Journal articles: 'Antimicrobial chemokine'

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Chensue, Stephen W. "Molecular Machinations: Chemokine Signals in Host-Pathogen Interactions." Clinical Microbiology Reviews 14, no. 4 (October 1, 2001): 821–35. http://dx.doi.org/10.1128/cmr.14.4.821-835.2001.

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SUMMARY Chemokines and their G-protein-coupled receptors represent an ancient and complex system of cellular communication participating in growth, development, homeostasis and immunity. Chemokine production has been detected in virtually every microbial infection examined; however, the precise role of chemokines is still far from clear. In most cases they appear to promote host resistance by mobilizing leukocytes and activating immune functions that kill, expel, or sequester pathogens. In other cases, the chemokine system has been pirated by pathogens, especially protozoa and viruses, which have exploited host chemokine receptors as modes of cellular invasion or developed chemokine mimics and binding proteins that act as antagonists or inappropriate agonists. Understanding microbial mechanisms of chemokine evasion will potentially lead to novel antimicrobial and anti-inflammatory therapeutic agents.

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Crawford, Matthew A., Yinghua Zhu, Candace S. Green, Marie D. Burdick, Patrick Sanz, Farhang Alem, Alison D. O'Brien, Borna Mehrad, Robert M. Strieter, and Molly A. Hughes. "Antimicrobial Effects of Interferon-Inducible CXC Chemokines against Bacillus anthracis Spores and Bacilli." Infection and Immunity 77, no. 4 (January 29, 2009): 1664–78. http://dx.doi.org/10.1128/iai.01208-08.

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ABSTRACT Based on previous studies showing that host chemokines exert antimicrobial activities against bacteria, we sought to determine whether the interferon-inducible Glu-Leu-Arg-negative CXC chemokines CXCL9, CXCL10, and CXCL11 exhibit antimicrobial activities against Bacillus anthracis. In vitro analysis demonstrated that all three CXC chemokines exerted direct antimicrobial effects against B. anthracis spores and bacilli including marked reductions in spore and bacillus viability as determined using a fluorometric assay of bacterial viability and CFU determinations. Electron microscopy studies revealed that CXCL10-treated spores failed to undergo germination as judged by an absence of cytological changes in spore structure that occur during the process of germination. Immunogold labeling of CXCL10-treated spores demonstrated that the chemokine was located internal to the exosporium in association primarily with the spore coat and its interface with the cortex. To begin examining the potential biological relevance of chemokine-mediated antimicrobial activity, we used a murine model of inhalational anthrax. Upon spore challenge, the lungs of C57BL/6 mice (resistant to inhalational B. anthracis infection) had significantly higher levels of CXCL9, CXCL10, and CXCL11 than did the lungs of A/J mice (highly susceptible to infection). Increased CXC chemokine levels were associated with significantly reduced levels of spore germination within the lungs as determined by in vivo imaging. Taken together, our data demonstrate a novel antimicrobial role for host chemokines against B. anthracis that provides unique insight into host defense against inhalational anthrax; these data also support the notion for an innovative approach in treating B. anthracis infection as well as infections caused by other spore-forming organisms.

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Boink, Mireille A., Sanne Roffel, Kamran Nazmi, Jan G. M. Bolscher, Enno C. I. Veerman, and Susan Gibbs. "Saliva-Derived Host Defense Peptides Histatin1 and LL-37 Increase Secretion of Antimicrobial Skin and Oral Mucosa Chemokine CCL20 in an IL-1α-Independent Manner." Journal of Immunology Research 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/3078194.

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Even though skin and oral mucosae are continuously in contact with commensal and opportunistic microorganisms, they generally remain healthy and uninflamed. Host defense peptides (HDPs) make up the body’s first line of defense against many invading pathogens and are involved in the orchestration of innate immunity and the inflammatory response. In this study, we investigated the effect of two salivary HDPs, LL-37 and Hst1, on the inflammatory and antimicrobial response by skin and oral mucosa (gingiva) keratinocytes and fibroblasts. The potent antimicrobial chemokine CCL20 was investigated and compared with chemokines CCL2, CXCL1, CXCL8, and CCL27 and proinflammatory cytokines IL-1αand IL-6. Keratinocyte-fibroblast cocultures showed a synergistic increase in CCL20 secretion upon Hst1 and LL-37 exposure compared to monocultures. These cocultures also showed increased IL-6, CXCL1, CXCL8, and CCL2 secretion, which was IL-1αdependent. Secretion of the antimicrobial chemokine CCL20 was clearly IL-1αindependent. These results indicate that salivary peptides can stimulate skin as well as gingiva cells to secrete antimicrobial chemokines as part of the hosts’ defense to counteract infection.

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Dishman, Acacia F., Jie He, Brian F. Volkman, and Anna R. Huppler. "Metamorphic Protein Folding Encodes Multiple Anti-Candida Mechanisms in XCL1." Pathogens 10, no. 6 (June 17, 2021): 762. http://dx.doi.org/10.3390/pathogens10060762.

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Candida species cause serious infections requiring prolonged and sometimes toxic therapy. Antimicrobial proteins, such as chemokines, hold great interest as potential additions to the small number of available antifungal drugs. Metamorphic proteins reversibly switch between multiple different folded structures. XCL1 is a metamorphic, antimicrobial chemokine that interconverts between the conserved chemokine fold (an α–β monomer) and an alternate fold (an all-β dimer). Previous work has shown that human XCL1 kills C. albicans but has not assessed whether one or both XCL1 folds perform this activity. Here, we use structurally locked engineered XCL1 variants and Candida killing assays, adenylate kinase release assays, and propidium iodide uptake assays to demonstrate that both XCL1 folds kill Candida, but they do so via different mechanisms. Our results suggest that the alternate fold kills via membrane disruption, consistent with previous work, and the chemokine fold does not. XCL1 fold-switching thus provides a mechanism to regulate the XCL1 mode of antifungal killing, which could protect surrounding tissue from damage associated with fungal membrane disruption and could allow XCL1 to overcome candidal resistance by switching folds. This work provides inspiration for the future design of switchable, multifunctional antifungal therapeutics.

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Lucero, Carissa M., Beth Fallert Junecko, Cynthia R. Klamar, Lauren A. Sciullo, Stella J. Berendam, Anthony R. Cillo, Shulin Qin, et al. "Macaque Paneth Cells Express Lymphoid Chemokine CXCL13 and Other Antimicrobial Peptides Not Previously Described as Expressed in Intestinal Crypts." Clinical and Vaccine Immunology 20, no. 8 (June 26, 2013): 1320–28. http://dx.doi.org/10.1128/cvi.00651-12.

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ABSTRACTCXCL13 is a constitutively expressed chemokine that controls migration of immune cells to lymphoid follicles. Previously, we found CXCL13 mRNA levels increased in rhesus macaque spleen tissues during AIDS. This led us to examine the levels and locations of CXCL13 by detailedin situmethods in cynomolgus macaque lymphoid and intestinal tissues. Our results revealed that there were distinct localization patterns of CXCL13 mRNA compared to protein in germinal centers. These patterns shifted during the course of simian immunodeficiency virus (SIV) infection, with increased mRNA expression within and around follicles during AIDS compared to uninfected or acutely infected animals. Unexpectedly, CXCL13 expression was also found in abundance in Paneth cells in crypts throughout the small intestine. Therefore, we expanded our analyses to include chemokines and antimicrobial peptides (AMPs) not previously demonstrated to be expressed by Paneth cells in intestinal tissues. We examined the expression patterns of multiple chemokines, including CCL25, as well as α-defensin 6 (DEFA6), β-defensin 2 (BDEF2), rhesus θ-defensin 1 (RTD-1), and Reg3γin situin intestinal tissues. Of the 10 chemokines examined, CXCL13 was unique in its expression by Paneth cells. BDEF2, RTD-1, and Reg3γ were also expressed by Paneth cells. BDEF2 and RTD-1 previously have not been shown to be expressed by Paneth cells. These findings expand our understanding of mucosal immunology, innate antimicrobial defenses, homeostatic chemokine function, and host protective mechanisms against microbial translocation.

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Xiao, Xun, Yanqi Zhang, Zhiwei Liao, and Jianguo Su. "Characterization and Antimicrobial Activity of the Teleost Chemokine CXCL20b." Antibiotics 9, no. 2 (February 12, 2020): 78. http://dx.doi.org/10.3390/antibiotics9020078.

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Fish are a potential source of diverse organic compounds with a broad spectrum of biological activities. Many fish-derived antimicrobial peptides and proteins are key components of the fish innate immune system. They are also potential candidates for development of new antimicrobial agents. CXCL20b is a grass carp (Ctenopharyngodon idella) CXC chemokine strongly transcribed at the early stage of bacterial infections, for which the immune role had not been reported to date. In the present study, we found that CXCL20b is a cationic amphipathic protein that displays potent antimicrobial activity against both Gram-positive and Gram-negative bacteria. The results of DiOC2(3) and atomic force microscopy (AFM) assays indicated that CXCL20b could induce bacterial membrane depolarization and disruption in a short time. By performing further structure-activity studies, we found that the antimicrobial activity of CXCL20b was mainly relative to the N-terminal random coil region. The central part of this cytokine representing β-sheet region was insoluble in water and the C-terminal α-helical region did not show an antimicrobial effect. The results presented in this article support the poorly understood function of CXCL20b, which fulfills an important role in bony fish antimicrobial immunity.

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Valdivia-Silva, Julio, Jaciel Medina-Tamayo, and Eduardo Garcia-Zepeda. "Chemokine-Derived Peptides: Novel Antimicrobial and Antineoplasic Agents." International Journal of Molecular Sciences 16, no. 12 (June 8, 2015): 12958–85. http://dx.doi.org/10.3390/ijms160612958.

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Schutte, Kirsten M., Debra J. Fisher, Marie D. Burdick, Borna Mehrad, Amy J. Mathers, Barbara J. Mann, Robert K. Nakamoto, and Molly A. Hughes. "Escherichia coli Pyruvate Dehydrogenase Complex Is an Important Component of CXCL10-Mediated Antimicrobial Activity." Infection and Immunity 84, no. 1 (November 9, 2015): 320–28. http://dx.doi.org/10.1128/iai.00552-15.

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Chemokines are best recognized for their role within the innate immune system as chemotactic cytokines, signaling and recruiting host immune cells to sites of infection. Certain chemokines, such as CXCL10, have been found to play an additional role in innate immunity, mediating CXCR3-independent killing of a diverse array of pathogenic microorganisms. While this is still not clearly understood, elucidating the mechanisms underlying chemokine-mediated antimicrobial activity may facilitate the development of novel therapeutic strategies effective against antibiotic-resistant Gram-negative pathogens. Here, we show that CXCL10 exerts antibacterial effects on clinical and laboratory strains ofEscherichia coliand report that disruption of pyruvate dehydrogenase complex (PDHc), which converts pyruvate to acetyl coenzyme A, enablesE. colito resist these antimicrobial effects. Through generation and screening of a transposon mutant library, we identified two mutants with increased resistance to CXCL10, both with unique disruptions of the gene encoding the E1 subunit of PDHc,aceE. Resistance to CXCL10 also occurred following deletion of eitheraceForlpdA, genes that encode the remaining two subunits of PDHc. Although PDHc resides within the bacterial cytosol, electron microscopy revealed localization of immunogold-labeled CXCL10 to the bacterial cell surface in both theE. coliparent andaceEdeletion mutant strains. Taken together, our findings suggest that while CXCL10 interacts with an as-yet-unidentified component on the cell surface, PDHc is an important mediator of killing by CXCL10. To our knowledge, this is the first description of PDHc as a key bacterial component involved in the antibacterial effect of a chemokine.

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Muñoz-Atienza, Estefanía, Carolina Aquilino, Khairul Syahputra, Azmi Al-Jubury, Carlos Araújo, Jakob Skov, Per W. Kania, et al. "CK11, a Teleost Chemokine with a Potent Antimicrobial Activity." Journal of Immunology 202, no. 3 (January 4, 2019): 857–70. http://dx.doi.org/10.4049/jimmunol.1800568.

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Rajasekaran, Ganesan, S. Dinesh Kumar, Jiyoung Nam, Dasom Jeon, Yangmee Kim, Chul Won Lee, Il-Seon Park, and Song Yub Shin. "Antimicrobial and anti-inflammatory activities of chemokine CXCL14-derived antimicrobial peptide and its analogs." Biochimica et Biophysica Acta (BBA) - Biomembranes 1861, no. 1 (January 2019): 256–67. http://dx.doi.org/10.1016/j.bbamem.2018.06.016.

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Nagaoka, Isao, Kaori Suzuki, François Niyonsaba, Hiroshi Tamura, and Michimasa Hirata. "Modulation of Neutrophil Apoptosis by Antimicrobial Peptides." ISRN Microbiology 2012 (March 27, 2012): 1–12. http://dx.doi.org/10.5402/2012/345791.

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Peptide antibiotics possess the potent antimicrobial activities against invading microorganisms and contribute to the innate host defense. Human antimicrobial peptides, α-defensins (human neutrophil peptides, HNPs), human β-defensins (hBDs), and cathelicidin (LL-37) not only exhibit potent bactericidal activities against Gram-negative and Gram-positive bacteria, but also function as immunomodulatory molecules by inducing cytokine and chemokine production, and inflammatory and immune cell activation. Neutrophil is a critical effector cell in host defense against microbial infection, and its lifespan is regulated by various pathogen- and host-derived substances. Here, we provided the evidence that HNP-1, hBD-3, and LL-37 cannot only destroy bacteria but also potently modulate (suppress) neutrophil apoptosis, accompanied with the phosphorylation of ERK-1/-2, the downregulation of tBid (an proapoptotic protein) and upregulation of Bcl-xL (an antiapoptotic protein), and the inhibition of mitochondrial membrane potential change and caspase 3 activity, possibly via the actions on the distinct receptors, the P2Y6 nucleotide receptor, the chemokine receptor CCR6, and the low-affinity formyl-peptide receptor FPRL1/the nucleotide receptor P2X7, respectively. Suppression of neutrophil apoptosis results in the prolongation of their lifespan and may be advantageous for the host defense against bacterial invasion.

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Holdren, Grant, David Rosenthal, Jianyi Yang, Amber Bates, Carol Fischer, Yang Zhang, Nicole Brogden, and Kim Brogden. "Antimicrobial Activity of Chemokine CXCL10 for Dermal and Oral Microorganisms." Antibiotics 3, no. 4 (October 23, 2014): 527–39. http://dx.doi.org/10.3390/antibiotics3040527.

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Nguyen, Leonard T., David I. Chan, Laura Boszhard, Sebastian A. J. Zaat, and Hans J. Vogel. "Structure–function studies of chemokine-derived carboxy-terminal antimicrobial peptides." Biochimica et Biophysica Acta (BBA) - Biomembranes 1798, no. 6 (June 2010): 1062–72. http://dx.doi.org/10.1016/j.bbamem.2009.11.021.

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Thammasit, Patcharin, Jirapas Sripetchwandee, Joshua D. Nosanchuk, Siriporn C. Chattipakorn, Nipon Chattipakorn, and Sirida Youngchim. "Cytokine and Chemokine Responses in Invasive Aspergillosis following Hematopoietic Stem Cell Transplantation: Past Evidence for Future Therapy of Aspergillosis." Journal of Fungi 7, no. 9 (September 13, 2021): 753. http://dx.doi.org/10.3390/jof7090753.

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Invasive pulmonary aspergillosis is a frequent complication in immunocompromised individuals, and it continues to be an important cause of mortality in patients undergoing hematopoietic stem cell transplantation. In addition to antifungal therapy used for mycoses, immune-modulatory molecules such as cytokines and chemokines can modify the host immune response and exhibit a promising form of antimicrobial therapeutics to combat invasive fungal diseases. Cytokine and chemokine profiles may also be applied as biomarkers during fungal infections and clinical research has demonstrated different activation patterns of cytokines in invasive mycoses such as aspergillosis. In this review, we summarize different aspects of cytokines that have been described to date and provide possible future directions in research on invasive pulmonary aspergillosis following hematopoietic stem cell transplantation. These findings suggest that cytokines and chemokines may serve as useful biomarkers to improve diagnosis and monitoring of infection.

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Bailer, Peter, Amanda E. Ward, Matthew Crawford, Debra Fisher, Lukas K. Tamm, and Molly Hughes. "Toxicity and Structure of Antimicrobial Peptides Derived from the Chemokine, CXCL10." Biophysical Journal 116, no. 3 (February 2019): 83a. http://dx.doi.org/10.1016/j.bpj.2018.11.492.

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Kina, Shinichiro, Toshiyuki Nakasone, Hiroyuki Takemoto, Akira Matayoshi, Shoko Makishi, Nao Sunagawa, Feixin Liang, Thongsavanh Phonaphonh, and Hajime Sunakawa. "Regulation of Chemokine Production via Oxidative Pathway in HeLa Cells." Mediators of Inflammation 2009 (2009): 1–5. http://dx.doi.org/10.1155/2009/183760.

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Inflammation is associated with disease progression and, by largely unknown mechanisms, has been said to drive oncogenesis. At inflamed sites, neutrophils deploy a potent antimicrobial arsenal that includes proteinases, antimicrobial peptides, and ROS. Reactive oxygen species (ROSs) induce chemokines. In the present study, the concentrations of IL-8 in culture supernatants of HeLa cells treated with ROS were determined by enzyme-linked immunosorbent assay. We used -phenanthroline to deplete in order to investigate the mechanisms through which ROSs induce IL-8 secretion in our system. The iron chelator -phenanthroline effectively inhibited -induced ERK2 activation. Enzyme-linked immunosorbent assays showed that IL-8 protein secretion was elevated in ROS-treated HeLa cells. When was removed from these cells, IL-8 secretion was inhibited. Collectively, these results indicate that -mediated Erk pathway activation is an important signal transduction pathway in ROS-induced IL-8 secretion in epithelial cells.

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Chan, David I., Howard N. Hunter, Brian F. Tack, and Hans J. Vogel. "Human Macrophage Inflammatory Protein 3α: Protein and Peptide Nuclear Magnetic Resonance Solution Structures, Dimerization, Dynamics, and Anti-Infective Properties." Antimicrobial Agents and Chemotherapy 52, no. 3 (December 17, 2007): 883–94. http://dx.doi.org/10.1128/aac.00805-07.

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ABSTRACT Human macrophage inflammatory protein 3α (MIP-3α), also known as CCL20, is a 70-amino-acid chemokine which exclusively binds to chemokine receptor 6. In addition, the protein also has direct antimicrobial, antifungal, and antiviral activities. The solution structure of MIP-3α was solved by the use of two-dimensional homonuclear proton nuclear magnetic resonance (NMR). The structure reveals the characteristic chemokine fold, with three antiparallel β strands followed by a C-terminal α helix. In contrast to the crystal structures of MIP-3α, the solution structure was found to be monomeric. Another difference between the NMR and crystal structures lies in the angle of the α helix with respect to the β strands, which measure 69 and ∼56.5° in the two structures, respectively. NMR diffusion and pH titration studies revealed a distinct tendency for MIP-3α to form dimers at neutral pH and monomers at lower pH, dependent on the protonation state of His40. Molecular dynamics simulations of both the monomeric and the dimeric forms of MIP-3α supported the notion that the chemokine undergoes a change in helix angle upon dimerization and also highlighted the important hydrophobic and hydrogen bonding contacts made by His40 in the dimer interface. Moreover, a constrained N terminus and a smaller binding groove were observed in dimeric MIP-3α simulations, which could explain why monomeric MIP-3α may be more adept at receptor binding and activation. The solution structure of a synthetic peptide consisting of the last 20 residues of MIP-3α displayed a highly amphipathic α helix, reminiscent of various antimicrobial peptides. Antimicrobial assays with this peptide revealed strong and moderate bactericidal activities against Escherichia coli and Staphylococcus aureus, respectively. This confirms that the C-terminal α-helical region of MIP-3α plays a significant part in its broad anti-infective activity.

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Nevins, Amanda M., Akshay Subramanian, Jazma L. Tapia, David P. Delgado, Robert C. Tyler, Davin R. Jensen, André J. Ouellette, and Brian F. Volkman. "A Requirement for Metamorphic Interconversion in the Antimicrobial Activity of Chemokine XCL1." Biochemistry 55, no. 27 (June 28, 2016): 3784–93. http://dx.doi.org/10.1021/acs.biochem.6b00353.

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Laneri, Sonia, Mariarita Brancaccio, Cristina Mennitti, Margherita G. De Biasi, Maria Elena Pero, Giuseppe Pisanelli, Olga Scudiero, and Raffaela Pero. "Antimicrobial Peptides and Physical Activity: A Great Hope against COVID 19." Microorganisms 9, no. 7 (June 30, 2021): 1415. http://dx.doi.org/10.3390/microorganisms9071415.

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Antimicrobial peptides (AMPs), α- and β-defensins, possess antiviral properties. These AMPs achieve viral inhibition through different mechanisms of action. For example, they can: (i) bind directly to virions; (ii) bind to and modulate host cell-surface receptors, disrupting intracellular signaling; (iii) function as chemokines to augment and alter adaptive immune responses. Given their antiviral properties and the fact that the development of an effective coronavirus disease 2019 (COVID-19) treatment is an urgent public health priority, they and their derivatives are being explored as potential therapies against COVID-19. These explorations using various strategies, range from their direct interaction with the virus to using them as vaccine adjuvants. However, AMPs do not work in isolation, specifically in their role as potent immune modulators, where they interact with toll-like receptors (TLRs) and chemokine receptors. Both of these receptors have been shown to play roles in COVID-19 pathogenesis. In addition, it is known that a healthy lifestyle accompanied by controlled physical activity can represent a natural weapon against COVID-19. In competitive athletes, an increase in serum defensins has been shown to function as self-protection from the attack of microorganisms, consequently a controlled physical activity could act as a support to any therapies in fighting COVID-19. Therefore, including information on all these players’ interactions would produce a complete picture of AMP-based therapies’ response.

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Majumdar, Shamik, and Philip Murphy. "Adaptive Immunodeficiency in WHIM Syndrome." International Journal of Molecular Sciences 20, no. 1 (December 20, 2018): 3. http://dx.doi.org/10.3390/ijms20010003.

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Cysteine-X-cysteine chemokine receptor 4 (CXCR4) is a broadly expressed and multifunctional G protein-coupled chemokine receptor critical for organogenesis, hematopoiesis, and antimicrobial host defense. In the hematopoietic system, the binding of CXCR4 to its cognate chemokine ligand, CXCL12, mediates leukocyte trafficking, distribution, survival, activation, and proliferation. Warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome is a rare, autosomal dominant, combined immunodeficiency disorder caused by mutations in the C-terminus of CXCR4 that prevent receptor downregulation and therefore result in pathologically increased signaling. The “M” in the acronym WHIM refers to myelokathexis, the retention of neutrophils in the bone marrow resulting in neutropenia, which explains in part the increased susceptibility to bacterial infection. However, WHIM patients also present with B and T lymphopenia, which may explain the susceptibility to human papillomavirus (HPV), the cause of warts. The impact of WHIM mutations on lymphocytes and adaptive immunity has received less attention than myelokathexis and is the focus of this review.

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Brogden, Kim A., Georgia K. Johnson, Steven D. Vincent, Taher Abbasi, and Shireen Vali. "Oral inflammation, a role for antimicrobial peptide modulation of cytokine and chemokine responses." Expert Review of Anti-infective Therapy 11, no. 10 (October 2013): 1097–113. http://dx.doi.org/10.1586/14787210.2013.836059.

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Ramamourthy, Gopal, Mauricio Arias, Leonard T. Nguyen, Hiroaki Ishida, and Hans J. Vogel. "Expression and Purification of Chemokine MIP-3α (CCL20) through a Calmodulin-Fusion Protein System." Microorganisms 7, no. 1 (January 8, 2019): 8. http://dx.doi.org/10.3390/microorganisms7010008.

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Human macrophage inflammatory protein 3α (MIP-3α), also known as CCL20, is a 70 amino acid chemokine that selectively binds and activates chemokine receptor 6 (CCR6). This chemokine is responsible for inducing the migration of immature dendritic cells, effector, or memory T-cells, and B-cells. Moreover, the MIP-3α protein has been shown to display direct antimicrobial, antiviral and antiprotozoal activities. Because of the potential therapeutic uses of this protein, the efficient production of MIP-3α is of great interest. However, bacterial recombinant production of the MIP-3α protein has been limited by the toxicity of this extremely basic protein (pI 9.7) toward prokaryotic cells, and by solubility problems during expression and purification. In an attempt to overcome these issues, we have investigated the bacterial recombinant expression of MIP-3α by using several common expression and fusion tags, including 6× histidine (His), small ubiquitin modifier protein (SUMO), thioredoxin (TRX), ketosteroid isomerase (KSI), and maltose binding protein (MBP). We have also evaluated a recently introduced calmodulin (CaM)-tag that has been used for the effective expression of many basic antimicrobial peptides (AMPs). Here, we show that the CaM fusion tag system effectively expressed soluble MIP-3α in the cytoplasm of Escherichia coli with good yields. Rapid purification was facilitated by the His-tag that was integrated in the CaM-fusion protein system. Multidimensional nuclear magnetic resonance (NMR) studies demonstrated that the recombinant protein was properly folded, with the correct formation of disulfide bonds. In addition, the recombinant MIP-3α had antibacterial activity, and was shown to inhibit the formation of Pseudomonas aeruginosa biofilms.

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Williams, Andrew E., and Rachel C. Chambers. "The mercurial nature of neutrophils: still an enigma in ARDS?" American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 3 (February 1, 2014): L217—L230. http://dx.doi.org/10.1152/ajplung.00311.2013.

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The acute respiratory distress syndrome (ARDS) is a life-threatening lung condition resulting from direct and indirect insults to the lung. It is characterized by disruption of the endothelial-epithelial barrier, alveolar damage, pulmonary edema, and respiratory failure. A key feature of ARDS is the accumulation of neutrophils in the lung microvasculature, interstitium, and alveolar space. Despite a clear association between neutrophil influx into the lung and disease severity, there is some debate as to whether neutrophils directly contribute to disease pathogenesis. The primary function of neutrophils is to provide immediate host defense against pathogenic microorganisms. Neutrophils release numerous antimicrobial factors such as reactive oxygen species, proteinases, and neutrophil extracellular traps. However, these factors are also toxic to host cells and can result in bystander tissue damage. The excessive accumulation of neutrophils in ARDS may therefore contribute to disease progression. Central to neutrophil recruitment is the release of chemokines, including the archetypal neutrophil chemoattractant IL-8, from resident pulmonary cells. However, the chemokine network in the inflamed lung is complex and may involve several other chemokines, including CXCL10, CCL2, and CCL7. This review will therefore focus on the experimental and clinical evidence supporting neutrophils as key players in ARDS and the chemokines involved in recruiting them into the lung.

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Björstad, Åse, Huamei Fu, Anna Karlsson, Claes Dahlgren, and Johan Bylund. "Interleukin-8-Derived Peptide Has Antibacterial Activity." Antimicrobial Agents and Chemotherapy 49, no. 9 (September 2005): 3889–95. http://dx.doi.org/10.1128/aac.49.9.3889-3895.2005.

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ABSTRACT Chemokines are inflammatory mediators with effects on diverse processes associated with the immune response. Some of the proteins belonging to the CXC chemokine subfamily, one of four groups in the family, possess inherent antibacterial activity against a wide range of bacteria. The CXC chemokine interleukin-8 (IL-8) has not been ascribed any direct antibacterial activity, but the fact that several of the amino acids in the carboxy-terminal part of the protein are identical or similar to those in a bactericidal cecropin-like peptide [Hp(2-20)] from Helicobacter pylori suggests that processing of the cytokine might generate peptide fragments with antibacterial properties. Synthetic peptides representing the carboxy-terminal part of IL-8 were investigated for antibacterial activities. These fragments possessed an antibacterial activity absent in the full-length IL-8. The antibacterial effects were reduced at increasing salt concentrations whereas the activity was increased when the pH was lowered. The IL-8-derived peptide shared structural similarity with and was also functionally additive to the Hp(2-20) peptide. The IL-8-derived peptide lacked the proinflammatory effects of the full-length protein. We also showed that acid hydrolysis of IL-8 generated a major peptide fragment corresponding to the antibacterial carboxyl terminus of the protein. The results presented are of special interest when put in the context of the suggested importance of antimicrobial peptides for microbial colonization of the gastric mucosa.

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Sun, Baiming, Yang Lei, Zhenjie Cao, Yongcan Zhou, Yun Sun, Ying Wu, Shifeng Wang, Weiliang Guo, and Chunsheng Liu. "TroCCL4, a CC chemokine of Trachinotus ovatus, is involved in the antimicrobial immune response." Fish & Shellfish Immunology 86 (March 2019): 525–35. http://dx.doi.org/10.1016/j.fsi.2018.11.080.

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Nguyen, Leonard T., Paulus H. S. Kwakman, David I. Chan, Zhihong Liu, Leonie de Boer, Sebastian A. J. Zaat, and Hans J. Vogel. "Exploring Platelet Chemokine Antimicrobial Activity: Nuclear Magnetic Resonance Backbone Dynamics of NAP-2 and TC-1." Antimicrobial Agents and Chemotherapy 55, no. 5 (February 14, 2011): 2074–83. http://dx.doi.org/10.1128/aac.01351-10.

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ABSTRACTThe platelet chemokines neutrophil-activating peptide-2 (NAP-2) and thrombocidin-1 (TC-1) differ by only two amino acids at their carboxy-terminal ends. Nevertheless, they display a significant difference in their direct antimicrobial activities, with the longer NAP-2 being inactive and TC-1 being active. In an attempt to rationalize this difference in activity, we studied the structure and the dynamics of both proteins by nuclear magnetic resonance (NMR) spectroscopy. Using15N isotope-labeled protein, we confirmed that the two monomeric proteins essentially have the same overall structure in aqueous solution. However, NMR relaxation measurements provided evidence that the negatively charged carboxy-terminal residues of NAP-2 experience a restricted motion, whereas the carboxy-terminal end of TC-1 moves in an unrestricted manner. The same behavior was also seen in molecular dynamic simulations of both proteins. Detailed analysis of the protein motions through model-free analysis, as well as a determination of their overall correlation times, provided evidence for the existence of a monomer-dimer equilibrium in solution, which seemed to be more prevalent for TC-1. This finding was supported by diffusion NMR experiments. Dimerization generates a larger cationic surface area that would increase the antimicrobial activities of these chemokines. Moreover, these data also show that the negatively charged carboxy-terminal end of NAP-2 (which is absent in TC-1) folds back over part of the positively charged helical region of the protein and, in doing so, interferes with the direct antimicrobial activity.

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Burkhardt, Amanda M., Kenneth P. Tai, Juan P. Flores-Guiterrez, Natalia Vilches-Cisneros, Karishma Kamdar, Oralia Barbosa-Quintana, Ricardo Valle-Rios, et al. "CXCL17 Is a Mucosal Chemokine Elevated in Idiopathic Pulmonary Fibrosis That Exhibits Broad Antimicrobial Activity." Journal of Immunology 188, no. 12 (May 18, 2012): 6399–406. http://dx.doi.org/10.4049/jimmunol.1102903.

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Park, Jong-Hwan, Yun-Gi Kim, Michael Shaw, Thirumala-Devi Kanneganti, Yukari Fujimoto, Koichi Fukase, Naohiro Inohara, and Gabriel Núñez. "Nod1/RICK and TLR Signaling Regulate Chemokine and Antimicrobial Innate Immune Responses in Mesothelial Cells." Journal of Immunology 179, no. 1 (June 19, 2007): 514–21. http://dx.doi.org/10.4049/jimmunol.179.1.514.

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Hieshima, Kunio, Haruo Ohtani, Michiko Shibano, Dai Izawa, Takashi Nakayama, Yuri Kawasaki, Fumio Shiba, et al. "CCL28 Has Dual Roles in Mucosal Immunity as a Chemokine with Broad-Spectrum Antimicrobial Activity." Journal of Immunology 170, no. 3 (February 1, 2003): 1452–61. http://dx.doi.org/10.4049/jimmunol.170.3.1452.

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Martínez-Becerra, Francisco, Daniel-Adriano Silva, Lenin Domínguez-Ramírez, Guillermo Mendoza-Hernández, Yolanda López-Vidal, Gloria Soldevila, and Eduardo A. García-Zepeda. "Analysis of the antimicrobial activities of a chemokine-derived peptide (CDAP-4) on Pseudomonas aeruginosa." Biochemical and Biophysical Research Communications 355, no. 2 (April 2007): 352–58. http://dx.doi.org/10.1016/j.bbrc.2007.01.188.

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Valore, Erika V., Dorothy J. Wiley, and Tomas Ganz. "Reversible Deficiency of Antimicrobial Polypeptides in Bacterial Vaginosis." Infection and Immunity 74, no. 10 (October 2006): 5693–702. http://dx.doi.org/10.1128/iai.00524-06.

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ABSTRACT Bacterial vaginosis is a common condition associated with increased risk of sexually transmitted diseases, including human immunodeficiency virus infections. In contrast, vulvovaginal candidiasis has a much weaker association with sexually transmitted diseases. We found that vaginal lavage fluid from women with bacterial vaginosis is deficient in antimicrobial polypeptides and antimicrobial activity compared to fluid from healthy women or women with vulvovaginal candidiasis. Effective treatment normalized the concentrations of antimicrobial polypeptides in both bacterial vaginosis and in vulvovaginal candidiasis, suggesting that the abnormalities were a result of the diseases. Unlike in vulvovaginal candidiasis, the neutrophil attractant chemokine interleukin-8 (IL-8) was not increased in bacterial vaginosis, accounting for low concentrations of neutrophil-derived defensins in vaginal fluid. In organotypic cultures of human vaginal epithelium containing dendritic cells, treatment with Lactobacillus jensenii, a typical vaginal resident, induced the synthesis of IL-8 mRNA and the epithelial human β-defensin-2 mRNA, but a typical bacterial vaginosis pathogen, Gardnerella vaginalis, had no effect. When the two bacteria were combined, Gardnerella vaginalis did not interfere with the immunostimulatory effect of Lactobacillus jensenii. The loss of normal immunostimulatory flora in bacterial vaginosis is thus associated with a local deficiency of multiple innate immune factors, and this deficiency could predispose individuals to sexually transmitted diseases.

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Di Liberto, Diana, Massimo Locati, Nadia Caccamo, Annunciata Vecchi, Serena Meraviglia, Alfredo Salerno, Guido Sireci, et al. "Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infection." Journal of Experimental Medicine 205, no. 9 (August 11, 2008): 2075–84. http://dx.doi.org/10.1084/jem.20070608.

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D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6−/− mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor α, interleukin 1β, and interferon γ) in bronchoalveolar lavage and serum. High levels of inflammatory cytokines in D6−/− infected mice were associated with liver and kidney damage, resulting in both liver and renal failure. Blocking inflammatory CC chemokines with a cocktail of antibodies reversed the inflammatory phenotype of D6−/− mice but led to less controlled growth of M. tuberculosis. Thus, the D6 decoy receptor plays a key role in setting the balance between antimicrobial resistance, immune activation, and inflammation in M. tuberculosis infection.

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Ghosh, Santosh K., Sanhita Gupta, Bin Jiang, and Aaron Weinberg. "Fusobacterium nucleatum and Human Beta-Defensins Modulate the Release of Antimicrobial Chemokine CCL20/Macrophage Inflammatory Protein 3α." Infection and Immunity 79, no. 11 (September 12, 2011): 4578–87. http://dx.doi.org/10.1128/iai.05586-11.

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ABSTRACTCells of the innate immune system regulate immune responses through the production of antimicrobial peptides, chemokines, and cytokines, including human beta-defensins (hBDs) and CCL20. In this study, we examined the kinetics of primary human oral epithelial cell (HOEC) production of CCL20 and hBDs in response toFusobacterium nucleatum, a commensal bacterium of the oral cavity, which we previously showed promotes HOEC induction of hBDs. HOECs secrete maximal levels of CCL20 at 6 h, following stimulation byF. nucleatumcell wall (FnCW). The kinetics of CCL20 release is distinct from that of hBD-2 and -3, which peaks after 24 h and 48 h of FnCW stimulation, respectively. FnCW-induced release of CCL20 by HOECs requires both transcriptional and translational activation. Release of CCL20 by HOECs is inhibited by brefeldin A, suggesting that it is secreted through a vesicle transport pathway. Other epithelium-derived agents that FnCW induces, such as hBD-2, hBD-3, tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β), are also able to release CCL20. By focusing on mitogen-activated protein kinases, we show that both extracellular signal-regulated kinase 1/2 and p38, but not JNK, are required for hBD-, TNF-α-, and IL-1β-induced secretion of CCL20 by HOECs. The ability of FnCW and its induced hBDs to produce proinflammatory cytokines and CCL20 suggests the broad role ofF. nucleatumand human antimicrobial peptides in primary immune responses elicited by oral epithelium.

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Chen, Lanlin, Zhimin Zhang, Kathryn E. Barletta, Marie D. Burdick, and Borna Mehrad. "Heterogeneity of lung mononuclear phagocytes during pneumonia: contribution of chemokine receptors." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 10 (November 15, 2013): L702—L711. http://dx.doi.org/10.1152/ajplung.00194.2013.

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Bacterial pneumonia is a common and dangerous illness. Mononuclear phagocytes, which comprise monocyte, resident and recruited macrophage, and dendritic cell subsets, are critical to antimicrobial defenses, but the dynamics of their recruitment to the lungs in pneumonia is not established. We hypothesized that chemokine-mediated traffic of mononuclear phagocytes is important in defense against bacterial pneumonia. In a mouse model of Klebsiella pneumonia, circulating Ly6Chiand, to a lesser extent, Ly6Clomonocytes expanded in parallel with accumulation of inflammatory macrophages and CD11bhidendritic cells and plasmacytoid dendritic cells in the lungs, whereas numbers of alveolar macrophages remained constant. CCR2 was expressed by Ly6Chimonocytes, recruited macrophages, and airway dendritic cells; CCR6 was prominently expressed by airway dendritic cells; and CX3CR1 was ubiquitously expressed by blood monocytes and lung CD11bhidendritic cells during infection. CCR2-deficient, but not CCL2-, CX3CR1-, or CCR6-deficient animals exhibited worse outcomes of infection. The absence of CCR2 had no detectable effect on neutrophils but resulted in reduction of all subsets of lung mononuclear phagocytes in the lungs, including alveolar macrophages and airway and plasmacytoid dendritic cells. In addition, absence of CCR2 skewed the phenotype of lung mononuclear phagocytes, abrogating the appearance of M1 macrophages and TNF-producing dendritic cells in the lungs. Taken together, these data define the dynamics of mononuclear phagocytes during pneumonia.

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Hosokawa, Yoshitaka, Ikuko Hosokawa, and Kazumi Ozaki. "Nobiletin Decreases Inflammatory Mediator Expression in Tumor Necrosis Factor-Stimulated Human Periodontal Ligament Cells." Mediators of Inflammation 2021 (July 10, 2021): 1–7. http://dx.doi.org/10.1155/2021/5535844.

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Nobiletin, a biologically active substance in the skin of citrus fruits, has been reported to be an effective anti-inflammatory, anticancer, and antimicrobial agent. In this study, we aimed to examine the anti-inflammatory effects of nobiletin on tumor necrosis factor- (TNF-) stimulated human periodontal ligament cells (HPDLCs). Our results demonstrated that nobiletin treatment could decrease the expressions of inflammatory cytokines (C-X-C motif chemokine ligand (CXCL)10, C-C motif chemokine ligand (CCL)2, and interleukin- (IL-) 8), matrix metalloproteinases (MMPs) (MMP1 and MMP3), and prostaglandin-endoperoxide synthase 2 (PTGS2) in TNF-stimulated HPDLCs. Moreover, we revealed that nobiletin could inhibit the activation of nuclear factor- (NF-) κB and protein kinase B (AKT1) pathways in TNF-stimulated HPDLCs. Furthermore, nobiletin treatment enhanced nuclear factor, erythroid 2 like 2 (NFE2L2) and heme oxygenase 1 (HMOX1) expressions in TNF-stimulated HPDLCs. In conclusion, these findings suggest that nobiletin can inhibit inflammatory responses in TNF-stimulated HPDLCs by inhibiting NF-κB and AKT1 activations and upregulating the NFE2L2 and HMOX1 expression.

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Ogawa, Hiroyuki, Mitsutoshi Iimura, Lars Eckmann, and Martin F. Kagnoff. "Regulated production of the chemokine CCL28 in human colon epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 5 (November 2004): G1062—G1069. http://dx.doi.org/10.1152/ajpgi.00162.2004.

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The chemokine CCL28 is constitutively expressed by epithelial cells at several mucosal sites and is thought to function as a homeostatic chemoattractant of subpopulations of T cells and IgA B cells and to mediate antimicrobial activity. We report herein on the regulation of CCL28 in human colon epithelium by the proinflammatory cytokine IL-1, bacterial flagellin, and n-butyrate, a product of microbial metabolism. In vivo, CCL28 was markedly increased in the epithelium of pathologically inflamed compared with normal human colon. Human colon and small intestinal xenografts were used to model human intestinal epithelium in vivo. Xenografts constitutively expressed little, if any, CCL28 mRNA or protein. After stimulation with the proinflammatory cytokine IL-1, CCL28 mRNA and protein were significantly increased in the epithelium of colon but not small intestinal xenografts, although both upregulated the expression of another prototypic chemokine, CXCL8, in response to the identical stimulus. In studies of CCL28 regulation using human colon epithelial cell lines, proinflammatory stimuli, including IL-1, bacterial flagellin, and bacterial infection, significantly upregulated CCL28 mRNA expression and protein production. In addition, CCL28 mRNA expression and protein secretion by those cells were significantly increased by the short-chain fatty acid n-butyrate, and IL-1- or flagellin-stimulated upregulation of CCL28 by colon epithelial cells was synergistically increased by pretreatment of cells with n-butyrate. Consistent with its upregulated expression by proinflammatory stimuli, CCL28 mRNA expression was attenuated by pharmacological inhibitors of NF-κB activation. These findings indicate that CCL28 functions as an “inflammatory” chemokine in human colon epithelium and suggest the notion that CCL28 may act to counterregulate colonic inflammation.

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Oudhoff, Menno J., Marjolein E. Blaauboer, Kamran Nazmi, Nina Scheres, Jan G. M. Bolscher, and Enno C. I. Veerman. "The role of salivary histatin and the human cathelicidin LL-37 in wound healing and innate immunity." Biological Chemistry 391, no. 5 (May 1, 2010): 541–48. http://dx.doi.org/10.1515/bc.2010.057.

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Abstract Antimicrobial peptides are multifunctional in innate immunity and wound repair of multicellular organisms. We were the first to discover that histatins, a family of salivary antimicrobial peptides, enhance epithelial cell migration, suggesting a role in oral wound healing. It is unknown whether histatins display innate-immunity activities, similar to other antimicrobial peptides such as LL-37. Therefore, we compared the effect of Histatin-2 and LL-37 on several activities within the context of wound healing and innate immunity. We found that Histatin-2 enhances fibroblast migration, but only weakly induces proliferation. LL-37 enhances both fibroblast migration and proliferation, but only at a narrow concentration optimum (approximately 1 μm). At higher concentrations LL-37 causes cell death, whereas Histatin-2 is not cytotoxic. Both peptides do not alter fibroblast-to-myofibroblast differentiation. Histatin-2 does not alter interleukin-8 (IL-8) expression and lipopolysaccharide (LPS)-elevated cytokine and chemokine expression. In contrast, LL-37 induces IL-8 expression, but dampens the LPS-induced immune response. Neither Histatin-2 nor LL-37 affects human-neutrophil migration. Histatins are, unlike other antimicrobial peptides, not cytotoxic or proinflammatory. It seems that they are important for the initial stage of wound healing in which fast wound coverage is important for healing without infection, inflammation, or fibrosis development. Interestingly, these characteristics are more typical for the mouth than for skin.

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Bourbigot, Sarah, Liam Fardy, Alan J. Waring, Michael R. Yeaman, and Valerie Booth. "Structure of Chemokine-Derived Antimicrobial Peptide Interleukin-8α and Interaction with Detergent Micelles and Oriented Lipid Bilayers." Biochemistry 48, no. 44 (November 10, 2009): 10509–21. http://dx.doi.org/10.1021/bi901311p.

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Jin, Ge, Hameem I. Kawsar, Stanley A. Hirsch, Chun Zeng, Xun Jia, Zhimin Feng, Santosh K. Ghosh, et al. "An Antimicrobial Peptide Regulates Tumor-Associated Macrophage Trafficking via the Chemokine Receptor CCR2, a Model for Tumorigenesis." PLoS ONE 5, no. 6 (June 8, 2010): e10993. http://dx.doi.org/10.1371/journal.pone.0010993.

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Reid-Yu, Sarah A., Brian R. Tuinema, Cherrie N. Small, Lydia Xing, and Brian K. Coombes. "CXCL9 Contributes to Antimicrobial Protection of the Gut during Citrobacter rodentium Infection Independent of Chemokine-Receptor Signaling." PLOS Pathogens 11, no. 2 (February 2, 2015): e1004648. http://dx.doi.org/10.1371/journal.ppat.1004648.

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Bourbigot, Sarah, and Valerie Booth. "Structure-Activity Relationships in Two Antimicrobial Peptides Based on Chemokine Helical Segments: RP-1 and IL-8α." Biophysical Journal 96, no. 3 (February 2009): 409a—410a. http://dx.doi.org/10.1016/j.bpj.2008.12.2088.

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Elass, Elisabeth, Maryse Masson, Joël Mazurier, and Dominique Legrand. "Lactoferrin Inhibits the Lipopolysaccharide-Induced Expression and Proteoglycan-Binding Ability of Interleukin-8 in Human Endothelial Cells." Infection and Immunity 70, no. 4 (April 2002): 1860–66. http://dx.doi.org/10.1128/iai.70.4.1860-1866.2002.

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ABSTRACT Interleukin-8 (IL-8), a C-X-C chemokine bound to endothelium proteoglycans, initiates the activation and selective recruitment of leukocytes at inflammatory foci. We demonstrate that human lactoferrin, an antimicrobial lipopolysaccharide (LPS)-binding protein, decreases both IL-8 mRNA and protein expression induced by the complex Escherichia coli 055:B5 LPS/sCD14 in human umbilical vein endothelial cells. The use of recombinant lactoferrins mutated in the LPS-binding sites indicates that this inhibitory effect is mediated by an interaction of lactoferrin with LPS and CD14s that suppresses the endotoxin biological activity. Furthermore, since dimeric IL-8 and lactoferrin are both proteoglycan-binding molecules, the competition between these proteins for heparin binding was investigated. Lactoferrin strongly inhibited the interaction of radiolabeled IL-8 to immobilized heparin, whereas a lactoferrin variant lacking the amino acid residues essential for heparin binding was not inhibitory. Moreover, this process is specific, since serum transferrin, a glycoprotein whose structure is close to that of lactoferrin, did not prevent the interaction of IL-8 with heparin. These results suggest that the anti-inflammatory properties of lactoferrin during septicemia are related, at least in part, to the regulation of IL-8 production and also to the ability of lactoferrin to compete with chemokines for their binding to proteoglycans.

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Yount, Nannette Y., Kimberly D. Gank, Yan Qiong Xiong, Arnold S. Bayer, Thomas Pender, William H. Welch, and Michael R. Yeaman. "Platelet Microbicidal Protein 1: Structural Themes of a Multifunctional Antimicrobial Peptide." Antimicrobial Agents and Chemotherapy 48, no. 11 (November 2004): 4395–404. http://dx.doi.org/10.1128/aac.48.11.4395-4404.2004.

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ABSTRACT Mammalian platelets release platelet microbicidal proteins (PMPs) as components of their antimicrobial armamentarium. The present studies defined the structure of PMP-1 and examined its structure-activity relationships. Amino acid sequencing and mass spectroscopy demonstrated that distinct N-terminal polymorphism variants of PMP-1 isolated from nonstimulated or thrombin-stimulated platelets arise from a single PMP-1 propeptide. Sequence data (NH2-[S]D1DPKE5SEGDL10HCVCV15KTTSL20 . . .) enabled cloning of PMP-1 from bone marrow and characterization of its full-length cDNA. PMP-1 is translated as a 106-amino-acid precursor and is processed to yield 73-residue (8,053 Da) and 72-residue (7,951-Da) variants. Searches with the BLAST program and sequence alignments demonstrated the homology of PMP-1 to members of the mammalian platelet factor 4 (PF-4) family of proteins. On the basis of phylogenetic relatedness, congruent sequence motifs, and predicted three-dimensional structures, PMP-1 shares the greatest homology with human PF-4 (hPF-4). By integration of its structural and antimicrobial properties, these results establish the identity of PMP-1 as a novel rabbit analogue of the microbicidal chemokine (kinocidin) hPF-4. These findings advance the hypothesis that stimuli in the setting of infection prompt platelets to release PF-4-class or related kinocidins, which have structures consistent with their likely multiple roles that bridge molecular and cellular mechanisms of antimicrobial host defense.

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Sperandio, Brice, Béatrice Regnault, Jianhua Guo, Zhi Zhang, Samuel L. Stanley, Philippe J. Sansonetti, and Thierry Pédron. "Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression." Journal of Experimental Medicine 205, no. 5 (April 21, 2008): 1121–32. http://dx.doi.org/10.1084/jem.20071698.

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Antimicrobial factors are efficient defense components of the innate immunity, playing a crucial role in the intestinal homeostasis and protection against pathogens. In this study, we report that upon infection of polarized human intestinal cells in vitro, virulent Shigella flexneri suppress transcription of several genes encoding antimicrobial cationic peptides, particularly the human β-defensin hBD-3, which we show to be especially active against S. flexneri. This is an example of targeted survival strategy. We also identify the MxiE bacterial regulator, which controls a regulon encompassing a set of virulence plasmid-encoded effectors injected into host cells and regulating innate signaling, as being responsible for this dedicated regulatory process. In vivo, in a model of human intestinal xenotransplant, we confirm at the transcriptional and translational level, the presence of a dedicated MxiE-dependent system allowing S. flexneri to suppress expression of antimicrobial cationic peptides and promoting its deeper progression toward intestinal crypts. We demonstrate that this system is also able to down-regulate additional innate immunity genes, such as the chemokine CCL20 gene, leading to compromised recruitment of dendritic cells to the lamina propria of infected tissues. Thus, S. flexneri has developed a dedicated strategy to weaken the innate immunity to manage its survival and colonization ability in the intestine.

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Coussens, Anna K., Robert J. Wilkinson, Yasmeen Hanifa, Vladyslav Nikolayevskyy, Paul T. Elkington, Kamrul Islam, Peter M. Timms, et al. "Vitamin D accelerates resolution of inflammatory responses during tuberculosis treatment." Proceedings of the National Academy of Sciences 109, no. 38 (September 4, 2012): 15449–54. http://dx.doi.org/10.1073/pnas.1200072109.

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Calcidiol, the major circulating metabolite of vitamin D, supports induction of pleiotropic antimicrobial responses in vitro. Vitamin D supplementation elevates circulating calcidiol concentrations, and thus has a potential role in the prevention and treatment of infection. The immunomodulatory effects of administering vitamin D to humans with an infectious disease have not previously been reported. To characterize these effects, we conducted a detailed longitudinal study of circulating and antigen-stimulated immune responses in ninety-five patients receiving antimicrobial therapy for pulmonary tuberculosis who were randomized to receive adjunctive high-dose vitamin D or placebo in a clinical trial, and who fulfilled criteria for per-protocol analysis. Vitamin D supplementation accelerated sputum smear conversion and enhanced treatment-induced resolution of lymphopaenia, monocytosis, hypercytokinaemia, and hyperchemokinaemia. Administration of vitamin D also suppressed antigen-stimulated proinflammatory cytokine responses, but attenuated the suppressive effect of antimicrobial therapy on antigen-stimulated secretion of IL-4, CC chemokine ligand 5, and IFN-α. We demonstrate a previously unappreciated role for vitamin D supplementation in accelerating resolution of inflammatory responses during tuberculosis treatment. Our findings suggest a potential role for adjunctive vitamin D supplementation in the treatment of pulmonary infections to accelerate resolution of inflammatory responses associated with increased risk of mortality.

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Serebryanaya, N. B., S. N. Shanin, E. E. Fomicheva, and P. P. Yakutseni. "BLOOD PLATELETS AS ACTIVATORS AND REGULATORS OF INFLAMMATORY AND IMMUNE REACTIONS. PART 2. THROMBOCYTES AS PARTICIPANTS OF IMMUNE REACTIONS." Medical Immunology (Russia) 21, no. 1 (January 24, 2019): 9–20. http://dx.doi.org/10.15789/1563-0625-2019-1-9-20.

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Thrombocytes keep a leading role in conjugating thrombosis, inflammation and congenital immune responses. The platelets provide stable adhesion and interaction with immune cells. Activated platelets express CD40L (CD154), a membrane glycoprotein of tumor necrosis factor (TNF) family. Hence, the platelets are the main source of sCD40L in blood plasma. Platelet CD154 may interact with CD40 receptor on endothelial cells, causing an inflammatory response, and enhancing production of immunoglobulins by B-lymphocytes. Membrane and soluble CD154 of platelets combined with other signals can induce maturation and activation of dendritic cells (DC). The platelets possess functional receptors, e.g., TLR2, TLR4, TLR7 and TLR9 they also bear Fc-receptors, including FcγRIIA, FcεRI and FcαRIA. FcγRIIA on platelets mediate protection against bacteria. Cross-linking of FcαRI on platelets results in production of prothrombotic and pro-inflammatory mediators such as tissue factor and IL-1β. Activation of platelets via FcεR1 causes release of chemokine RANTES and serotonin, which contribute to the pro-inflammatory response of other immune cells. Platelets possess receptors for activated complement components and its fragments (CR2, CR3, CR4, C1q, C1 inhibitor and factors D and H). Activated platelets trigger the complement system through the release of protein kinases and ATP, and also by phosphorylation of C3 and C3b. α-granules of platelets contain chemokines which represent the most numerous group of antimicrobial proteins of platelets (kinocidins), and there is an antimicrobial protein of the defensin family – hBD-1 in the cytoplasm of platelets. Ligand and receptor of the TNF superfamily (TRAIL and LIGHT), the SDF-1 chemokine (CXCL12), the IL-1βinterleukins, IL-8 and the soluble IL-6 receptor (sRIL-6) are recognized as platelet products belonging to the family of cytokines and their receptors. The HMGB-1 protein classified as an inflammatory cytokine, is expressed by activated platelets and causes formation of the extracellular traps by neutrophils. Platelets produce numerous growth factors, including EGF-α and EGF-β1, EGF-β2, TGF-α and TGF-β1, TGF-β2, PDGF, HGF, FGF-β, IGF, pro- and antiangiogenic factors, e.g., VEGF-F and angiopoietins Ang-1 and Ang-2. Fulfillment of immune functions by the platelets is carried out by their interaction with leukocytes, which are attracted to the site of infection and inflammation and retained during the development of an “immune thrombus” under conditions of high shear stress. Platelets can not only maintain and guide the immune response, but also initiate these events. They are able to present the antigen in the context of MHC class I molecules, and activate naїve CD8+T lymphocytes. Potential consequences of platelet interaction with neutrophils, monocytes, dendritic cells and lymphocytes are discussed in the review article.

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Marth, Christina D., Simon M. Firestone, Dave Hanlon, Lisa Y. Glenton, Glenn F. Browning, Neil D. Young, and Natali Krekeler. "Innate immune genes in persistent mating-induced endometritis in horses." Reproduction, Fertility and Development 30, no. 3 (2018): 533. http://dx.doi.org/10.1071/rd17157.

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Persistent mating-induced endometritis (PMIE) severely decreases fertility in horses. The aim of the present study was to evaluate differences between horses susceptible to PMIE and a control group in terms of the expression of selected immune response and effector genes, and the effects of oestrous cycle stage on this expression. Endometrial biopsies from 18 uterine samples of mares in the control group (eight in dioestrus, 10 in oestrus) and 16 PMIE-susceptible mares (four in dioestrus, 12 in oestrus) were analysed by quantitative real-time reverse transcription–polymerase chain reaction. Genes for pathogen recognition receptors Toll-like receptor 2 (TLR2) and NLR family CARD domain containing 5 (NLRC5), as well as tissue-specific inhibitor of metalloproteinase 1 (TIMP1), C-X-C motif chemokine ligand (CXCL) 9, CXCL10 and CXCL11 and uteroferrin were expressed at similar levels in the control group and in susceptible mares. Genes for C-C motif chemokine ligand 2 (CCL2) and the antimicrobial peptides secreted phospholipase A2 (sPLA2), lipocalin 2 and lactoferrin were all expressed at higher levels in susceptible compared with control mares. The expression of genes for the antimicrobial peptides equine β-defensin 1 (EBD1), lysozyme (LYZ) and secretory leukoprotease inhibitor (SLPI) was also higher in susceptible than control mares. The diagnostic sensitivity of assays for EBD1, LYZ and SLP1 gene expression to detect susceptibility to PMIE was estimated to be 100%, 94% and 100% respectively, with specificities of 83%, 78% and 78% respectively. When all three tests were positive, the specificity increased to 94%, with an overall sensitivity of 94%. The present study has yielded insights into pathophysiological changes in mares susceptible to PMIE and identified robust diagnostic markers (EBD1, LYZ and SLPI) for susceptibility to this disease.

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Kumar, Manish, Vanessa Kissoon-Singh, Aralia Leon Coria, France Moreau, and Kris Chadee. "Probiotic mixture VSL#3 reduces colonic inflammation and improves intestinal barrier function in Muc2 mucin-deficient mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 1 (January 1, 2017): G34—G45. http://dx.doi.org/10.1152/ajpgi.00298.2016.

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MUC2 mucin is the major glycoprotein in colonic mucus that separates intestinal microbiota from underlying host cells and serves as a food source for some eubacteria. MUC2 deficiency results in impaired epithelial barrier function, imbalance in gut microbiota, and spontaneous colitis. Probiotics have been shown to have a protective effect against colitis. In this study we used Muc2 mucin-deficient ( Muc2−/−) and Muc2+/+ littermates to test whether the probiotic mixture VSL#3 requires an intact mucin barrier to exert its beneficial effect. VSL#3 alone reduced basal colonic proinflammatory cytokine levels and improved epithelial barrier function in Muc2−/− animals. Similarly, in dextran sulfate sodium-induced colitis, VSL#3 dampened the proinflammatory chemokines KC, monocyte chemoattractant protein-1, and macrophage inflammatory protein-2 and upregulated the tissue regeneration growth factors transforming growth factor-β, fibroblast growth factor-1, and vascular endothelial growth factor-A, which accelerated resolution of colitis symptoms in Muc2−/− animals. Importantly, improved colonic health in VSL#3-treated animals was associated with attenuated reactive oxygen species production by peritoneal macrophages, restoration of antimicrobial peptide gene expression in the small intestine, and increased abundance of bacterial commensals in the gut. The beneficial effects of VSL#3 in Muc2−/− animals were mediated by acetate, an important short-chain fatty acid produced by gut bacteria. These studies provide evidence for the first time that VSL#3 can enhance epithelial barrier function by dampening the proinflammatory cytokine and chemokine response, accelerating restitution, and altering commensal microbiota in the absence of a functional mucus barrier. NEW & NOTEWORTHY It is unclear whether probiotics require an intact mucin barrier to first colonize and/or exert their protective functions. In this study we used mucin-deficient (Muc2 −/−) mice to interrogate if the multispecies probiotic mixture VSL#3 could enhance epithelial barrier function. In the absence of a mucus bilayer, VSL#3 dampened proinflammatory and chemokine production, accelerated restitution, and markedly improved gut permeability mediated by the short-chain fatty acid acetate in the colon.

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Crawford, M. A., D. E. Lowe, D. J. Fisher, S. Stibitz, R. D. Plaut, J. W. Beaber, J. Zemansky, et al. "Identification of the bacterial protein FtsX as a unique target of chemokine-mediated antimicrobial activity against Bacillus anthracis." Proceedings of the National Academy of Sciences 108, no. 41 (September 26, 2011): 17159–64. http://dx.doi.org/10.1073/pnas.1108495108.

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Cross, A. L., J. Hawkes, H. L. Wright, R. J. Moots, and S. W. Edwards. "APPA (apocynin and paeonol) modulates pathological aspects of human neutrophil function, without supressing antimicrobial ability, and inhibits TNFα expression and signalling." Inflammopharmacology 28, no. 5 (May 7, 2020): 1223–35. http://dx.doi.org/10.1007/s10787-020-00715-5.

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Abstract Neutrophils are key players in the pathophysiological process underlying inflammatory conditions not only by release of tissue-damaging cytotoxic enzymes, reactive oxygen species (ROS) but also by secretion of important immunomodulatory chemokines and cytokines. Here, we report the effects of the novel agent APPA, undergoing formal clinical development for treatment of osteoarthritis, and its constituent components, apocynin (AP) and paeonol (PA) on a number of neutrophil functions, including effects on TNFα- expression and signalling. Neutrophils were treated with APPA (10–1000 µg/mL) prior to the measurement of cell functions, including ROS production, chemotaxis, apoptosis and surface receptor expression. Expression levels of several key genes and proteins were measured after incubation with APPA and the chromatin re-modelling agent, R848. APPA did not significantly affect phagocytosis, bacterial killing or expression of surface receptors, while chemotactic migration was affected only at the highest concentrations. However, APPA down-regulated neutrophil degranulation and ROS levels, and decreased the formation of neutrophil extracellular traps. APPA also decreased cytokine-stimulated gene expression, inhibiting both TNFα- and GM-CSF-induced cell signalling. APPA was as effective as infliximab in down-regulating chemokine and IL-6 expression following incubation with R848. Whilst APPA does not interfere with neutrophil host defence against infections, it does inhibit neutrophil degranulation, and cytokine-driven signalling pathways (e.g. autocrine signalling and NF-κB activation), processes that are associated with inflammation. These observations may explain the mechanisms by which APPA exerts anti-inflammatory effects and suggests a potential therapeutic role in inflammatory diseases in which neutrophils and TNFα signalling are important in pathology, such as rheumatoid arthritis.

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Journal articles on the topic 'Antimicrobial chemokine'

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