Journal articles: 'HILP'

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Duckett, Colin S., Feng Li, Yu Wang, Kevin J. Tomaselli, Craig B. Thompson, and Robert C. Armstrong. "Human IAP-Like Protein Regulates Programmed Cell Death Downstream of Bcl-xL and Cytochrome c." Molecular and Cellular Biology 18, no. 1 (January 1, 1998): 608–15. http://dx.doi.org/10.1128/mcb.18.1.608.

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ABSTRACT The gene encoding human IAP-like protein (hILP) is one of several mammalian genes with sequence homology to the baculovirus inhibitor-of-apoptosis protein (iap) genes. Here we show that hILP can block apoptosis induced by a variety of extracellular stimuli, including UV light, chemotoxic drugs, and activation of the tumor necrosis factor and Fas receptors. hILP also protected against cell death induced by members of the caspase family, cysteine proteases which are thought to be the principal effectors of apoptosis. hILP and Bcl-xL were compared for their ability to affect several steps in the apoptotic pathway. Redistribution of cytochromec from mitochondria, an early event in apoptosis, was not blocked by overexpression of hILP but was inhibited by Bcl-xL. In contrast, hILP, but not Bcl-xL, inhibited apoptosis induced by microinjection of cytochromec. These data suggest that while Bcl-xL may control mitochondrial integrity, hILP can function downstream of mitochondrial events to inhibit apoptosis.

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REYES-JURADO, FATIMA, ADDÍ RHODE NAVARRO-CRUZ, JOSUÉ MÉNDEZ-AGUILAR, CARLOS ENRIQUE OCHOA-VELASCO, EMMA MANI-LÓPEZ, MARÍA TERESA JIMÉNEZ-MUNGUÍA, ENRIQUE PALOU, AURELIO LÓPEZ-MALO, and RAÚL ÁVILA-SOSA. "High-Intensity Light Pulses To Inactivate Salmonella Typhimurium on Mexican Chia (Salvia hispanica L.) Seeds." Journal of Food Protection 82, no. 8 (July 11, 2019): 1272–77. http://dx.doi.org/10.4315/0362-028x.jfp-18-577.

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ABSTRACT Chia seeds provide a suitable environment for microorganisms. However, it is difficult to disinfect these seeds with water and/or chemical disinfectant solutions because the mucilage in the seeds can absorb water and consequently form gels. High-intensity light pulses (HILP) is one of the most promising emerging technologies for inactivating microorganisms on surfaces, in clear liquids and beverages, and on solid foods. The aim of this work was to evaluate the effect of HILP on Salmonella Typhimurium in culture medium (in vitro tests) and inoculated onto chia seeds (in vivo tests). HILP was effective against Salmonella Typhimurium under both conditions: 8 s of treatment (10.32 J/cm2) resulted in a 9-log reduction during in vitro tests, and 15 s of treatment (19.35 J/cm2) resulted in a 4-log reduction on the inoculated chia seeds. Salmonella Typhimurium inactivation kinetics were accurately described using the Weibull model (R2 > 0.939). These results indicate that the use of HILP for microbial inactivation on seeds could generate products suitable for human consumption.

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Birmpa, Angeliki, Apostolos Vantarakis, Spyros Paparrodopoulos, Paul Whyte, and James Lyng. "Efficacy of Three Light Technologies for Reducing Microbial Populations in Liquid Suspensions." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/673939.

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The aim of the current study was to evaluate the effectiveness of three nonthermal light technologies (NUV-Vis, continuous UV, and HILP) on their ability to inactivateEscherichia coliK12 andListeria innocua. E. coliK12 was selected as a representative microorganism for the enterohaemorrhagic foodborne pathogenE. coliO157:H7 andL. innocuaas a surrogate microorganism for the common foodborne pathogenListeria monocytogenes, respectively. The liquid matrix used for the disinfection experiments was a liquid matrix (MRD solution). The results of the present study show that the HILP treatment inactivated bothE. coliandL. innocuamore rapidly and effectively than either continuous UV-C or NUV-vis treatment. With HILP at 2.5 cm from the lamp,E. coliandL. innocuapopulations were reduced by 3.07 and 3.77 log10CFU/mL, respectively, after a 5 sec treatment time, and were shown to be below the limit of detection (<0.22 log10CFU/mL) following 30 sec exposure to HILP (106.2 J/cm2). These studies demonstrate the bactericidal efficacy of alternative nonthermal light technologies and their potential as decontamination strategies in the food industry.

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G??hl, J., T. h. Meyer, and W. Hohenberger. "Hyperthermic isolated limb perfusion (HILP)." Melanoma Research 7, Supplement 1 (June 1997): S101. http://dx.doi.org/10.1097/00008390-199706001-00354.

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Lacivita, Valentina, Amalia Conte, James G. Lyng, Cristina Arroyo, Vittorio A. Zambrini, and Matteo A. Del Nobile. "High intensity light pulses to reduce microbial load in fresh cheese." Journal of Dairy Research 85, no. 2 (May 2018): 232–37. http://dx.doi.org/10.1017/s0022029918000134.

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The present study focused on the utilisation of High Intensity Light Pulses (HILP) treatment to preserve mozzarella cheese. First, the susceptibility of Pseudomonas fluorescens and Enterobacteriaceae to HILP (fluences from 0·39 to 28·0 J/cm2) in a transparent liquid was evaluated (in-vitro tests). Afterwards, the effects on inoculated mozzarella cheese were also assessed. Then untreated (Control) and HILP treated samples were packaged and stored at 10 °C for 2 weeks. Enterobacteriaceae, Pseudomonas spp. and pH were monitored during storage. In a transparent liquid (in-vitro tests) there was a significant microbial inactivation just with 2 s of treatment. On the inoculated cheese a relevant microbial reduction of about 1 log cycle was observed, according to the exposure to the treatments. For Pseudomonas spp. in particular, in the treated samples, the microbiological acceptability limit (106 cfu/g) was never reached after 2 weeks of refrigerated storage. To sum up, the efficacy of this treatment is very interesting because a microbial reduction was observed in treated samples. HILP treatment is able to control the microbial growth and may be considered a promising way to decontaminate the surface of mozzarella cheese.

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Teras, Jüri, Michael J. Carr, Jonathan S. Zager, and Hidde M. Kroon. "Molecular Aspects of the Isolated Limb Infusion Procedure." Biomedicines 9, no. 2 (February 7, 2021): 163. http://dx.doi.org/10.3390/biomedicines9020163.

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For decades, isolated limb infusion (ILI) and hyperthermic isolated limb perfusion (HILP) have been used to treat melanoma in-transit metastases and unresectable sarcoma confined to the limb utilizing the effect of loco-regional high-dose chemotherapy to the isolated limb. Both procedures are able to provide high response rates in patients with numerous or bulky lesions in whom other loco-regional treatments are becoming ineffective. In comparison to systemic therapies, on the other hand, ILI and HILP have the advantage of not being associated with systemic side-effects. Although in principle ILI and HILP are similar procedures, ILI is technically simpler to perform and differs from HILP in that it takes advantage of the hypoxic and acidotic environment that develops in the isolated limb, potentiating anti-tumour activity of the cytotoxic agents melphalan +/− actinomycin-D. Due to its simplicity, ILI can be used in both preclinical and clinical studies to test new cytotoxic regimens and combinations with the aim to overcome tumour resistance. In the future, administration of cytotoxic agents by ILI, in combination with systemic treatments such as BRAF/MEK/KIT inhibitors, immunotherapy (CTLA-4 blockade), and/or programmed death (PD-1) pathway inhibitors, has the potential to improve responses further by inducing increased tumour cell death while limiting the ability of the tumour to suppress the immune response.

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Cano, María J. "New records and range extension of some mosses in tropical areas of Chile." Bryophyte Diversity and Evolution 24, no. 1 (December 30, 2003): 15–20. http://dx.doi.org/10.11646/bde.24.1.6.

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A total of thirteen mosses are reported as new for Chile: Aloinella andina Delgad., Coscinodontella bryanii R.S. Williams, Didymodon acutus (Brid.) K. Saito, Erythrophyllopsis fuscula (Müll. Hal.) Hilp., Fissidens excurrentinervis R.S. Williams, Grimmia molesta J. Muñoz, Grimmia pseudoanodon Deguchi, Jaffueliobryum williamsii (Deguchi) Delgad., Leptopteriginandrum austroalpinum Müll. Hal., Pseudocrossidium elatum (R.S. Williams) Delgad., Rhexophyllum subnigrum (Mitt.) Hilp., Saitobryum lorentzii (Müll. Hal.) Ochyra, and Syntrichia fragilis (Taylor) Ochyra. In addition, Grimmia plagiopodia Hedw., which was previosly known from Southern Chile, is reported ca. 3500 km more to the north, near the Bolivian border.

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Knorr, C., J. O. Pelz, J. Göhl, W. Hohenberger, and T. Meyer. "Expression of Chemoresistance-Related Genes and Heat Shock Protein 72 in Hyperthermic Isolated Limb Perfusion of Malignant Melanoma: An Experimental Study." Journal of Oncology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/138758.

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Hyperthermic isolated limb perfusion (HILP) is considered an established treatment for multiple locoregional intransit metastases in malignant melanoma of the extremities. Various mechanisms such as the expression of chemoresistance genes and heat shock proteins by the tumor may be responsible for varying response rates and locoregional recurrences of the treatment. The aim of the experimental animal study was to investigate the direct impact of HILP on such mechanisms of resistance. Tissue temperature, administration of the cytostatic drug, and duration of perfusion were varied. Expression of the chemoresistance genes mdr1, mrp1, mrp2, and lrp and of heat shock protein 72 (HSP72) in the tumor tissue was analysed using RT-PCR and western blot analysis. The untreated SK-MEL-3 tumor expressed mdr1, mrp1, and lrp, but not mrp2. Neither variation of temperature, administration of the cytostatic drug, nor duration of perfusion changed the expression of this “resistance pattern”. In contrast to the cytostatic drug, hyperthermia causes a persistent induction of HSP72. Both observations could offer a potential explanation for failure of HILP in malignant melanoma.

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Trezzi, M., A. Parolari, C. Loardi, and F. Alamanni. "Vascular Complications following Isolated Limb Perfusion for Local Recurrence of Extremity Melanoma: A Case Report and Literature Review." International Journal of Vascular Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/204148.

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Introduction. To evaluate the role of hyperthermic isolated limb perfusion (HILP) in arterial thrombosis following melanoma-soft tissue sarcoma chemotherapy.Report. Here is presented one case of iliac-common femoral artery subacute thrombosis and a review of the appropriate literature performed using a MEDLINE search. Acute/subacute arterial occlusion is one of the most feared vascular complications of HILP, located nearly always in the external iliac-femoral artery axis, being those vessels cannulated for perfusion.Conclusions. The small number of reported cases indicates either the rarity of this complication or unawareness of its existence. The true incidence of this complication is probably underreported.

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Baxter, M. Aaron, and Bradley D. Jones. "The fimYZ Genes Regulate Salmonella enterica Serovar Typhimurium Invasion in Addition to Type 1 Fimbrial Expression and Bacterial Motility." Infection and Immunity 73, no. 3 (March 2005): 1377–85. http://dx.doi.org/10.1128/iai.73.3.1377-1385.2005.

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ABSTRACT An important step in Salmonella enterica serovar Typhimurium virulence is the ability to invade the intestinal epithelium. The invasion process requires a large number of genes encoded on Salmonella pathogenicity island 1 (SPI-1) at centisome 63 as well as genes located in other positions throughout the chromosome. Expression of the invasive phenotype is tightly regulated by environmental cues that are processed by a complex regulatory scheme. A central player in the invasion regulatory pathway is the HilA protein, which is transcriptional activator belonging to the OmpR/ToxR family. A number of positive regulators (hilC, hilD, fis, sirA/barA, csrAB, phoBR, fadD, envZ/ompR, and fliZ) and negative regulators (hha, hilE, lon, ams, phoP c and pag) have been identified that are able to alter expression of hilA transcription. Recent work has found that hilA transcription requires the HilD protein for activation. Other work has emphasized the importance of HilE as a negative regulator of hilA. Overexpression of hilE superrepresses hilA transcription, as well as the invasive phenotype. Two-hybrid experiments suggest that HilE exerts its regulatory influence on hilA through protein-protein interactions with HilD as the protein does not bind to the hilA promoter nor does it affect hilD transcription. As it seems likely that hilE plays an important role in translating environmental signals into invasion gene regulation, we have attempted to identify how the hilE gene itself is regulated. Our results indicate that the fimYZ genes, response regulatory proteins involved in type 1 fimbrial gene expression and recently implicated in motility gene regulation, are important activators of hilE expression. These findings indicate that invasion gene expression is coregulated with motility and adherence and provide experimental evidence that the expression of these virulence phenotypes is a subset of the overall regulation of bacterial physiology.

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Main-Hester, Kara L., Katherine M. Colpitts, Gracie A. Thomas, Ferric C. Fang, and Stephen J. Libby. "Coordinate Regulation of Salmonella Pathogenicity Island 1 (SPI1) and SPI4 in Salmonella enterica Serovar Typhimurium." Infection and Immunity 76, no. 3 (December 26, 2007): 1024–35. http://dx.doi.org/10.1128/iai.01224-07.

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ABSTRACT Salmonella enterica serovar Typhimurium harbors five pathogenicity islands (SPI) required for infection in vertebrate hosts. Although the role of SPI1 in promoting epithelial invasion and proinflammatory cell death has been amply documented, SPI4 has only more recently been implicated in Salmonella virulence. SPI4 is a 24-kb pathogenicity island containing six open reading frames, siiA to siiF. Secretion of the 595-kDa SiiE protein requires a type I secretory system encoded by siiC, siiD, and siiF. An operon polarity suppressor (ops) sequence within the 5′ untranslated region upstream of siiA is required for optimal SPI4 expression and predicted to bind the antiterminator RfaH. SiiE concentrations are decreased in a SPI1 mutant strain, suggesting that SPI1 and SPI4 may have common regulatory inputs. SPI1 gene expression is positively regulated by the transcriptional activators HilA, HilC, and HilD, encoded within SPI1, and negatively regulated by the regulators HilE and PhoP. Here, we show that mutations in hilA, hilC, or hilD similarly reduce expression of siiE, and mutations in hilE or phoP enhance siiE expression. Individual overexpression of HilA, HilC, or HilD in the absence of SPI1 cannot activate siiE expression, suggesting that these transcriptional regulators act in concert or in combination with additional SPI1-encoded regulatory loci to activate SPI4. HilA is no longer required for siiE expression in an hns mutant strain, suggesting that HilA promotes SPI4 expression by antagonizing the global transcriptional silencer H-NS. Coordinate regulation suggests that SPI1 and SPI4 play complementary roles in the interaction of S. enterica serovar Typhimurium with the host intestinal mucosa.

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Baxter, M. Aaron, Thomas F. Fahlen, Rebecca L. Wilson, and Bradley D. Jones. "HilE Interacts with HilD and Negatively Regulates hilA Transcription and Expression of the Salmonella enterica Serovar Typhimurium Invasive Phenotype." Infection and Immunity 71, no. 3 (March 2003): 1295–305. http://dx.doi.org/10.1128/iai.71.3.1295-1305.2003.

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ABSTRACT The ability of Salmonella enterica serovar Typhimurium to traverse the intestinal mucosa of a host is an important step in its ability to initiate gastrointestinal disease. The majority of the genes required for this invasive characteristic are encoded on Salmonella pathogenicity island 1 (SPI1), and their expression is controlled by the transcriptional activator HilA, a member of the OmpR/ToxR family of proteins. A variety of genes (hilC, hilD, fis, sirA/barA, csrAB, phoB, fadD, envZ/ompR, fliZ, hilE, ams, lon, pag, and hha) have been identified that exert positive or negative effects on hilA expression, although the mechanisms by which these gene products function remain relatively unclear. Recent work indicates that the small DNA-binding protein, Hha, has a significant role in repressing hilA transcription and the invasive phenotype, particularly in response to osmolarity signals. We have characterized the Salmonella-specific gene, hilE, and found that it plays an important regulatory role in hilA transcription and invasion gene expression. Mutation of hilE causes derepression of hilA transcription, and overexpression of hilE superrepresses hilA expression and the invasive phenotype. Bacterial two-hybrid experiments indicate that the HilE protein interacts with HilD, suggesting a possible mechanism for HilE negative regulation of hilA gene expression and the Salmonella invasive phenotype. Finally, we have found that the hilE gene resides on a region of the serovar Typhimurium chromosome that has many characteristics of a pathogenicity island.

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Cornett, Wendy R., Linda M. McCall, Rebecca P. Petersen, Merrick I. Ross, Henry A. Briele, R. Dirk Noyes, Jeffrey J. Sussman, et al. "Randomized Multicenter Trial of Hyperthermic Isolated Limb Perfusion With Melphalan Alone Compared With Melphalan Plus Tumor Necrosis Factor: American College of Surgeons Oncology Group Trial Z0020." Journal of Clinical Oncology 24, no. 25 (September 1, 2006): 4196–201. http://dx.doi.org/10.1200/jco.2005.05.5152.

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Purpose To determine in a randomized prospective multi-institutional trial whether the addition of tumor necrosis factor alpha (TNF-α) to a melphalan-based hyperthermic isolated limb perfusion (HILP) treatment would improve the complete response rate for locally advanced extremity melanoma. Patients and Methods Patients with locally advanced extremity melanoma were randomly assigned to receive melphalan or melphalan plus TNF-α during standard HILP. Patient randomization was stratified according to disease/treatment status and regional nodal disease status. Results The intervention was completed in 124 patients of the 133 enrolled. Grade 4 adverse events were observed in 14 (12%) of 129 patients, with three (4%) of 64 in the melphalan-alone arm and 11 (16%) of 65 in the melphalan-plus-TNF-α arm (P = .0436). There were two toxicity-related lower extremity amputations in the melphalan-plus-TNF-α arm, and one disease progression–related upper extremity amputation in the melphalan-alone arm. There was no treatment-related mortality in either arm of the study. One hundred sixteen patients were assessable at 3 months postoperatively. Sixty-four percent of patients (36 of 58) in the melphalan-alone arm and 69% of patients (40 of 58) in the melphalan-plus-TNF-α arm showed a response to treatment at 3 months, with a complete response rate of 25% (14 of 58 patients) in the melphalan-alone arm and 26% (15 of 58 patients) in the melphalan-plus-TNF-α arm (P = .435 and P = .890, respectively). Conclusion In locally advanced extremity melanoma treated with HILP, the addition of TNF-α to melphalan did not demonstrate a significant enhancement of short-term response rates over melphalan alone by the 3-month follow-up, and TNF-α plus melphalan was associated with a higher complication rate.

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Olekhnovich, Igor N., and Robert J. Kadner. "DNA-Binding Activities of the HilC and HilD Virulence Regulatory Proteins of Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 184, no. 15 (August 1, 2002): 4148–60. http://dx.doi.org/10.1128/jb.184.15.4148-4160.2002.

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ABSTRACT The HilC and HilD proteins of Salmonella enterica serovar Typhimurium are members of the AraC/XylS family of transcription regulators. They are encoded on Salmonella pathogenicity island 1 (SPI1) and control expression of the hilA gene, which encodes the major transcriptional activator for many genes encoded on SPI1 and elsewhere that contribute to invasion of host cells. Gel electrophoretic shift and DNase footprinting assays revealed that purified HilC and HilD proteins can bind to multiple regions in the hilA and hilC promoters and to a single region in the hilD promoter. Although both HilC and -D proteins can bind to the same DNA regions, they showed different dependencies on the sequence and lengths of their DNA targets. To identify the binding-sequence specificity of HilC and HilD, a series of single base substitutions changing each position in a DNA fragment corresponding to positions −92 to −52 of the hilC promoter was tested for binding to HilC and HilD in a gel shift DNA-binding assay. This mutational analysis in combination with sequence alignments allowed deduction of consensus sequences for binding of both proteins. The consensus sequences overlap but differ so that HilC can bind to both types of sites but HilD only to one. The hilA and hilC promoters contain multiple binding sites of each type, whereas the hilD promoter contains a site that binds HilC but not HilD without additional binding elements. The HilC and HilD proteins had no major effect on transcription from the hilA or hilD promoters using purified proteins in vitro but changed the choice of promoter at hilC. These results are consistent with a model derived from analysis of lacZ fusions stating that HilC and HilD enhance hilA expression by counteracting a repressing activity.

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Ellermeier, Jeremy R., and James M. Slauch. "Fur Regulates Expression of the Salmonella Pathogenicity Island 1 Type III Secretion System through HilD." Journal of Bacteriology 190, no. 2 (November 9, 2007): 476–86. http://dx.doi.org/10.1128/jb.00926-07.

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ABSTRACT The invasion of intestinal epithelial cells by Salmonella enterica serovar Typhimurium is mediated by a type III secretion system (T3SS) encoded on Salmonella pathogenicity island 1 (SPI1). Expression of the SPI1 T3SS is tightly regulated by the combined action of HilC, HilD, and RtsA, three AraC family members that can independently activate hilA, which encodes the direct regulator of the SPI1 structural genes. Expression of hilC, hilD, and rtsA is controlled by a number of regulators that respond to a variety of environmental signals. In this work, we show that one such signal is iron mediated by Fur (ferric uptake regulator). Fur activates hilA transcription in a HilD-dependent manner. Fur regulation of HilD does not appear to be simply at the transcriptional or translational level but rather requires the presence of the HilD protein. Fur activation of SPI1 is not mediated through the Fur-regulated small RNAs RfrA and RfrB, which are the Salmonella ortholog and paralog of RyhB that control expression of sodB. Fur regulation of HilD is also not mediated through the known SPI1 repressor HilE or the CsrABC system. Although understanding the direct mechanism of Fur action on HilD requires further analysis, this work is an important step toward elucidating how various global regulatory systems control SPI1.

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Knorr, >C, N. Melling, J. Goehl, T. Drachsler, W. Hohenberger, and T. Meyer. "Long-term functional outcome after hyperthermic isolated limb perfusion (HILP)." International Journal of Hyperthermia 24, no. 5 (January 2008): 409–14. http://dx.doi.org/10.1080/02656730801975249.

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Lucas, Robin L., and Catherine A. Lee. "Roles of hilC and hilD in Regulation of hilA Expression in Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 183, no. 9 (May 1, 2001): 2733–45. http://dx.doi.org/10.1128/jb.183.9.2733-2745.2001.

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ABSTRACT Sequences between −332 and −39 upstream of the hilApromoter are required for repression of hilA. An unidentified repressor is thought to bind these upstream repressing sequences (URS) to inhibit hilA expression. Two AraC-like transcriptional regulators encoded on Salmonellapathogenicity island 1 (SPI1), HilC and HilD, bind to the URS to counteract the repression of hilA. The URS is required for regulation of hilA by osmolarity, oxygen, PhoP/PhoQ, and SirA/BarA. Here, we show that FadD, FliZ, PhoB, and EnvZ/OmpR also require the URS to regulate hilA. These environmental and regulatory factors may affect hilA expression by altering the expression or activity of HilC, HilD, or the unknown repressor. To begin investigating these possibilities, we tested the effects of environmental and regulatory factors on hilC andhilD expression. We also examined hilAregulation when hilC or hilD was disrupted or expressed to a high level. Although hilC is regulated by all environmental conditions and regulatory factors that modulatehilA expression, hilC is not required for the regulation of hilA by any conditions or factors except EnvZ/OmpR. In contrast, hilD is absolutely required forhilA expression, but environmental conditions and regulatory factors have little or no effect on hilDexpression. We speculate that EnvZ/OmpR regulates hilA by altering the expression and/or activity of hilC, while all other regulatory conditions and mutations regulate hilA by modulating hilD posttranscriptionally. We also discuss models in which the regulation of hilA expression is mediated by modulation of the expression or activity of one or more repressors.

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Meyer, Th, C. Christl, I. Muckenschnabel, G. Bernhardt, J. Göhl, W. Hohenberger, and A. Buschauer. "Essential factors in hyperthermic isolated limb perfusion (HILP)-in vitro studies." Journal of Cancer Research and Clinical Oncology 121, S1 (January 1995): A59. http://dx.doi.org/10.1007/bf02572201.

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Coit, D. G. "Hyperthermic isolation limb perfusion (HILP) with cisplatin (CDDP) for metastatic intransit melanoma." Melanoma Research 3, no. 1 (March 1993): 98. http://dx.doi.org/10.1097/00008390-199303000-00367.

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Knorr, C., T. Meyer, T. Janssen, J. Goehl, and W. Hohenberger. "Hyperthermic isolated limb perfusion (HILP) in malignant melanoma. Experience with 101 patients." European Journal of Surgical Oncology (EJSO) 32, no. 2 (March 2006): 224–27. http://dx.doi.org/10.1016/j.ejso.2005.09.007.

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Olekhnovich, Igor N., and Robert J. Kadner. "Contribution of the RpoA C-Terminal Domain to Stimulation of the Salmonella enterica hilA Promoter by HilC and HilD." Journal of Bacteriology 186, no. 10 (May 15, 2004): 3249–53. http://dx.doi.org/10.1128/jb.186.10.3249-3253.2004.

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ABSTRACT Expression of invasion genes in Salmonella pathogenicity island 1 (SPI-1) is mainly driven by the transcriptional activator HilA. Transcription of hilA is subject to complex control and is stimulated by the SPI-1-encoded HilC and HilD proteins. The C-terminal domain of RpoA contributes to hilA activation by HilC/D under certain inducing conditions.

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Sanna, M. G., C. S. Duckett, B. W. M. Richter, C. B. Thompson, and R. J. Ulevitch. "Selective activation of JNK1 is necessary for the anti-apoptotic activity of hILP." Proceedings of the National Academy of Sciences 95, no. 11 (May 26, 1998): 6015–20. http://dx.doi.org/10.1073/pnas.95.11.6015.

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Fletcher, W. S., R. F. Pommier, and E. A. Woltering. "Pharmacokinetics and results of dose escalation in cisplatin hyperthermic isolation limb perfusion (HILP)." Melanoma Research 3, no. 1 (March 1993): 96. http://dx.doi.org/10.1097/00008390-199303000-00361.

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Chubiz, Jessica E. Cott, Yekaterina A. Golubeva, Dongxia Lin, Lucas D. Miller, and James M. Slauch. "FliZ Regulates Expression of the Salmonella Pathogenicity Island 1 Invasion Locus by Controlling HilD Protein Activity in Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 192, no. 23 (October 1, 2010): 6261–70. http://dx.doi.org/10.1128/jb.00635-10.

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ABSTRACT A prerequisite for Salmonella enterica to cause both intestinal and systemic disease is the direct injection of effector proteins into host intestinal epithelial cells via a type three secretion system (T3SS); the T3SS genes are carried on Salmonella pathogenicity island 1 (SPI1). These effector proteins induce inflammatory diarrhea and bacterial invasion. Expression of the SPI1 T3SS is tightly regulated in response to environmental signals through a variety of global regulatory systems. We have previously shown that three AraC-like regulators, HilD, HilC, and RtsA, act in a complex feed-forward regulatory loop to control the expression of the hilA gene, which encodes the direct regulator of the SPI1 structural genes. In this work, we characterize a major positive regulator of this system, the flagellar protein FliZ. Through genetic and biochemical analyses, we show that FliZ posttranslationally controls HilD to positively regulate hilA expression. This mechanism is independent of other flagellar components and is not mediated through the negative regulator HilE or through FliZ-mediated RpoS regulation. We demonstrate that FliZ controls HilD protein activity and not stability. FliZ regulates HilD in the absence of Lon protease, previously shown to degrade HilD. Indeed, it appears that FliZ, rather than HilD, is the most relevant target of Lon as it relates to SPI1 expression. Mutants lacking FliZ are significantly attenuated in their ability to colonize the intestine but are unaffected during systemic infection. The intestinal attenuation is partially dependent on SPI1, but FliZ has additional pleiotropic effects.

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Meyer, T., W. Hohenberger, and H. Schönenberger. "Investigations regarding the choice of the cytostatic agent in hyperthermic isolated limb perfusion (HILP)." Melanoma Research 3, no. 1 (March 1993): 98. http://dx.doi.org/10.1097/00008390-199303000-00369.

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Boddicker, Jennifer D., Boyd M. Knosp, and Bradley D. Jones. "Transcription of the Salmonella Invasion Gene Activator, hilA, Requires HilD Activation in the Absence of Negative Regulators." Journal of Bacteriology 185, no. 2 (January 15, 2003): 525–33. http://dx.doi.org/10.1128/jb.185.2.525-533.2003.

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ABSTRACT Salmonella enterica serovar Typhimurium causes human gastroenteritis and a systemic typhoid-like infection in mice. Infection is initiated by entry of the bacteria into intestinal epithelial cells and is mediated by a type III secretion system that is encoded by genes in Salmonella pathogenicity island 1. The expression of invasion genes is tightly regulated by environmental conditions such as oxygen and osmolarity, as well as by many bacterial factors. The hilA gene encodes an OmpR/ToxR family transcriptional regulator that activates the expression of invasion genes in response to both environmental and genetic regulatory factors. HilD is an AraC/XylS regulator that has been postulated to act as a derepressor of hilA expression that promotes transcription by interfering with repressor binding at the hilA promoter. Our research group has identified four genes (hilE, hha, pag, and ams) that negatively affect hilA transcription. Since the postulated function of HilD at the hilA promoter is to counteract the effects of repressors, we examined this model by measuring hilA::Tn5lacZY expression in strains containing negative regulator mutations in the presence or absence of functional HilD. Single negative regulator mutations caused significant derepression of hilA expression, and two or more negative regulator mutations led to very high level expression of hilA. However, in all strains tested, the absence of hilD resulted in low-level expression of hilA, suggesting that HilD is required for activation of hilA expression, whether or not negative regulators are present. We also observed that deletion of the HilD binding sites in the chromosomal hilA promoter severely decreased hilA expression. In addition, we found that a single point mutation at leucine 289 in the C-terminal domain of the α subunit of RNA polymerase leads to very low levels of hilA::Tn5lacZY expression, suggesting that HilD activates transcription of hilA by contacting and recruiting RNA polymerase to the hilA promoter.

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Meyer, Th, J. Goehl, G. Bernhardt, Th Spru, and W. Hohenberger. "An experimental concept optimizing hyperthermic isolated limb perfusion (HILP) for malignant melanoma of the extremities." Melanoma Research 3 (September 1993): 31. http://dx.doi.org/10.1097/00008390-199309002-00116.

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Bedard, V., A. Vataire, C. Desouche, C. Le Péchoux, J. Muret, D. Vanel, P. Terrier, A. Le Cesne, and S. Bonvalot. "A prospective database of 100 patients with locally soft tissue sarcoma (STS) treated by isolated limb perfusion with melphalan and TNFα 1mg." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 10010. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.10010.

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10010 Background: In a prior randomized phase II trial comparing hyperthermic isolated limb perfusion (HILP) with melphalan and 4 different doses of TNFa (0.5 mg; 1 mg; 2mg, 3 mg/4mg superior/ inferior limb), there was no dose effect detected for the tumour response but systemic toxicity was significantly lower with low doses TNF-a (Bonvalot S et al. 2005). The objective of the present study was to confirm these datas on a larger population of locally advanced or recurrent STS of the extremity using low dose TNFa. Methods: Prospective database including 100 HILP (38–40°) with melphalan (10 mg/L) and TNFa 1 mg. Resection of the remnant tumour was performed 2 months after ILP. The main endpoint was complete response on MRI. Secondary endpoints were histological response, rate of amputation and toxicity. Results: Sex ratio was and median age was 43 years. Location/ median size were 30/48 mm and 70/72 mm for upper and lower limbs respectively. There were 26 multifocal tumors, 52 recurrences of which 18 arising in a pre irradiated field. Grade (FNCLCC) were 1 (23 pts), 2 (34 pts), 3 (43 pts). Fifty one pts had pre ILP systemic chemotherapy. A complete radiological response was obtained in 30% of pts while 48%, 9% and 13% of pts exhibited a partial, no change and disease progression. There was no mortality and no systemic toxicity. Local toxicity were (Wieberdink) grade 2 (16 pts), 3 (5 pts) and 4 (1 pt). A limb salvage surgery was achieved in 88% pts. With a median follow-up of 27 months, 3 years overall survival and local recurrence rate were 89% and 15% respectively. Age, gender, tumor size, recurrence, uni/multifocality, grade, pre op chemotherapy, pre irradiated field, were not predictive of the responses rates. Conclusions: This study confirm that 1mg TNFa is as effective as the standard dose without its systemic toxicity. A wide population of pts may benefit from this approach. No significant financial relationships to disclose.

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Göhl, J., Th Meyer, and W. Hohenberger. "Hyperthermic isolated limb perfusion (HILP) — A therapeutic concept in locoreglonal metastasized malignant melanoma — Experiences over 20 years." European Journal of Cancer 33 (September 1997): S256. http://dx.doi.org/10.1016/s0959-8049(97)86068-6.

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Meyer, Th, J. Göhl, W. Hohenberger, and I. Muckenschnabel. "Essential factors in hyperthermic isolated limb perfusion (HILP) — Experimental results of in-vitro and in-vivo studies." European Journal of Cancer 33 (September 1997): S257. http://dx.doi.org/10.1016/s0959-8049(97)86073-x.

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Boddicker, Jennifer D., and Bradley D. Jones. "Lon Protease Activity Causes Down-Regulation of Salmonella Pathogenicity Island 1 Invasion Gene Expression after Infection of Epithelial Cells." Infection and Immunity 72, no. 4 (April 2004): 2002–13. http://dx.doi.org/10.1128/iai.72.4.2002-2013.2004.

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ABSTRACT Salmonella enterica serovar Typhimurium causes self-limiting gastroenteritis in humans and a typhoid-like disease in mice that serves as a model for typhoid infections in humans. A critical step in Salmonella pathogenesis is the invasion of enterocytes and M cells of the small intestine via expression of a type III secretion system, encoded on Salmonella pathogenicity island 1 (SPI-1), that secretes effector proteins into host cells, leading to engulfment of the bacteria within large membrane ruffles. The in vitro regulation of invasion genes has been the subject of much scientific investigation. Transcription of the hilA gene, which encodes an OmpR/ToxR-type transcriptional activator of downstream invasion genes, is increased during growth under high-osmolarity and low-oxygen conditions, which presumably mimic the environment found within the small intestine. Several negative regulators of invasion gene expression have been identified, including HilE, Hha, and Lon protease. Mutations within the respective genes increase the expression of hilA when the bacteria are grown under environmental conditions that are not favorable for hilA expression and invasion. In this study, the intracellular expression of invasion genes was examined, after bacterial invasion of HEp-2 epithelial cells, using Salmonella strains containing plasmid-encoded short-half-life green fluorescent protein reporters of hilA, hilD, hilC, or sicA expression. Interestingly, the expression of SPI-1 genes was down-regulated after invasion, and this was important for the intracellular survival of the bacteria. In addition, the effects of mutations in genes encoding negative regulators of invasion on intracellular hilA expression were examined. Our results indicate that Lon protease is important for down-regulation of hilA expression and intracellular survival after the invasion of epithelial cells.

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Ellermeier, Craig D., and James M. Slauch. "RtsA and RtsB Coordinately Regulate Expression of the Invasion and Flagellar Genes in Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 185, no. 17 (September 1, 2003): 5096–108. http://dx.doi.org/10.1128/jb.185.17.5096-5108.2003.

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ABSTRACT Salmonella enterica serovar Typhimurium encounters numerous host environments and defense mechanisms during the infection process. The bacterium responds by tightly regulating the expression of virulence genes. We identified two regulatory proteins, termed RtsA and RtsB, which are encoded in an operon located on an island integrated at tRNAPheU in S. enterica serovar Typhimurium. RtsA belongs to the AraC/XylS family of regulators, and RtsB is a helix-turn-helix DNA binding protein. In a random screen, we identified five RtsA-regulated fusions, all belonging to the Salmonella pathogenicity island 1 (SPI1) regulon, which encodes a type III secretion system (TTSS) required for invasion of epithelial cells. We show that RtsA increases expression of the invasion genes by inducing hilA expression. RtsA also induces expression of hilD, hilC, and the invF operon. However, induction of hilA is independent of HilC and HilD and is mediated by direct binding of RtsA to the hilA promoter. The phenotype of an rtsA null mutation is similar to the phenotype of a hilC mutation, both of which decrease expression of SPI1 genes approximately twofold. We also show that RtsA can induce expression of a SPI1 TTSS effector, slrP, independent of any SPI1 regulatory protein. RtsB represses expression of the flagellar genes by binding to the flhDC promoter region. Repression of the positive activators flhDC decreases expression of the entire flagellar regulon. We propose that RtsA and RtsB coordinate induction of invasion and repression of motility in the small intestine.

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Lerminiaux, Nicole A., Keith D. MacKenzie, and Andrew D. S. Cameron. "Salmonella Pathogenicity Island 1 (SPI-1): The Evolution and Stabilization of a Core Genomic Type Three Secretion System." Microorganisms 8, no. 4 (April 16, 2020): 576. http://dx.doi.org/10.3390/microorganisms8040576.

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Salmonella Pathogenicity Island 1 (SPI-1) encodes a type three secretion system (T3SS), effector proteins, and associated transcription factors that together enable invasion of epithelial cells in animal intestines. The horizontal acquisition of SPI-1 by the common ancestor of all Salmonella is considered a prime example of how gene islands potentiate the emergence of new pathogens with expanded niche ranges. However, the evolutionary history of SPI-1 has attracted little attention. Here, we apply phylogenetic comparisons across the family Enterobacteriaceae to examine the history of SPI-1, improving the resolution of its boundaries and unique architecture by identifying its composite gene modules. SPI-1 is located between the core genes fhlA and mutS, a hotspot for the gain and loss of horizontally acquired genes. Despite the plasticity of this locus, SPI-1 demonstrates stable residency of many tens of millions of years in a host genome, unlike short-lived homologous T3SS and effector islands including Escherichia ETT2, Yersinia YSA, Pantoea PSI-2, Sodalis SSR2, and Chromobacterium CPI-1. SPI-1 employs a unique series of regulatory switches, starting with the dedicated transcription factors HilC and HilD, and flowing through the central SPI-1 regulator HilA. HilA is shared with other T3SS, but HilC and HilD may have their evolutionary origins in Salmonella. The hilA, hilC, and hilD gene promoters are the most AT-rich DNA in SPI-1, placing them under tight control by the transcriptional repressor H-NS. In all Salmonella lineages, these three promoters resist amelioration towards the genomic average, ensuring strong repression by H-NS. Hence, early development of a robust and well-integrated regulatory network may explain the evolutionary stability of SPI-1 compared to T3SS gene islands in other species.

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Mizusaki, Hideaki, Akiko Takaya, Tomoko Yamamoto, and Shin-Ichi Aizawa. "Signal Pathway in Salt-Activated Expression of the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium." Journal of Bacteriology 190, no. 13 (April 25, 2008): 4624–31. http://dx.doi.org/10.1128/jb.01957-07.

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ABSTRACT Salmonella enterica serovar Typhimurium secretes virulence factors for invasion called Sip proteins or Sips into its hosts through a type III secretion system (T3SS). In the absence of a host, S. enterica induces Sip secretion in response to sucrose or simple salts, such as NaCl. We analyzed induction of host-independent Sip secretion by monitoring protein secretion by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), assembly of needle complexes by electron microscopy, and transcription of virulence regulatory genes by quantitative reverse transcriptase PCR (real-time PCR). SDS-PAGE showed that addition of sucrose or simple salts, such as NaCl, to the growth medium induced Sip secretion without altering flagellar protein secretion, which requires a distinct T3SS. Electron microscopy confirmed that the amount of secreted Sips increased as the number of assembled needle complexes increased. Real-time PCR revealed that added sucrose or NaCl enhanced transcription of hilA, hilC, and hilD, which encode known regulators of Salmonella virulence. However, epistasis analysis implicated HilD and HilA, but not HilC, in the direct pathway from the salt stimulus to the Sip secretion response. Further analyses showed that the BarA/SirA two-component signal transduction pathway, but not the two-component sensor kinase EnvZ, directly activated hilD and hilA transcription and thus Sip secretion in response to either sucrose or NaCl. Finally, real-time PCR showed that salt does not influence transcription of the BarA/SirA-dependent csrB and csrC genes. A model is proposed for the major pathway in which sucrose or salt signals to enhance virulence gene expression.

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SHIBATA, Satoko, Yoshiyuki MURAKAMI, Yoichi MOROI, Shonosuke NAGAE, Kazunori URABE, Tetsuya KOGA, Masutaka FURUE, and Juichiro NAKAYAMA. "Evaluation of Clinical Prognosis of Stage II and III Melanoma Patients Treated with Hyperthermic Isolated Limb Perfusion(HILP)." Nishi Nihon Hifuka 67, no. 2 (2005): 147–51. http://dx.doi.org/10.2336/nishinihonhifu.67.147.

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Kage, Hirokazu, Akiko Takaya, Mai Ohya, and Tomoko Yamamoto. "Coordinated Regulation of Expression of Salmonella Pathogenicity Island 1 and Flagellar Type III Secretion Systems by ATP-Dependent ClpXP Protease." Journal of Bacteriology 190, no. 7 (February 1, 2008): 2470–78. http://dx.doi.org/10.1128/jb.01385-07.

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ABSTRACT Salmonella enterica serovar Typhimurium delivers a variety of proteins via the Salmonella pathogenicity island 1 (SPI1)-encoded type III secretion system into host cells, where they elicit several physiological changes, including bacterial invasion, macrophage apoptosis, and enteropathogenesis. Once Salmonella has established a systemic infection, excess macrophage apoptosis would be detrimental to the pathogen, as it utilizes macrophages as vectors for systemic dissemination throughout the host. Therefore, SPI1 expression must be restricted to one or a few specific locations in the host. In the present study, we have demonstrated that the expression of this complex of genes is repressed by the ATP-dependent ClpXP protease, which therefore suppresses macrophage apoptosis. Depletion of ClpXP caused significant increases in the amounts of two SPI1-encoded transcriptional regulators, HilC and HilD, leading to the stimulation of hilA induction and therefore activation of SPI1 expression. Our evidence shows that ClpXP regulates cellular levels of HilC and HilD via the control of flagellar gene expression. Subsequent experiments demonstrated that the flagellum-related gene product FliZ controls HilD posttranscriptionally, and this in turn activates HilC. These findings suggest that the ClpXP protease coregulates SPI1-related virulence phenotypes and motility. ClpXP is a member of the stress protein family induced in bacteria exposed to hostile environments such as macrophages.

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Boesch, Cedric E., Thomas Meyer, Lena Waschke, Susanne Merkel, Jonas Goehl, Werner Hohenberger, and Christian Knorr. "Long-term outcome of hyperthermic isolated limb perfusion (HILP) in the treatment of locoregionally metastasised malignant melanoma of the extremities." International Journal of Hyperthermia 26, no. 1 (January 2010): 16–20. http://dx.doi.org/10.3109/02656730903236086.

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Michelakis, Dimosthenis, Konstantinos Lasithiotakis, Ippokratis Messaritakis, Christos Ioannou, Kostas Perisynakis, Ioannis Souglakos, Dimitrios Stamatiou, et al. "A feasibility study of circulating melanoma cells in the perioperative context of hyperthermic isolated limb perfusion (HILP) in 20 patients." International Journal of Hyperthermia 38, no. 1 (January 1, 2021): 70–78. http://dx.doi.org/10.1080/02656736.2021.1874062.

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Teplitski, Max, Robert I. Goodier, and Brian M. M. Ahmer. "Pathways Leading from BarA/SirA to Motility andVirulence Gene Expression inSalmonella." Journal of Bacteriology 185, no. 24 (December 15, 2003): 7257–65. http://dx.doi.org/10.1128/jb.185.24.7257-7265.2003.

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ABSTRACT The barA and sirA genes of Salmonella enterica serovar Typhimurium encode a two-component sensor kinase and a response regulator, respectively. This system increases the expression of virulence genes and decreases the expression of motility genes. In this study, we examined the pathways by which SirA affects these genes. We found that the master regulator of flagellar genes, flhDC, had a positive regulatory effect on the primary regulator of intestinal virulence determinants, hilA, but that hilA had no effect on flhDC. SirA was able to repress flhDC in a hilA mutant and activate hilA in an flhDC mutant. Therefore, although the flhDC and hilA regulatory cascades interact, sirA affects each of them independently. A form of BarA lacking the two N-terminal membrane-spanning domains, BarA198, autophosphorylates in the presence of ATP and transfers the phosphate to purified SirA. Phosphorylated SirA was found to directly bind the hilA and hilC promoters in gel mobility shift assays but not the flhD, fliA, hilD, and invF promoters. Given that the CsrA/csrB system is known to directly affect flagellar gene expression, we tested the hypothesis that SirA affects flagellar gene expression indirectly by regulating csrA or csrB. The sirA gene did not regulate csrA but did activate csrB expression. Consistent with these results, phosphorylated SirA was found to directly bind the csrB promoter but not the csrA promoter. We propose a model in which SirA directly activates virulence expression via hilA and hilC while repressing the flagellar regulon indirectly via csrB.

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Nait Belaid, Youba, Patrick Coudray, José Sanchez-Torres, Yi-Ping Fang, Zhiguo Zeng, and Anne Barros. "Resilience Quantification of Smart Distribution Networks—A Bird’s Eye View Perspective." Energies 14, no. 10 (May 17, 2021): 2888. http://dx.doi.org/10.3390/en14102888.

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The introduction of pervasive telecommunication devices, in the scope of smart grids (SGs), has accentuated interest in the distribution network, which integrates a huge portion of new grid applications. High impact low probability (HILP) events, such as natural hazards, manmade errors, and cyber-attacks, as well as the inherent fragility of the distribution grid have propelled the development of effective resilience tools and methods for the power distribution network (PDN) to avoid catastrophic infrastructural and economical losses. Multiple resilience evaluation frameworks are proposed in the literature in order to assist distribution system operators (DSOs) in managing their networks when faced with exogenous threats. We conduct detailed analysis of existing quantitative resilience studies in both electric and telecommunication domains of a PDN, focusing on event type, metrics, temporal phases, uncertainty, and critical load. Our work adopts the standpoint of a DSO, whose target is to identify feasible resilience assessment frameworks, which apply to pre-defined requirements in terms of resilience evaluation objectives (planning, reactive response, or simple assessment), time of evaluation, and available enhancement strategies. Finally, results and observations on selected works are presented, followed by discussion of identified challenges and opportunities.

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Kiel, Erlend Sandø, and Gerd Hovin Kjølle. "Reliability of Supply and the Impact of Weather Exposure and Protection System Failures." Applied Sciences 11, no. 1 (December 27, 2020): 182. http://dx.doi.org/10.3390/app11010182.

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Extreme weather is known to cause failure bunching in electrical transmission systems. However, protection systems can also contribute to the worsening of the system state through various failure modes—spontaneous, missing or unwanted operation. The latter two types of failures only occur when an initial failure has happened, and thus are more likely to happen when the probability of failure of transmission lines is high, such as in an extreme weather scenario. This causes an exacerbation of failure bunching effects, increasing the risk of blackouts, or High Impact Low Probability (HILP) events. This paper describes a method to model transmission line failure rates, considering both protection system reliability and extreme weather exposure. A case study is presented using the IEEE 24 bus Reliability Test System (RTS) test system. The case study, using both an approximate method as well as a time-series approach to calculate reliability indices, demonstrates both a compact generalization of including protection system failures in reliability analysis, as well as the interaction between weather exposure and protection system failures and its impact on power system reliability indices. The results show that the inclusion of protection system failures can have a large impact on the estimated occurrence of higher order contingencies for adjacent lines, especially for lines with correlated weather exposure.

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Di Filippo, F., F. Cavaliere, R. Garinei, M. Anzà, P. Di Angelo, A. Psaila, L. Piarulli, et al. "TNFα-Based Isolated Hyperthermic Limb Perfusion (HILP) in the Treatment of Limb Recurrent Melanoma: Update 16 Years after Its First Clinical Application." Journal of Chemotherapy 16, sup5 (November 2004): 62–65. http://dx.doi.org/10.1080/1120009x.2004.11782388.

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Pérez-Morales, Deyanira, Jessica Nava-Galeana, Roberto Rosales-Reyes, Paige Teehan, Helen Yakhnin, Erika I. Melchy-Pérez, Yvonne Rosenstein, Miguel A. De la Cruz, Paul Babitzke, and Víctor H. Bustamante. "An incoherent feedforward loop formed by SirA/BarA, HilE and HilD is involved in controlling the growth cost of virulence factor expression by Salmonella Typhimurium." PLOS Pathogens 17, no. 5 (May 28, 2021): e1009630. http://dx.doi.org/10.1371/journal.ppat.1009630.

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An intricate regulatory network controls the expression of Salmonella virulence genes. The transcriptional regulator HilD plays a central role in this network by controlling the expression of tens of genes mainly required for intestinal colonization. Accordingly, the expression/activity of HilD is highly regulated by multiple factors, such as the SirA/BarA two-component system and the Hcp-like protein HilE. SirA/BarA positively regulates translation of hilD mRNA through a regulatory cascade involving the small RNAs CsrB and CsrC, and the RNA-binding protein CsrA, whereas HilE inhibits HilD activity by protein-protein interaction. In this study, we show that SirA/BarA also positively regulates translation of hilE mRNA through the same mentioned regulatory cascade. Thus, our results reveal a paradoxical regulation exerted by SirA/BarA-Csr on HilD, which involves simultaneous opposite effects, direct positive control and indirect negative control through HilE. This kind of regulation is called an incoherent type-1 feedforward loop (I1-FFL), which is a motif present in certain regulatory networks and represents a complex biological problem to decipher. Interestingly, our results, together with those from a previous study, indicate that HilE, the repressor component of the I1-FFL reported here (I1-FFLSirA/BarA-HilE-HilD), is required to reduce the growth cost imposed by the expression of the genes regulated by HilD. Moreover, we and others found that HilE is necessary for successful intestinal colonization by Salmonella. Thus, these findings support that I1-FFLSirA/BarA-HilE-HilD cooperates to control the precise amount and activity of HilD, for an appropriate balance between the growth cost and the virulence benefit generated by the expression of the genes induced by this regulator. I1-FFLSirA/BarA-HilE-HilD represents a complex regulatory I1-FFL that involves multiple regulators acting at distinct levels of gene expression, as well as showing different connections to the rest of the regulatory network governing Salmonella virulence.

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Palgan, I., I. M. Caminiti, A. Muñoz, F. Noci, P. Whyte, D. J. Morgan, D. A. Cronin, and J. G. Lyng. "Effectiveness of High Intensity Light Pulses (HILP) treatments for the control of Escherichia coli and Listeria innocua in apple juice, orange juice and milk." Food Microbiology 28, no. 1 (February 2011): 14–20. http://dx.doi.org/10.1016/j.fm.2010.07.023.

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Caminiti, Irene M., Izabela Palgan, Francesco Noci, Arantxa Muñoz, Paul Whyte, Denis A. Cronin, Desmond J. Morgan, and James G. Lyng. "The effect of pulsed electric fields (PEF) in combination with high intensity light pulses (HILP) on Escherichia coli inactivation and quality attributes in apple juice." Innovative Food Science & Emerging Technologies 12, no. 2 (April 2011): 118–23. http://dx.doi.org/10.1016/j.ifset.2011.01.003.

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Schechter, Lisa M., and Catherine A. Lee. "AraC/XylS family members, HilC and HilD, directly bind and derepress the Salmonella typhimurium hilA promoter." Molecular Microbiology 40, no. 6 (June 2001): 1289–99. http://dx.doi.org/10.1046/j.1365-2958.2001.02462.x.

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Olekhnovich, Igor N., and Robert J. Kadner. "Role of Nucleoid-Associated Proteins Hha and H-NS in Expression of Salmonella enterica Activators HilD, HilC, and RtsA Required for Cell Invasion." Journal of Bacteriology 189, no. 19 (August 3, 2007): 6882–90. http://dx.doi.org/10.1128/jb.00905-07.

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ABSTRACT The coordinate expression of Salmonella enterica invasion genes on Salmonella pathogenicity island 1 is under the control of the complex circuits of regulation that involve the AraC/XylS family transcriptional activators HilD, HilC, and RtsA and nucleoid-associated proteins. Single-copy transcription fusions were used to assess the effects of nucleoid-associated proteins Hha and H-NS on hilD, hilC, and rtsA expression. The data show that all three genes, hilD, hilC, and rtsA, were repressed by H-NS and/or Hha. The repression of rtsA was the highest among tested genes. The level of rtsA-lac was equally elevated in hns and hha mutants and was further enhanced in the hns hha double mutant under low-osmolarity conditions. Electrophoretic mobility shift experiments showed that H-NS and Hha directly bind to the rtsA promoter. In addition to the negative control that was exerted by H-NS/Hha under low-osmolarity conditions, the homologous virulence activators HilD, HilC, and RtsA (Hil activators) induced rtsA-lac expression in a high-salt medium. A DNase footprinting assay of the rtsA promoter revealed one common DNA-binding site for all three Hil activators centered at position −54 relative to the transcriptional start site. In the absence of Hha and H-NS, however, osmoregulation of the rtsA promoter was lost, and Hil activators were not required for rtsA transcription. These results taken together suggest that the HilD, HilC, and RtsA proteins induce the transcription of the rtsA promoter by counteracting H-NS/Hha-mediated repression.

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Lin, Dongxia, Christopher V. Rao, and James M. Slauch. "The Salmonella SPI1 Type Three Secretion System Responds to Periplasmic Disulfide Bond Status via the Flagellar Apparatus and the RcsCDB System." Journal of Bacteriology 190, no. 1 (October 19, 2007): 87–97. http://dx.doi.org/10.1128/jb.01323-07.

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ABSTRACT Upon contact with intestinal epithelial cells, Salmonella enterica serovar Typhimurium injects a set of effector proteins into the host cell cytoplasm via the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS) to induce inflammatory diarrhea and bacterial uptake. The master SPI1 regulatory gene hilA is controlled directly by three AraC-like regulators: HilD, HilC, and RtsA. Previous work suggested a role for DsbA, a periplasmic disulfide bond oxidase, in SPI1 T3SS function. RtsA directly activates dsbA, and deletion of dsbA leads to loss of SPI1-dependent secretion. We have studied the dsbA phenotypes by monitoring expression of SPI1 regulatory, structural, and effector genes. Here we present evidence that loss of DsbA independently affects SPI1 regulation and SPI1 function. The dsbA-mediated feedback inhibition of SPI1 transcription is not due to defects in the SPI1 T3SS apparatus. Rather, the transcriptional response is dependent on both the flagellar protein FliZ and the RcsCDB system, which also affects fliZ transcription. Thus, the status of disulfide bonds in the periplasm affects expression of the SPI1 system indirectly via the flagellar apparatus. RcsCDB can also affect SPI1 independently of FliZ. All regulation is through HilD, consistent with our current model for SPI1 regulation.

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Schechter, Lisa M., Sumita Jain, Samina Akbar, and Catherine A. Lee. "The Small Nucleoid-Binding Proteins H-NS, HU, and Fis Affect hilA Expression in Salmonella enterica Serovar Typhimurium." Infection and Immunity 71, no. 9 (September 2003): 5432–35. http://dx.doi.org/10.1128/iai.71.9.5432-5435.2003.

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ABSTRACT hilA encodes an activator of Salmonella enterica serovar Typhimurium virulence genes and is transcriptionally modulated by environmental conditions. We show that H-NS represses hilA under low-osmolarity conditions. H-NS, HU, and Fis also appear to affect the derepression of hilA by HilD. Modulation of hilA by counteracting repressing and derepressing mechanisms may allow Salmonella serovar Typhimurium to regulate its virulence genes in response to different situations in vivo.

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Altier, Craig, Mitsu Suyemoto, and Sara D. Lawhon. "Regulation of Salmonella entericaSerovar Typhimurium Invasion Genes by csrA." Infection and Immunity 68, no. 12 (December 1, 2000): 6790–97. http://dx.doi.org/10.1128/iai.68.12.6790-6797.2000.

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ABSTRACT Penetration of intestinal epithelial cells by Salmonella enterica serovar Typhimurium requires the expression of invasion genes, found in Salmonella pathogenicity island 1 (SPI1), that encode components of a type III secretion apparatus. These genes are controlled in a complex manner by regulators within SPI1, including HilA and InvF, and those outside SPI1, such as the two-component regulators PhoP/PhoQ and BarA/SirA. We report here that epithelial cell invasion requires the serovar Typhimurium homologue ofEscherichia coli csrA, which encodes a regulator that alters the stability of specific mRNA targets. A deletion mutant ofcsrA was unable to efficiently invade cultured epithelial cells and showed reduced expression of four tested SPI1 genes,hilA, invF, sipC, and prgH. Overexpression ofcsrA from an induced araBAD promoter also negatively affected the expression of these genes, indicating that CsrA can act as both a positive and a negative regulator of SPI1 genes and suggesting that the bacterium must tightly control the level or activity of CsrA to achieve maximal invasion. We found that CsrA affected hilA, a regulator of the other three genes we tested, probably by controlling one or more genetic elements that regulate hilA. We also found that both the loss and the overexpression of csrA reduced the expression of two regulators of hilA, hilC and hilD, suggesting that csrA exerts its control of hilAthrough one or both of these regulators. We further found, however, that CsrA could affect the expression of both invF andsipC independent of its effects on hilA. One additional striking phenotype of the csrA mutant, not observed in a comparable E. coli mutant, was its slow growth. Phenotypic revertants that had normal growth rates, while maintaining the csrA mutation, were common. These suppressed strains, however, did not recover the ability to invade cultured cells, indicating that the csrA-mediated loss of invasion cannot be attributed simply to poor growth and that the growth and invasion deficits of the csrA mutant arise from effects of CsrA on different targets.

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Journal articles on the topic 'HILP'

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