Although five flg22-insensitive awf mutants harbored mutations in FLS2 itself, Lumi-Map revealed three genes not previously associated with PTI. Lumi-Map has the potential to identify novel PAMPs and their receptors as well as signaling components downstream of the receptors. [Formula: see text] Copyright © 2020 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
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Samson, Willis K., Tonya C. Murphy, and Zachary T. Resch. "Central mechanisms for the hypertensive effects of preproadrenomedullin-derived peptides in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 5 (May 1, 1998): R1505—R1509. http://dx.doi.org/10.1152/ajpregu.1998.274.5.r1505.
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Peptides derived from postranslational processing of preproadrenomedullin exert potent hypotensive effects in the periphery. One of those peptides, adrenomedullin (AM) also has been demonstrated to act centrally in conscious rats to inhibit water drinking and salt appetite and, in anesthetized rats, surprisingly to increase blood pressure. We examined the effects of AM and the other postranslational product, proadrenomedullin NH2-terminal 20 peptide (PAMP), on blood pressure in conscious rats. Both AM and PAMP elicited dose-related increases in mean arterial pressure after cerebroventricular administration. The hypertensive effects of both AM and PAMP and of ANG II were blocked by peripheral administration of phentolamine, indicating actions of the peptides in brain to stimulate sympathetic nervous system function. Blockade of central ANG II receptors with saralasin prevented the hypertensive effects of both ANG II and PAMP, suggesting recruitment of endogenous angiotensinergic systems by central PAMP. The structural homolog of AM, calcitonin gene-related peptide (CGRP), at similar doses did not significantly affect blood pressure. Furthermore, the hypertensive effects of ANG II, AM, and PAMP were not abrogated by prior administration of the CGRP antagonist. We hypothesize that AM and PAMP exert cardioprotective effects in brain, which may counterbalance the volume-unloading actions of the peptides in the periphery.
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Stączek, Sylwia, Agnieszka Zdybicka-Barabas, Iwona Wojda, Adrian Wiater, Paweł Mak, Piotr Suder, Krzysztof Skrzypiec, and Małgorzata Cytryńska. "Fungal α-1,3-Glucan as a New Pathogen-Associated Molecular Pattern in the Insect Model Host Galleria mellonella." Molecules 26, no. 16 (August 23, 2021): 5097. http://dx.doi.org/10.3390/molecules26165097.
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Recognition of pathogen-associated molecular patterns (PAMPs) by appropriate pattern recognition receptors (PRRs) is a key step in activating the host immune response. The role of a fungal PAMP is attributed to β-1,3-glucan. The role of α-1,3-glucan, another fungal cell wall polysaccharide, in modulating the host immune response is not clear. This work investigates the potential of α-1,3-glucan as a fungal PAMP by analyzing the humoral immune response of the greater wax moth Galleria mellonella to Aspergillus niger α-1,3-glucan. We demonstrated that 57-kDa and 61-kDa hemolymph proteins, identified as β-1,3-glucan recognition proteins, bound to A. niger α-1,3-glucan. Other hemolymph proteins, i.e., apolipophorin I, apolipophorin II, prophenoloxidase, phenoloxidase activating factor, arylphorin, and serine protease, were also identified among α-1,3-glucan-interacting proteins. In response to α-1,3-glucan, a 4.5-fold and 3-fold increase in the gene expression of antifungal peptides galiomicin and gallerimycin was demonstrated, respectively. The significant increase in the level of five defense peptides, including galiomicin, corresponded well with the highest antifungal activity in hemolymph. Our results indicate that A. niger α-1,3-glucan is recognized by the insect immune system, and immune response is triggered by this cell wall component. Thus, the role of a fungal PAMP for α-1,3-glucan can be postulated.
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Toda, Shizuo. "Antioxidant and Hepatoprotective Effects of Polyphenols in Leaves of Artemisia Princeps Pamp." Natural Product Communications 2, no. 11 (November 2007): 1934578X0700201. http://dx.doi.org/10.1177/1934578x0700201117.
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The leaves of Artemisia princeps Pamp have been used for tea and food in Japan. The polyphenols of the leaves have inhibitory effects against lipid peroxidation and protein fragmentation by free radicals in vitro and an inhibitory effect on galactosamine -lipopolysaccharide induced hepatotoxicity in vivo. The levels of serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, lipid peroxidation in serum and liver by hepatotoxity were depressed by polyphenols in A. princeps Pamp. The depression of gluthathione and superoxide dismutase in plasma and liver by hepatotoxity were elevated by polyphenols in A. princeps Pamp. These results demonstrated that polyphenols in A. princeps Pamp have antioxidant and hepatoprotective effects.
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Göhre, Vera, Alexandra M. E. Jones, Jan Sklenář, Silke Robatzek, and Andreas P. M. Weber. "Molecular Crosstalk Between PAMP-Triggered Immunity and Photosynthesis." Molecular Plant-Microbe Interactions® 25, no. 8 (August 2012): 1083–92. http://dx.doi.org/10.1094/mpmi-11-11-0301.
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The innate immune system allows plants to respond to potential pathogens in an appropriate manner while minimizing damage and energy costs. Photosynthesis provides a sustained energy supply and, therefore, has to be integrated into the defense against pathogens. Although changes in photosynthetic activity during infection have been described, a detailed and conclusive characterization is lacking. Here, we addressed whether activation of early defense responses by pathogen-associated molecular patterns (PAMPs) triggers changes in photosynthesis. Using proteomics and chlorophyll fluorescence measurements, we show that activation of defense by PAMPs leads to a rapid decrease in nonphotochemical quenching (NPQ). Conversely, NPQ also influences several responses of PAMP-triggered immunity. In a mutant impaired in NPQ, apoplastic reactive oxygen species production is enhanced and defense gene expression is differentially affected. Although induction of the early defense markers WRKY22 and WRKY29 is enhanced, induction of the late markers PR1 and PR5 is completely abolished. We propose that regulation of NPQ is an intrinsic component of the plant's defense program.
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Crane-Godreau, Mardi A., and Charles R. Wira. "CCL20/Macrophage Inflammatory Protein 3α and Tumor Necrosis Factor Alpha Production by Primary Uterine Epithelial Cells in Response to Treatment with Lipopolysaccharide or Pam3Cys." Infection and Immunity 73, no. 1 (January 2005): 476–84. http://dx.doi.org/10.1128/iai.73.1.476-484.2005.
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ABSTRACT Having previously shown that CCL20/macrophage inflammatory protein 3α and tumor necrosis factor alpha (TNF-α) are released by polarized primary rat uterine epithelial cells (UEC) in response to Escherichia coli but not to Lactobacillus rhamnosus, we sought to determine if epithelial cells are responsive to pathogen-associated molecular patterns (PAMP), including lipopolysaccharide (LPS), lipoteichoic acid (LTA), and Pam3Cys, a bacterial lipoprotein analog. Epithelial cells were grown to confluence on Nunc cell culture inserts prior to apical treatment with PAMPs. In response to LPS, LTA, and Pam3Cys (EMC Microcollection GmbH, Tübingen, Germany), CCL20 levels increased (4- to 10-fold) while PAMPs caused increased TNF-α (1- to 4-fold) in the medium collected after 24 h of incubation. Both apical and basolateral secretion of CCL20 and TNF-α increased in response to PAMPs, but treatments had no effect on cell viability and integrity, as measured by transepithelial resistance. Time course studies of CCL20 and TNF-α release in response to Pam3Cys and LPS indicated that CCL20 release peaked between 2 and 4 h after treatment, whereas TNF-α release was gradual over the length of the incubation. Freeze-thaw and cell lysis experiments, along with actinomycin D studies, suggested that CCL20 and TNF-α are synthesized in response to PAMP stimulation. Taken together, these studies demonstrate that E. coli and selected PAMPs have direct effects on the production of CCL20 and TNF-α without affecting cell integrity. Since CCL20 is known to be both chemotactic and antimicrobial, the increase in apical and basolateral release by UEC in response to PAMPs suggests a new mechanism of innate immune protection in the female reproductive tract.
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Shen, Qiujing, Gildas Bourdais, Huairong Pan, Silke Robatzek, and Dingzhong Tang. "Arabidopsis glycosylphosphatidylinositol-anchored protein LLG1 associates with and modulates FLS2 to regulate innate immunity." Proceedings of the National Academy of Sciences 114, no. 22 (May 15, 2017): 5749–54. http://dx.doi.org/10.1073/pnas.1614468114.
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Plants detect and respond to pathogen invasion with membrane-localized pattern recognition receptors (PRRs), which recognize pathogen-associated molecular patterns (PAMPs) and activate downstream immune responses. Here we report that Arabidopsis thaliana LORELEI-LIKE GPI-ANCHORED PROTEIN 1 (LLG1), a coreceptor of the receptor-like kinase FERONIA, regulates PRR signaling. In a forward genetic screen for suppressors of enhanced disease resistance 1 (edr1), we identified the point mutation llg1-3, which suppresses edr1 disease resistance but does not affect plant growth and development. The llg1 mutants show enhanced susceptibility to various virulent pathogens, indicating that LLG1 has an important role in plant immunity. LLG1 constitutively associates with the PAMP receptor FLAGELLIN SENSING 2 (FLS2) and the elongation factor-Tu receptor, and forms a complex with BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 in a ligand-dependent manner, indicating that LLG1 functions as a key component of PAMP-recognition immune complexes. Moreover, LLG1 contributes to accumulation and ligand-induced degradation of FLS2, and is required for downstream innate immunity responses, including ligand-induced phosphorylation of BOTRYTIS-INDUCED KINASE 1 and production of reactive oxygen species. Taken together, our findings reveal that LLG1 associates with PAMP receptors and modulates their function to regulate disease responses. As LLG1 functions as a coreceptor of FERONIA and plays central roles in plant growth and development, our findings indicate that LLG1 participates in separate pathways, and may suggest a potential connection between development and innate immunity in plants.
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Dilsky, Stefan, and Wolfdieter A. Schenk. "Diastereomeric Halfsandwich Rhenium Complexes Containing Thiolate and Thioaldehyde Ligands." Zeitschrift für Naturforschung B 59, no. 10 (October 1, 2004): 1093–102. http://dx.doi.org/10.1515/znb-2004-1003.
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Abstract The reaction of diastereomeric methyl rhenium complexes [CpRe(NO)(NMDPP)(CH3)] (NMDPP = neomenthyl-diphenylphosphine) and [CpRe(NO)(PAMP)(CH3)] (PAMP = phenyl-2- anisyl-methylphosphine) with thiols in the presence of HBF4 gave thiolate complexes [CpRe(NO)(NMDPP)(SCH2Ph)] and [CpRe(NO)(PAMP)(SCH2R)] (R = Ph, 4-C6H4Cl, 4-C6H4OMe, 2-C4H3O, CH3, CH=CH2). Treatment of [CpRe(NO)(PAMP)(THF)]BF4 with the thiols and Na2CO3 gave the same compounds under neutral conditions. Similarly, the reaction of the chelate complex {CpRe(NO)[κP(Ph)(Me)(CH2C4H3κS)]}BF4 with thiols and NaOEt yielded the ring-opened products {CpRe(NO)[P(Ph)(Me)(CH2C4H3S)](SCH2R)} (R = Ph, 4-C6H4Cl, 4-C6H4OMe). One of the benzylic hydrogen atoms can be abstracted with [Ph3C]BF4 to give the diastereomeric thiobenzaldehyde complexes [CpRe(NO)(PAMP)(S=CHR)]BF4 (R = Ph, 4-C6H4Cl, 4-C6H4OMe) and {CpRe(NO)[P(Ph)(Me)(CH2C4H3S)](S=CHPh)}BF4. In these products, the thioformyl group is predominantly η2(C,S) coordinated to rhenium, but in a few cases the corresponding η1(S) isomers were also detected by IR and NMR spectroscopy.
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Martínez-Herrero, Sonia, and Alfredo Martínez. "Adrenomedullin: Not Just Another Gastrointestinal Peptide." Biomolecules 12, no. 2 (January 18, 2022): 156. http://dx.doi.org/10.3390/biom12020156.
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Adrenomedullin (AM) and proadrenomedullin N-terminal 20 peptide (PAMP) are two bioactive peptides derived from the same precursor with several biological functions including vasodilation, angiogenesis, or anti-inflammation, among others. AM and PAMP are widely expressed throughout the gastrointestinal (GI) tract where they behave as GI hormones, regulating numerous physiological processes such as gastric emptying, gastric acid release, insulin secretion, bowel movements, or intestinal barrier function. Furthermore, it has been recently demonstrated that AM/PAMP have an impact on gut microbiome composition, inhibiting the growth of bacteria related with disease and increasing the number of beneficial bacteria such as Lactobacillus or Bifidobacterium. Due to their wide functions in the GI tract, AM and PAMP are involved in several digestive pathologies such as peptic ulcer, diabetes, colon cancer, or inflammatory bowel disease (IBD). AM is a key protective factor in IBD onset and development, as it regulates cytokine production in the intestinal mucosa, improves vascular and lymphatic regeneration and function and mucosal epithelial repair, and promotes a beneficial gut microbiome composition. AM and PAMP are relevant GI hormones that can be targeted to develop novel therapeutic agents for IBD, other GI disorders, or microbiome-related pathologies.
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Goto, Yukihisa, Noriko Maki, Yasunori Ichihashi, Daisuke Kitazawa, Daisuke Igarashi, Yasuhiro Kadota, and Ken Shirasu. "Exogenous Treatment with Glutamate Induces Immune Responses in Arabidopsis." Molecular Plant-Microbe Interactions® 33, no. 3 (March 2020): 474–87. http://dx.doi.org/10.1094/mpmi-09-19-0262-r.
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Plant resistance inducers (PRIs) are compounds that protect plants from diseases by activating immunity responses. Exogenous treatment with glutamate (Glu), an important amino acid for all living organisms, induces resistance against fungal pathogens in rice and tomato. To understand the molecular mechanisms of Glu-induced immunity, we used the Arabidopsis model system. We found that exogenous treatment with Glu induces resistance against pathogens in Arabidopsis. Consistent with this, transcriptome analyses of Arabidopsis seedlings showed that Glu significantly induces the expression of wound-, defense-, and stress-related genes. Interestingly, Glu activates the expression of genes induced by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns at much later time points than the flg22 peptide, which is a bacterial-derived PAMP. The Glu receptor-like (GLR) proteins GLR3.3 and GLR3.6 are involved in the early expression of Glu-inducible genes; however, the sustained expression of these genes does not require the GLR proteins. Glu-inducible gene expression is also not affected by mutations in genes that encode PAMP receptors (EFR, FLS2, and CERK1), regulators of pattern-triggered immunity (BAK1, BKK1, BIK1, and PBL1), or a salicylic acid biosynthesis enzyme (SID2). The treatment of roots with Glu activates the expression of PAMP-, salicylic acid-, and jasmonic acid-inducible genes in leaves. Moreover, the treatment of roots with Glu primes chitin-induced responses in leaves, possibly through transcriptional activation of LYSIN-MOTIF RECEPTOR-LIKE KINASE 5 (LYK5), which encodes a chitin receptor. Because Glu treatment does not cause discernible growth retardation, Glu can be used as an effective PRI.
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Martinez, A., DL Hodge, M. Garayoa, HA Young, and F. Cuttitta. "Alternative splicing of the proadrenomedullin gene results in differential expression of gene products." Journal of Molecular Endocrinology 27, no. 1 (August 1, 2001): 31–41. http://dx.doi.org/10.1677/jme.0.0270031.
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The adrenomedullin (AM) gene codifies for two bioactive peptides, AM and proAM N-terminal 20 peptide (PAMP). We have found two forms of the AM mRNA. Form A is devoid of introns and results in a prohormone containing both peptides. Form B retains the third intron, which introduces a premature stop codon, producing a shorter prohormone with only PAMP. Tissues with a higher B/A ratio were more immunoreactive for PAMP than for AM. The form B message was found in the cytoplasmic compartment, thus excluding that the longer message was a result of contaminating nuclear mRNA. Form B was found in cells that express PAMP but not AM. mRNA expression in a variety of cell lines was investigated by ribonuclease protection assay and form B was found in significant amounts in two of them. Treatments that modify AM expression, such as exposure to hypoxia, were shown to change the B/A ratio and the relative secretion of AM and PAMP, indicating that the splicing mechanism for AM can be modulated and is physiologically relevant. Analysis of the sequence of the third intron and the fourth exon of the AM gene found motifs compatible with a highly regulated alternative splicing mechanism.
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Xia, Lin, Zhongqiu Wang, Ying Zhang, Xiao Yang, Yibei Zhan, Rui Cheng, Shiming Wang, and Jianfa Zhang. "Reciprocal regulation of insulin and plasma 5′-AMP in glucose homeostasis in mice." Journal of Endocrinology 224, no. 3 (December 15, 2014): 225–34. http://dx.doi.org/10.1530/joe-14-0501.
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A previous investigation has demonstrated that plasma 5′-AMP (pAMP) exacerbates and causes hyperglycemia in diabetic mice. However, the crosstalk between pAMP and insulin signaling to regulate glucose homeostasis has not been investigated in depth. In this study, we showed that the blood glucose level was more dependent on the ratio of insulin to pAMP than on the absolute level of these two factors. Administration of 5′-AMP significantly attenuated the insulin-stimulated insulin receptor (IR) autophosphorylation in the liver and muscle tissues, resulting in the inhibition of downstream AKT phosphorylation. A docking analysis indicated that adenosine was a potential inhibitor of IR tyrosine kinase. Moreover, the 5′-AMP treatment elevated the ATP level in the pancreas and in the isolated islets, stimulating insulin secretion and increasing the plasma level of insulin. The insulin administration decreased the 5′-AMP-induced hyper-adenosine level by the up-regulation of adenosine kinase activities. Our results indicate that blood glucose homeostasis is reciprocally regulated by pAMP and insulin.
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Suresh, J., N. M. Mahesh, J. Ahuja, and K. S. Santilna. "Review onArtemisia nilagirica(Clarke) Pamp." Journal of Biologically Active Products from Nature 1, no. 2 (January 2011): 97–104. http://dx.doi.org/10.1080/22311866.2011.10719075.
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Jutila, Mark A., Jeff Holderness, Jill C. Graff, and Jodi F. Hedges. "Antigen-independent priming: a transitional response of bovine γδ T-cells to infection." Animal Health Research Reviews 9, no. 1 (March 17, 2008): 47–57. http://dx.doi.org/10.1017/s1466252307001363.
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AbstractAnalysis of global gene expression in immune cells has provided unique insights into immune system function and response to infection. Recently, we applied microarray and serial analysis of gene expression (SAGE) techniques to the study of γδ T-cell function in humans and cattle. The intent of this review is to summarize the knowledge gained since our original comprehensive studies of bovine γδ T-cell subsets. More recently, we have characterized the effects of mucosal infection or treatment with microbial products or mitogens on gene expression patterns in sorted γδ and αβ T-cells. These studies provided new insights into the function of bovine γδ T-cells and led to a model in which response to pathogen-associated molecular patterns (PAMPs) induces ‘priming’ of γδ T-cells, resulting in more robust responses to downstream cytokine and/or antigen signals. PAMP primed γδ T-cells are defined by up-regulation of a select number of cytokines, including MIP1α and MIP1β, and by antigens such as surface IL2 receptor α (IL-2Rα) and CD69, in the absence of a prototypic marker for an activated γδ T-cell, IFN-γ. Furthermore, PAMP primed γδ T-cells are more capable of proliferation in response to IL-2 or IL-15 in the absence of antigen. PAMPs such as endotoxin, peptidoglycan and β-glucan are effective γδ T-cell priming agents, but the most potent antigen-independent priming agonists defined to date are condensed oligomeric tannins produced by some plants.
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Andersson, Ulf, Kevin J. Tracey, and Huan Yang. "Post-Translational Modification of HMGB1 Disulfide Bonds in Stimulating and Inhibiting Inflammation." Cells 10, no. 12 (November 26, 2021): 3323. http://dx.doi.org/10.3390/cells10123323.
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High mobility group box 1 protein (HMGB1), a highly conserved nuclear DNA-binding protein, is a “damage-associated molecular pattern” molecule (DAMP) implicated in both stimulating and inhibiting innate immunity. As reviewed here, HMGB1 is an oxidation-reduction sensitive DAMP bearing three cysteines, and the post-translational modification of these residues establishes its proinflammatory and anti-inflammatory activities by binding to different extracellular cell surface receptors. The redox-sensitive signaling mechanisms of HMGB1 also occupy an important niche in innate immunity because HMGB1 may carry other DAMPs and pathogen-associated molecular pattern molecules (PAMPs). HMGB1 with DAMP/PAMP cofactors bind to the receptor for advanced glycation end products (RAGE) which internalizes the HMGB1 complexes by endocytosis for incorporation in lysosomal compartments. Intra-lysosomal HMGB1 disrupts lysosomal membranes thereby releasing the HMGB1-transported molecules to stimulate cytosolic sensors that mediate inflammation. This HMGB1-DAMP/PAMP cofactor pathway slowed the development of HMGB1-binding antagonists for diagnostic or therapeutic use. However, recent discoveries that HMGB1 released from neurons mediates inflammation via the TLR4 receptor system, and that cancer cells express fully oxidized HMGB1 as an immunosuppressive mechanism, offer new paths to targeting HMGB1 for inflammation, pain, and cancer.
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Peng, Yujun, Rowan van Wersch, and Yuelin Zhang. "Convergent and Divergent Signaling in PAMP-Triggered Immunity and Effector-Triggered Immunity." Molecular Plant-Microbe Interactions® 31, no. 4 (April 2018): 403–9. http://dx.doi.org/10.1094/mpmi-06-17-0145-cr.
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Plants use diverse immune receptors to sense pathogen attacks. Recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors localized on the plasma membrane leads to PAMP-triggered immunity (PTI). Detection of pathogen effectors by intracellular or plasma membrane–localized immune receptors results in effector-triggered immunity (ETI). Despite the large variations in the magnitude and duration of immune responses triggered by different PAMPs or pathogen effectors during PTI and ETI, plasma membrane–localized immune receptors activate similar downstream molecular events such as mitogen-activated protein kinase activation, oxidative burst, ion influx, and increased biosynthesis of plant defense hormones, indicating that defense signals initiated at the plasma membrane converge at later points. On the other hand, activation of ETI by immune receptors localized to the nucleus appears to be more directly associated with transcriptional regulation of defense gene expression. Here, we review recent progress in signal transductions downstream of different groups of plant immune receptors, highlighting the converging and diverging molecular events.
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Yamamoto, Ayumi, Noriko N. Miura, Toshiaki Oharaseki, Kei Takahashi, Shiro Naoe, Kazuo Suzuki, and Naohito Ohno. "Suppression of PAMPs, Pathogen-Associated Microbial Patterns, Induced Cytokine Synthesis of PBMC, Human Blood Mononuclear Cells, by Immunoglobulin Preparation." Open Allergy Journal 5, no. 1 (August 24, 2012): 53–61. http://dx.doi.org/10.2174/1874838401205010053.
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The applications of immunoglobulin preparation for intravenous injection (IVIg) for various intractable diseases are increasing. The two major clinical indications for IVIg are the replacement therapy and the anti-inflammation therapy for a variety of acute and chronic autoimmune diseases. One of the proposed mechanisms of IVIg activity is the modulation of cytokine expression and function; therefore, we analyzed the effect of IVIg on pathogen-associated molecular pattern (PAMP)-induced cytokine production by peripheral blood mononuclear cells (PBMCs). The production of tumor necrosis factor-α (TNF-α) as a result of stimulation with lipopolysaccharide (LPS), polyinosinic-polycytidylic acid sodium salt (Poly I:C), or Pam3CysSerLys4 (Pam3) was significantly inhibited by sulfonated-IVIg (S-IVIg), or by F(ab')2. Assessed by one-color microarray analysis, the expressions of 229 genes were inhibited to 1/200 or less by F(ab')2. On the other hand, the expressions of 159 genes were increased by more than 100-fold by F(ab')2. According to these results, it was suggested that IVIg inhibits inflammatory PAMPs-induced cytokine production by PBMCs, due to the modulation of varieties of gene expression.
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Faye, Therese, Dag Anders Brede, Thor Langsrud, Ingolf F. Nes, and Helge Holo. "Prevalence of the Genes Encoding Propionicin T1 and Protease-Activated Antimicrobial Peptide and Their Expression in Classical Propionibacteria." Applied and Environmental Microbiology 70, no. 4 (April 2004): 2240–44. http://dx.doi.org/10.1128/aem.70.4.2240-2244.2004.
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ABSTRACT The purpose of this study was to investigate the frequency of production of the bacteriocin propionicin T1 and the protease-activated antimicrobial peptide (PAMP) and their corresponding genes in 64 isolates of classical propionibacteria. This study revealed that these genes are widespread in Propionibacterium jensenii and Propionibacterium thoenii but absent from the remaining species of classical propionibacteria that were studied. The pro-PAMP-encoding gene (pamA) was found in 63% of the P. jensenii strains and 61% of the P. thoenii strains, and all of these strains displayed PAMP activity. The propionicin T1-encoding gene (pctA) was present in 89% of the P. thoenii strains and 54% of the P. jensenii strains. All P. thoenii strains containing the pctA gene exhibited antimicrobial activity corresponding to propionicin T1 activity, whereas only 38% of the pctA-containing P. jensenii strains displayed this activity. Sequencing of the pctA genes revealed the existence of two allelic variants that differed in a single nucleotide in six strains of P. jensenii; in these strains the glycine at position 55 of propionicin T1 was replaced by an aspartate residue (A variant). No strains harboring the A variant showed any antimicrobial activity against propionicin T1-sensitive bacteria. An open reading frame (orf2) located immediately downstream from the pctA gene was absent in three strains containing the G variant of propionicin T1. Two of these strains showed low antimicrobial activity, while the third strain showed no antimicrobial activity at all. The protein encoded by orf2 showed strong homology to ABC transporters, and it has been proposed previously that this protein is involved in the producer immunity against propionicin T1. The limited antimicrobial activity exhibited by the strains lacking orf2 further suggests that this putative ABC transporter plays an important role in propionicin T1 activity.
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Masada, Kimiya, Takahiro Nagayama, Akio Hosokawa, Makoto Yoshida, Mizue Suzuki-Kusaba, Hiroaki Hisa, Tomohiko Kimura, and Susumu Satoh. "Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (April 1, 1999): R1118—R1124. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r1118.
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We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 μg) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng ⋅ kg−1 ⋅ min−1) or its selective antagonist adrenomedullin-(22—52) (5, 15, and 50 ng ⋅ kg−1 ⋅ min−1). Proadrenomedullin NH2-terminal 20 peptide (PAMP; 5, 15, and 50 ng ⋅ kg−1 ⋅ min−1) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 μg) and to muscarine (0.5, 1, and 2 μg), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.
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Zhang, Ying, Zhongqiu Wang, Yue Zhao, Ming Zhao, Shiming Wang, Zichun Hua, and Jianfa Zhang. "The plasma 5′-AMP acts as a potential upstream regulator of hyperglycemia in type 2 diabetic mice." American Journal of Physiology-Endocrinology and Metabolism 302, no. 3 (February 2012): E325—E333. http://dx.doi.org/10.1152/ajpendo.00424.2011.
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Increased plasma free fatty acid (FFA) level is a hallmark of type 2 diabetes. However, the underlying molecular basis for FFA-caused hyperglycemia remains unclear. Here we identified plasma 5′-adenosine monophosphate (pAMP) markedly elevated in the plasma of type 2 diabetic mice. High levels of FFAs induced damage in vein endothelial cells and contributed to an increase in pAMP. Administration of synthetic 5′-AMP caused hyperglycemia and impaired insulin action in lean wild-type mice. 5′-AMP elevated blood glucose in mice deficient in adenosine receptors with equal efficiency as wild-type mice. The function of pAMP was initiated by the elevation of cellular adenosine levels, directly stimulating G-6-Pase enzyme activity, attenuating insulin-dependent GLUT4 translocation in skeletal muscle, and displaying a rapid and steep increase in blood glucose and a decrease in hepatic glycogen level. It was followed by an increase in the gene expression of hepatic Foxo1 and its targeting gene Pepck and G6Pase, which was similar to diabetic phenotype in db/db mice. Our results suggest that pAMP is a potential upstream regulator of hyperglycemia in type 2 diabetes.
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Pandya, Unnati, Chinaza Egbuta, Trefa Abdullah Norman, Chih-Yuan Chiang, Valerie Wiersma, Rekha Panchal, Edwin Bremer, Paul Eggleton, and Leslie Gold. "The Biophysical Interaction of the Danger-Associated Molecular Pattern (DAMP) Calreticulin with the Pattern-Associated Molecular Pattern (PAMP) Lipopolysaccharide." International Journal of Molecular Sciences 20, no. 2 (January 18, 2019): 408. http://dx.doi.org/10.3390/ijms20020408.
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The endoplasmic reticulum (ER) chaperone protein, calreticulin (CRT), is essential for proper glycoprotein folding and maintaining cellular calcium homeostasis. During ER stress, CRT is overexpressed as part of the unfolded protein response (UPR). In addition, CRT can be released as a damage-associated molecular pattern (DAMP) molecule that may interact with pathogen-associated molecular patterns (PAMPs) during the innate immune response. One such PAMP is lipopolysaccharide (LPS), a component of the gram-negative bacterial cell wall. In this report, we show that recombinant and native human placental CRT strongly interacts with LPS in solution, solid phase, and the surface of gram-negative and gram-positive bacteria. Furthermore, LPS induces oilgomerization of CRT with a disappearance of the monomeric form. The application of recombinant CRT (rCRT) to size exclusion and anion exchange chromatography shows an atypical heterogeneous elution profile, indicating that LPS affects the conformation and ionic charge of CRT. Interestingly, LPS bound to CRT is detected in sera of bronchiectasis patients with chronic bacterial infections. By ELISA, rCRT dose-dependently bound to solid phase LPS via the N- and C-domain globular head region of CRT and the C-domain alone. The specific interaction of CRT with LPS may be important in PAMP innate immunity.
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Sun, Lifan, and Jie Zhang. "Regulatory role of receptor-like cytoplasmic kinases in early immune signaling events in plants." FEMS Microbiology Reviews 44, no. 6 (July 27, 2020): 845–56. http://dx.doi.org/10.1093/femsre/fuaa035.
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ABSTRACT Receptor-like cytoplasmic kinases (RLCKs) play crucial roles in regulating plant development and immunity. Conserved pathogen-associated molecular patterns (PAMPs) derived from microbes are recognized by plant pattern recognition receptors to activate PAMP-triggered immunity (PTI). Microbial effectors, whose initial function is to promote virulence, are recognized by plant intracellular nucleotide-binding domain and leucine-rich repeat receptors (NLRs) to initiate effector-triggered immunity (ETI). Both PTI and ETI trigger early immune signaling events including the production of reactive oxygen species, induction of calcium influx and activation of mitogen-activated protein kinases. Research progress has revealed the important roles of RLCKs in the regulation of early PTI signaling. Accordingly, RLCKs are often targeted by microbial effectors that are evolved to evade PTI via diverse modulations. In some cases, modulation of RLCKs by microbial effectors triggers the activation of NLRs. This review covers the mechanisms by which RLCKs engage diverse substrates to regulate early PTI signaling and the regulatory roles of RLCKs in triggering NLR activation. Accumulating evidence suggests evolutionary links and close connections between PAMP- and effector-triggered early immune signaling that are mediated by RLCKs. As key immune regulators, RLCKs can be considered targets with broad prospects for the improvement of plant resistance via genetic engineering.
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Crane-Godreau, Mardi A., and Charles R. Wira. "Effects of Estradiol on Lipopolysaccharide and Pam3Cys Stimulation of CCL20/Macrophage Inflammatory Protein 3 Alpha and Tumor Necrosis Factor Alpha Production by Uterine Epithelial Cells in Culture." Infection and Immunity 73, no. 7 (July 2005): 4231–37. http://dx.doi.org/10.1128/iai.73.7.4231-4237.2005.
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ABSTRACT We have previously demonstrated that rat uterine epithelial cells (UEC) produce CCL20/macrophage inflammatory protein 3 alpha (MIP3α) and tumor necrosis factor alpha (TNF-α) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys. To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3α and TNF-α secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h. E2 inhibited the constitutive secretion of TNF-α and CCL20/MIP3α into culture media. Interestingly, E2 pretreatment enhanced CCL20/MIP3α secretion due to LPS and Pam3Cys administration. In contrast, and at the same time, E2 lowered the TNF-α response to both PAMP. To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial cells were incubated with E2 and/or ICI 182,780, a known ER antagonist. ICI 182,780 had no effect on E2 inhibition of constitutive TNF-α and CCL20/MIP3α secretion. In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3α secretion as well as partially reversed the inhibitory effect of E2 on TNF-α production by epithelial cells. Overall, these results indicate that E2 regulates the production of TNF-α and CCL20/MIP3α by UEC in the absence as well as presence of PAMP. Since CCL20/MIP3α has antimicrobial activity and is chemotactic for immune cells, these studies suggest that regulation of CCL20/MIP3α and TNF-α by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.
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Hong, Jung-Hee, Jeong-Lan Jeon, Ju-Hyun Lee, and In-Seon Lee. "Antioxidative Properties of Artemisia princeps Pamp." Journal of the Korean Society of Food Science and Nutrition 36, no. 6 (June 30, 2007): 657–62. http://dx.doi.org/10.3746/jkfn.2007.36.6.657.
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Scanlon, Seth Thomas. "SAA1 sees PAMP in the mite." Science 369, no. 6501 (July 16, 2020): 265.5–266. http://dx.doi.org/10.1126/science.369.6501.265-e.
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Nguyen, Hanh P., Suma Chakravarthy, André C. Velásquez, Heather L. McLane, Lirong Zeng, Hitoshi Nakayashiki, Duck-Hwan Park, Alan Collmer, and Gregory B. Martin. "Methods to Study PAMP-Triggered Immunity Using Tomato and Nicotiana benthamiana." Molecular Plant-Microbe Interactions® 23, no. 8 (August 2010): 991–99. http://dx.doi.org/10.1094/mpmi-23-8-0991.
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Understanding the molecular basis of plant responses to pathogen-associated molecular patterns (PAMPs) is an active area of research in the field of plant–microbe interactions. A growing number of plant genes involved in various steps of PAMP-triggered immunity (PTI) pathways and microbial factors involved in the elicitation or suppression of PTI have been identified. These studies have largely relied on Arabidopsis thaliana and, therefore, most of the PTI assays have been developed and optimized for that model plant system. Although PTI is a conserved feature among plants, the response spectra vary across different species. Thus, there is a need for robust PTI assays in other pathosystems, such as those involving Solanaceae plant–pathogen interactions, which include many economically important plants and their diseases. We have optimized molecular, cellular, and whole-plant methods to measure PTI responses in two widely studied solanaceous species, tomato (Solanum lycopersicum) and Nicotiana benthamiana. Here, we provide detailed protocols for measuring various PTI-associated phenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition, activation of mitogen-activated protein kinases, and a luciferase-based reporter system. These methods will facilitate limited genetic screens and detailed characterization of potential PTI-related genes in model and economically important Solanaceae spp.–pathogen interactions.
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Chen, Shiu-Jau, Tzer-Bin Lin, Hsien-Yu Peng, Cheng-Hsien Lin, An-Sheng Lee, Hsiang-Jui Liu, Chun-Chieh Li, and Kuang-Wen Tseng. "Protective Effects of Fucoxanthin Dampen Pathogen-Associated Molecular Pattern (PAMP) Lipopolysaccharide-Induced Inflammatory Action and Elevated Intraocular Pressure by Activating Nrf2 Signaling and Generating Reactive Oxygen Species." Antioxidants 10, no. 7 (July 7, 2021): 1092. http://dx.doi.org/10.3390/antiox10071092.
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Inflammation and oxidative stress are closely related processes in the pathogenesis of various ocular diseases. Uveitis is a disorder of the uvea and ocular tissues that causes extreme pain, decreases visual acuity, and can eventually lead to blindness. The pharmacological functions of fucoxanthin, isolated from brown algae, induce a variety of therapeutic effects such as oxidative stress reduction and repression of inflammation reactions. However, the specific anti-inflammatory effects of fucoxanthin on pathogen-associated molecular pattern (PAMP) lipopolysaccharide-induced uveitis have yet to be extensively described. Therefore, the aim of present study was to investigate the anti-inflammatory effects of fucoxanthin on uveitis in rats. The results showed that fucoxanthin effectively enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in ocular tissues. Furthermore, fucoxanthin significantly increased the ocular activities of superoxide dismutase and decreased the levels of malondialdehyde stimulated by PAMP-induced uveitis. Ocular hypertension and the levels of inflammatory cells and proinflammatory cytokine tumor necrosis factor-alpha in the aqueous humor were alleviated with fucoxanthin treatment. Consequently, compared to the observed effects in lipopolysaccharide groups, fucoxanthin treatment significantly preserved iris sphincter innervation and pupillary function. Additionally, PAMP-induced corneal endothelial disruption was significantly inhibited by fucoxanthin treatment. Overall, these findings suggest that fucoxanthin may protect against inflammation from PAMP-induced uveitis by promoting the Nrf2 pathway and inhibiting oxidative stress.
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Noh, Ji-Yoon, Suk Ran Yoon, Tae-Don Kim, Inpyo Choi, and Haiyoung Jung. "Toll-Like Receptors in Natural Killer Cells and Their Application for Immunotherapy." Journal of Immunology Research 2020 (January 4, 2020): 1–9. http://dx.doi.org/10.1155/2020/2045860.
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Innate immunity represents the first barrier for host defense against microbial infection. Toll-like receptors (TLRs) are the most well-defined PRRs with respect to PAMP recognition and induction of innate immune responses. They recognize pathogen-associated molecular patterns (PAMPs) and trigger innate immune responses by inducing inflammatory cytokines, chemokines, antigen-presenting molecules, and costimulatory molecules. TLRs are expressed either on the cell surface or within endosomes of innate immune cells. NK cells are one of the innate immune cells and also express TLRs to recognize or respond to PAMPs. TLRs in NK cells induce the innate immune responses against bacterial and viral infections via inducing NK cytotoxicity and cytokine production. In this review, we will discuss the expression and cellular function of TLRs in NK cells and also introduce some therapeutic applications of TLR agonists for NK cell-mediated immunotherapy.
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Saur, Isabel M. L., Yasuhiro Kadota, Jan Sklenar, Nicholas J. Holton, Elwira Smakowska, Youssef Belkhadir, Cyril Zipfel, and John P. Rathjen. "NbCSPR underlies age-dependent immune responses to bacterial cold shock protein inNicotiana benthamiana." Proceedings of the National Academy of Sciences 113, no. 12 (March 4, 2016): 3389–94. http://dx.doi.org/10.1073/pnas.1511847113.
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Plants use receptor kinases (RKs) and receptor-like proteins (RLPs) as pattern recognition receptors (PRRs) to sense pathogen-associated molecular patterns (PAMPs) that are typical of whole classes of microbes. After ligand perception, many leucine-rich repeat (LRR)-containing PRRs interact with the LRR-RK BRI1-ASSOCIATED KINASE 1 (BAK1). BAK1 is thus expected to interact with unknown PRRs. Here, we used BAK1 as molecular bait to identify a previously unknown LRR-RLP required for the recognition of the csp22 peptide derived from bacterial cold shock protein. We established a method to identify proteins that interact with BAK1 only after csp22 treatment. BAK1 was expressed transiently inNicotiana benthamianaand immunopurified after treatment with csp22. BAK1-associated proteins were identified by mass spectrometry. We identified several proteins including known BAK1 interactors and a previously uncharacterized LRR-RLP that we termed RECEPTOR-LIKE PROTEIN REQUIRED FOR CSP22 RESPONSIVENESS (NbCSPR). This RLP associates with BAK1 upon csp22 treatment, andNbCSPR-silenced plants are impaired in csp22-induced defense responses.NbCSPRconfers resistance to bacteria in an age-dependent and flagellin-induced manner. As such, it limits bacterial growth andAgrobacterium-mediated transformation of floweringN. benthamianaplants. Transgenic expression ofNbCSPRintoArabidopsis thalianaconferred responsiveness to csp22 and antibacterial resistance. Our method may be used to identify LRR-type RKs and RLPs required for PAMP perception/responsiveness, even when the active purified PAMP has not been defined.
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Oth, Tammy, Joris Vanderlocht, Catharina H. M. J. Van Elssen, Gerard M. J. Bos, and Wilfred T. V. Germeraad. "Pathogen-Associated Molecular Patterns Induced Crosstalk between Dendritic Cells, T Helper Cells, and Natural Killer Helper Cells Can Improve Dendritic Cell Vaccination." Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/5740373.
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A coordinated cellular interplay is of crucial importance in both host defense against pathogens and malignantly transformed cells. The various interactions of Dendritic Cells (DC), Natural Killer (NK) cells, and T helper (Th) cells can be influenced by a variety of pathogen-associated molecular patterns (PAMPs) and will lead to enhanced CD8+effector T cell responses. Specific Pattern Recognition Receptor (PRR) triggering during maturation enables DC to enhance Th1 as well as NK helper cell responses. This effect is correlated with the amount of IL-12p70 released by DC. Activated NK cells are able to amplify the proinflammatory cytokine profile of DC via the release of IFN-γ. The knowledge on how PAMP recognition can modulate the DC is of importance for the design and definition of appropriate therapeutic cancer vaccines. In this review we will discuss the potential role of specific PAMP-matured DC in optimizing therapeutic DC-based vaccines, as some of these DC are efficiently activating Th1, NK cells, and cytotoxic T cells. Moreover, to optimize these vaccines, also the inhibitory effects of tumor-derived suppressive factors, for example, on the NK-DC crosstalk, should be taken into account. Finally, the suppressive role of the tumor microenvironment in vaccination efficacy and some proposals to overcome this by using combination therapies will be described.
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Spears, Benjamin J., T. C. Howton, Fei Gao, Christopher M. Garner, M. Shahid Mukhtar, and Walter Gassmann. "Direct Regulation of the EFR-Dependent Immune Response by Arabidopsis TCP Transcription Factors." Molecular Plant-Microbe Interactions® 32, no. 5 (May 2019): 540–49. http://dx.doi.org/10.1094/mpmi-07-18-0201-fi.
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One layer of the innate immune system allows plants to recognize pathogen-associated molecular patterns (PAMPS), activating a defense response known as PAMP-triggered immunity (PTI). Maintaining an active immune response, however, comes at the cost of plant growth and development; accordingly, optimization of the balance between defense and development is critical to plant fitness. The TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTOR (TCP) transcription factor family consists of well-characterized transcriptional regulators of plant development and morphogenesis. The three closely related class I TCP transcription factors TCP8, TCP14, and TCP15 have also been implicated in the regulation of effector-triggered immunity, but there has been no previous characterization of PTI-related phenotypes. To identify TCP targets involved in PTI, we screened a PAMP-induced gene promoter library in a yeast one-hybrid assay and identified interactions of these three TCPs with the EF-Tu RECEPTOR (EFR) promoter. The direct interactions between TCP8 and EFR were confirmed to require an intact TCP binding site in planta. A tcp8 tcp14 tcp15 triple mutant was impaired in EFR-dependent PTI and exhibited reduced levels of PATHOGENESIS-RELATED PROTEIN 2 and induction of EFR expression after elicitation with elf18 but also increased production of reactive oxygen species relative to Col-0. Our data support an increasingly complex role for TCPs at the nexus of plant development and defense.