The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Carolina Tafalla - One of the best experts on this subject based on the ideXlab platform.
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immune Responses elicited in rainbow trout through the administration of infectious pancreatic necrosis virus like particles
Developmental and Comparative Immunology, 2012Co-Authors: S Martinezalonso, Vikram N Vakharia, Sylvia Rodriguez Saintjean, Sara I Perezprieto, Carolina TafallaAbstract:Virus like particles (VLPs) against viral pathogens not only constitute a novel approach for the development of antiviral vaccines for an specific virus, but also for the creation of multivalent vaccines in which antigens from other pathogens may be expressed on the surface of these VLPs. Despite positive results on protection for many of these VLPs in both fish and mammals, not many studies have focused on the immune Response triggered by these particles; studies that may provide hints for the identification of immune mechanisms responsible for antiviral protection, which are mostly unknown in fish. In the current work, we have studied the levels of transcription of several immune genes in the spleen of rainbow trout (Oncorhynchus mykiss) intraperitoneally injected with VLPs from infectious pancreatic necrosis virus (IPNV) focusing on the Chemokine Response as well as the Response of genes related to interferon (IFN) production. Surprisingly, the capacity of VLPs to induce Chemokines differed from that of live IPNV, suggesting a direct effect of viral replication on the Chemokine Response in this organ. While VLPs up-regulated the transcription of CK3, CK10 and CXCd and down-modulated CK5B, CK6 and CK9 transcription, a previous study in which the transcription of γIP, CXCd, CK1, CK3, CK5B, CK6, CK7A, CK9 and CK12 had been studied demonstrated that IPNV only significantly up-regulated CK6 and down-modulated CK3 in the spleen. On the other hand, the administration of VLPs produced a strong mobilization to the peritoneum of CD4+, IgM+, IgT+ and CD83+ leukocytes similar to that induced by the live viral infection. In both cases, this leukocyte recruitment seemed to be greatly mediated through CK3, CK5B, CK9 and CK10 Chemokine production. These results together with the fact that VLPs strongly induced non-specific lymphocyte proliferation and specific anti-IPNV antibody production point to VLPs as excellent candidates for vaccine development.
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Specific regulation of the Chemokine Response to viral hemorrhagic septicemia virus at the entry site.
Journal of virology, 2011Co-Authors: Jana Montero, Jessica Garcia, M. Camino Ordas, Isabel Casanova, Antonia Gonzalez, Alberto J. Villena, Julio Coll, Carolina TafallaAbstract:The fin bases constitute the main portal of rhabdovirus entry into rainbow trout (Oncorhynchus mykiss), and replication in this first site strongly conditions the outcome of the infection. In this context, we studied the Chemokine Response elicited in this area in Response to viral hemorrhagic septicemia virus (VHSV), a rhabdovirus. Among all the rainbow trout Chemokine genes studied, only the transcription levels of CK10 and CK12 were significantly upregulated in Response to VHSV. As the virus had previously been shown to elicit a much stronger Chemokine Response in internal organs, we compared the effect of VHSV on the gills, another mucosal site which does not constitute the main site of viral entry or rhabdoviral replication. In this case, a significantly stronger Chemokine Response was triggered, with CK1, CK3, CK9, and CK11 being upregulated in Response to VHSV and CK10 and CK12 being down-modulated by the virus. We then conducted further experiments to understand how these different Chemokine Responses of mucosal tissues could correlate with their capacity to support VHSV replication. No viral replication was detected in the gills, while at the fin bases, only the skin and the muscle were actively supporting viral replication. Within the skin, viral replication took place in the dermis, while viral replication was blocked within epidermal cells at some point before protein translation. The different susceptibilities of the different skin layers to VHSV correlated with the effect that VHSV has on their capacity to secrete chemotactic factors. Altogether, these results suggest a VHSV interference mechanism on the early Chemokine Response at its active replication sites within mucosal tissues, a possible key process that may facilitate viral entry.
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Viral hemorrhagic septicemia and infectious pancreatic necrosis viruses replicate differently in rainbow trout gonad and induce different Chemokine transcription profiles.
Developmental and comparative immunology, 2010Co-Authors: Elena Chaves-pozo, Jana Montero, Alberto Cuesta, Carolina TafallaAbstract:Viral hemorrhagic septicemia virus (VHSV) and infectious pancreatic necrosis virus (IPNV) are two rainbow trout (Oncorhynchus mykiss) pathogens. While IPNV is known to be vertically transmitted to the next generation through the oocyte, VHSV is known to replicate in the ovary and be transmitted horizontally through the ovarian fluid. In this work, we wanted to study whether these differences had an effect on the immune Response triggered in the ovary, with a focus on the Chemokine Response. We have studied the kinetics of viral gene expression and the sites of replication, confirming that great differences exist between the replication of the two viruses in the gonad. Next, we studied the levels of expression of several CXC and CC Chemokines in the ovary and found that while VHSV strongly triggered Chemokine transcription, IPNV had almost no effect. This lack of immune Response might be an advantage that permits its vertical transmission.
Peter T Soboslay - One of the best experts on this subject based on the ideXlab platform.
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inflammatory and regulatory ccl and cxcl Chemokine and cytokine cellular Responses in patients with patent mansonella perstans filariasis
Clinical and Experimental Immunology, 2019Co-Authors: B. Wangala, Richard G. Gantin, A Vovor, Wiyao Poutouli, Kossi Komlan, Meba Banla, Carsten Köhler, P S Vosberg, Peter T SoboslayAbstract:: Mansonella perstans (Mp) filariasis is present in large populations in sub-Saharan Africa, and to what extent patent Mp infection modulates the expression of immunity in patients, notably their cellular cytokine and Chemokine Response profile, remains not well known. We studied the spontaneous and inducible cellular production of Chemokines (C-X-C motif) ligand 9 (CXCL9) [monokine induced by interferon (IFN)-γ (MIG)], CXCL-10 [inducible protein (IP)-10], Chemokine (C-C motif) ligand 24 (CCL24) (eotaxin-2), CCL22 [macrophage-derived Chemokine (MDC)], CCL13 [monocyte chemotactic protein-4 (MCP-4)], CCL18 [pulmonary and activation-regulated Chemokine (PARC)], CCL17 [thymus- and activation-regulated Chemokine (TARC)] and interleukin (IL)-27 in mansonelliasis patients (Mp-PAT) and mansonelliasis-free controls (CTRL). Freshly isolated peripheral mononuclear blood cells (PBMC) were stimulated with helminth, protozoan and bacterial antigens and mitogen [phytohaemagglutinin (PHA)]. PBMC from Mp-PAT produced spontaneously (without antigen stimulation) significantly higher levels of eotaxin-2, IL-27, IL-8, MCP-4 and MDC than cells from CTRL, while IFN-γ-IP-10 was lower in Mp-PAT. Helminth antigens activated IL-27 and MCP-4 only in CTRL, while Ascaris antigen, Onchocerca antigen, Schistosoma antigen, Entamoeba antigen, Streptococcus antigen, Mycobacteria antigen and PHA stimulated MIG release in CTRL and Mp-PAT. Notably, Entamoeba antigen and PHA strongly depressed (P < 0·0001) eotaxin-2 (CCL24) production in both study groups. Multiple regression analyses disclosed in Mp-PAT and CTRL dissimilar cellular Chemokine and cytokine production levels being higher in Mp-PAT for CCL24, IL-27, IL-8, MCP-4, MDC and PARC (for all P < 0·0001), at baseline (P < 0·0001), in Response to Entamoeba histolytica strain HM1 antigen (EhAg) (P < 0·0001), Onchocerca volvulus adult worm-derived antigen (OvAg) (P = 0·005), PHA (P < 0·0001) and purified protein derivative (PPD) (P < 0·0001) stimulation. In Mp-PAT with hookworm co-infection, the cellular Chemokine production of CXCL10 (IP-10) was diminished. In summary, the Chemokine and cytokine Responses in Mp-PAT were in general not depressed, PBMC from Mp-PAT produced spontaneously and selectively inducible inflammatory and regulatory Chemokines and cytokines at higher levels than CTRL and such diverse and distinctive reactivity supports that patent M. perstans infection will not polarize innate and adaptive cellular immune responsiveness in patients.
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coinfections with schistosoma haematobium necator americanus and entamoeba histolytica entamoeba dispar in children Chemokine and cytokine Responses and changes after antiparasite treatment
The Journal of Infectious Diseases, 2009Co-Authors: David M Hamm, Richard G. Gantin, Meba Banla, Abram Agossou, Lars Kocherscheidt, Klaus Dietz, Peter T SoboslayAbstract:The effect of polyparasite infections on cytokine and Chemokine Responses as well as the effect of antiparasite treatment was studied in children without parasite infection (the G0 group), in children singly infected with Schistosoma haematobium (the G1 group), and in children multiply infected with S. haematobium/Schistosoma mansoni, Entamoeba histolytica/Entamoeba dispar, and Necator americanus (the G3+ group). Linear regression analysis disclosed a significant risk for coinfection with hookworm and Schistosoma species. Polyparasite infections detected in 23% of children before treatment were present in 5% at 15 months after treatment. Chemokine Responses to S. mansoni adult worm antigen (SmAg) diminished after treatment for macrophage inflammatory Chemokine (MIP)-1alpha/Chemokine (C-C motif) ligand (CCL)-3 (among G3+ children, by a factor of 200 [95% confidence interval {CI}, 33-1111]) and for MIP-1beta/CCL-4 (among G3+ children, by a factor of 26 [95% CI, 6-117]) but were enhanced for thymus- and activation-regulated Chemokine/CCL-17 (among G3+ children, by a factor of 10 [95% CI, 3-32]) (P < .001 for all). In Response to E. histolytica antigen, interleukin (IL)-13 levels increased after treatment among G1 children by a factor of 138 (95% CI, 12-1569) and among G3+ children by a factor of 21 (95% CI, 7-64) (P < .001 for both). Cellular production of interferon (IFN)-gamma in Response to SmAg decreased 4 weeks after treatment among G3+ children, whereas T helper cell type 2 (Th2) IL-13 production was enhanced among G1 and G3+ children. In summary, polyparasite infections with S. haematobium/S. mansoni, E. histolytica/E. dispar, and N. americanus generated prominent proinflammatory cytokine and Chemokine Responses, and, after antihelminth treatment, the inflammatory Chemokine Response lessened as the Th2 responsiveness in coinfected children increased.
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coinfections with schistosoma haematobium necator americanus and entamoeba histolytica entamoeba dispar in children Chemokine and cytokine Responses and changes after antiparasite treatment
The Journal of Infectious Diseases, 2009Co-Authors: David M Hamm, Richard G. Gantin, Meba Banla, Abram Agossou, Lars Kocherscheidt, Klaus Dietz, Peter T SoboslayAbstract:The effect of polyparasite infections on cytokine and Chemokine Responses as well as the effect of antiparasite treatment was studied in children without parasite infection (the G0 group), in children singly infected with Schistosoma haematobium (the G1 group), and in children multiply infected with S. haematobium/Schistosoma mansoni, Entamoeba histolytica/Entamoeba dispar, and Necator americanus (the G3 group). Linear regression analysis disclosed a significant risk for coinfection with hookworm and Schistosoma species. Polyparasite infections detected in 23% of children before treatment were present in 5% at 15 months after treatment. Chemokine Responses to S. mansoni adult worm antigen (SmAg) diminished after treatment for macrophage inflammatory Chemokine (MIP)‐1/Chemokine (C-C motif) ligand (CCL)‐3 (among G3 children, by a factor of 200 [95% confidence interval {CI}, 33‐1111]) and for MIP-1/CCL-4 (among G3 children, by a factor of 26 [95% CI, 6‐117])butwereenhancedforthymus-andactivation-regulatedChemokine/CCL-17(amongG3children,bya factor of 10 [95% CI, 3‐32]) (P<.001 for all). In Response to E. histolytica antigen, interleukin (IL)‐13 levels increased after treatment among G1 children by a factor of 138 (95% CI, 12‐1569) and among G3children by a factor of 21 (95% CI, 7‐64) (P<.001 for both). Cellular production of interferon (IFN)‐ in Response to SmAg decreased 4 weeks after treatment among G3children, whereas T helper cell type 2 (Th2) IL-13 production was enhancedamongG1andG3children.Insummary,polyparasiteinfectionswithS.haematobium/S.mansoni,E. histolytica/E. dispar, and N. americanus generated prominent proinflammatory cytokine and Chemokine Responses, and, after antihelminth treatment, the inflammatory Chemokine Response lessened as the Th2 responsiveness in coinfected children increased. In large parts of sub-Saharan Africa, intestinal and intravascular helminth and protozoan infections often occur concurrently [1]. Up to 90% of schoolchildren may be found to be infected with helminths or
Peter J Hutchinson - One of the best experts on this subject based on the ideXlab platform.
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recombinant human interleukin 1 receptor antagonist promotes m1 microglia biased cytokines and Chemokines following human traumatic brain injury
Journal of Cerebral Blood Flow and Metabolism, 2016Co-Authors: Adel Helmy, Mathew R Guilfoyle, Keri L H Carpenter, John D Pickard, David K Menon, Peter J HutchinsonAbstract:Interleukin-1 receptor antagonist (IL1ra) has demonstrated efficacy in a wide range of animal models of neuronal injury. We have previously published a randomised controlled study of IL1ra in human severe TBI, with concomitant microdialysis and plasma sampling of 42 cytokines and Chemokines. In this study, we have used partial least squares discriminant analysis to model the effects of drug administration and time following injury on the cytokine milieu within the injured brain. We demonstrate that treatment with rhIL1ra causes a brain-specific modification of the cytokine and Chemokine Response to injury, particularly in samples from the first 48 h following injury. The magnitude of this Response is dependent on the concentration of IL1ra achieved in the brain extracellular space. Chemokines related to recruitment of macrophages from the plasma compartment (MCP-1) and biasing towards a M1 microglial phenotype (GM-CSF, IL1) are increased in patient samples in the rhIL1ra-treated patients. In control patients, cytokines and Chemokines biased to a M2 microglia phenotype (IL4, IL10, MDC) are relatively increased. This pattern of Response suggests that a simple classification of IL1ra as an 'anti-inflammatory' cytokine may not be appropriate and highlights the importance of the microglial Response to injury.
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principal component analysis of the cytokine and Chemokine Response to human traumatic brain injury
PLOS ONE, 2012Co-Authors: Adel Helmy, Chrystalina A Antoniades, Mathew R Guilfoyle, Keri L H Carpenter, Peter J HutchinsonAbstract:There is a growing realisation that neuro-inflammation plays a fundamental role in the pathology of Traumatic Brain Injury (TBI). This has led to the search for biomarkers that reflect these underlying inflammatory processes using techniques such as cerebral microdialysis. The interpretation of such biomarker data has been limited by the statistical methods used. When analysing data of this sort the multiple putative interactions between mediators need to be considered as well as the timing of production and high degree of statistical co-variance in levels of these mediators. Here we present a cytokine and Chemokine dataset from human brain following human traumatic brain injury and use principal component analysis and partial least squares discriminant analysis to demonstrate the pattern of production following TBI, distinct phases of the humoral inflammatory Response and the differing patterns of Response in brain and in peripheral blood. This technique has the added advantage of making no assumptions about the Relative Recovery (RR) of microdialysis derived parameters. Taken together these techniques can be used in complex microdialysis datasets to summarise the data succinctly and generate hypotheses for future study.
Gabriela Godaly - One of the best experts on this subject based on the ideXlab platform.
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Chemokine Response to febrile urinary tract infection
Kidney International, 2005Co-Authors: Gisela Otto, Marie D Burdick, Robert M Strieter, Gabriela GodalyAbstract:Chemokine Response to febrile urinary tract infection. Background Mucosal CXC Chemokines recruit inflammatory cells to the infected urinary tract. The Chemokine Response repertoire of the urinary tract and the relationship to disease severity have not been examined, however. Methods This study quantified CXC (CXCL1, CXCL3, CXCL5, CXCL8, CXCL9, and CXCL10) and CC (CCL2, CCL4, and CCL5) Chemokines in sequential urine samples obtained from 50 patients with febrile urinary tract infections during 24 hours after diagnosis. Results All patients had elevated Chemokine levels, but bacteremic infections caused higher CXCL1, CXCL3, CXCL5, CXCL8, and CCL2 Responses. CCL2 and CXCL8 levels were higher in patients with acute pyelonephritis symptoms and CCL2, CXCL3, CCL4, CXCL5, and CXCL10 were significantly correlated to C-reactive protein (CRP) and temperature. Women and men showed different Chemokine Responses. Conclusion Febrile urinary tract infections are accompanied by a complex Chemokine Response. The Response magnitude reflects disease severity, and the repertoire is influenced by gender and underlying disease.
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interleukin 8 receptor knockout mice have subepithelial neutrophil entrapment and renal scarring following acute pyelonephritis
The Journal of Infectious Diseases, 2000Co-Authors: Long Hang, Gabriela Godaly, Bjorn Frendeus, Catharina SvanborgAbstract:Interleukin (IL)-8 receptor knockout (KO) mice were shown to have a dysfunctional neutrophil Response to urinary tract infection and to develop renal scarring. Intravesical Escherichia coli infection stimulated epithelial Chemokine secretion and IL-8 receptor expression in control mice. Neutrophils migrated through the tissues and crossed the epithelial barrier into the urinary tract lumen. In murine IL-8 receptor homologue (mIL-8Rh) KO mice, infection triggered a Chemokine Response, and neutrophils were recruited but failed to traverse the mucosal barrier and accumulated under the epithelium. After 7 days, control mice were healthy, and infection was cleared, but mIL-8Rh KO mice had swollen kidneys, with neutrophil abscesses and high numbers of bacteria. After 35 days, they developed kidney pathology and renal scarring. The results demonstrate that Chemokine receptors drive transepithelial neutrophil migration. In their absence, the neutrophils are trapped, and the tissues are destroyed. This molecular deficiency may determine the progression from acute pyelonephritis to renal scarring.
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interleukin 8 receptor deficiency confers susceptibility to acute experimental pyelonephritis and may have a human counterpart
Journal of Experimental Medicine, 2000Co-Authors: Bjorn Frendeus, Gabriela Godaly, Long Hang, Diana Karpman, Anncharlotte Lundstedt, Catharina SvanborgAbstract:Neutrophils migrate to infected mucosal sites that they protect against invading pathogens. Their interaction with the epithelial barrier is controlled by CXC Chemokines and by their receptors. This study examined the change in susceptibility to urinary tract infection (UTI) after deletion of the murine interleukin 8 receptor homologue (mIL-8Rh). Experimental UTIs in control mice stimulated an epithelial Chemokine Response and increased Chemokine receptor expression. Neutrophils migrated through the tissues to the epithelial barrier that they crossed into the lumen, and the mice developed pyuria. In mIL-8Rh knockout (KO) mice, the Chemokine Response was intact, but the epithelial cells failed to express IL-8R, and neutrophils accumulated in the tissues. The KO mice were unable to clear bacteria from kidneys and bladders and developed bacteremia and symptoms of systemic disease, but control mice were fully resistant to infection. The experimental UTI model demonstrated that IL-8R–dependent mechanisms control the urinary tract defense, and that neutrophils are essential host effector cells. Patients prone to acute pyelonephritis also showed low CXC Chemokine receptor 1 expression compared with age-matched controls, suggesting that Chemokine receptor expression may also influence the susceptibility to UTIs in humans. The results provide a first molecular clue to disease susceptibility of patients prone to acute pyelonephritis.
Jana Montero - One of the best experts on this subject based on the ideXlab platform.
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Specific regulation of the Chemokine Response to viral hemorrhagic septicemia virus at the entry site.
Journal of virology, 2011Co-Authors: Jana Montero, Jessica Garcia, M. Camino Ordas, Isabel Casanova, Antonia Gonzalez, Alberto J. Villena, Julio Coll, Carolina TafallaAbstract:The fin bases constitute the main portal of rhabdovirus entry into rainbow trout (Oncorhynchus mykiss), and replication in this first site strongly conditions the outcome of the infection. In this context, we studied the Chemokine Response elicited in this area in Response to viral hemorrhagic septicemia virus (VHSV), a rhabdovirus. Among all the rainbow trout Chemokine genes studied, only the transcription levels of CK10 and CK12 were significantly upregulated in Response to VHSV. As the virus had previously been shown to elicit a much stronger Chemokine Response in internal organs, we compared the effect of VHSV on the gills, another mucosal site which does not constitute the main site of viral entry or rhabdoviral replication. In this case, a significantly stronger Chemokine Response was triggered, with CK1, CK3, CK9, and CK11 being upregulated in Response to VHSV and CK10 and CK12 being down-modulated by the virus. We then conducted further experiments to understand how these different Chemokine Responses of mucosal tissues could correlate with their capacity to support VHSV replication. No viral replication was detected in the gills, while at the fin bases, only the skin and the muscle were actively supporting viral replication. Within the skin, viral replication took place in the dermis, while viral replication was blocked within epidermal cells at some point before protein translation. The different susceptibilities of the different skin layers to VHSV correlated with the effect that VHSV has on their capacity to secrete chemotactic factors. Altogether, these results suggest a VHSV interference mechanism on the early Chemokine Response at its active replication sites within mucosal tissues, a possible key process that may facilitate viral entry.
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Viral hemorrhagic septicemia and infectious pancreatic necrosis viruses replicate differently in rainbow trout gonad and induce different Chemokine transcription profiles.
Developmental and comparative immunology, 2010Co-Authors: Elena Chaves-pozo, Jana Montero, Alberto Cuesta, Carolina TafallaAbstract:Viral hemorrhagic septicemia virus (VHSV) and infectious pancreatic necrosis virus (IPNV) are two rainbow trout (Oncorhynchus mykiss) pathogens. While IPNV is known to be vertically transmitted to the next generation through the oocyte, VHSV is known to replicate in the ovary and be transmitted horizontally through the ovarian fluid. In this work, we wanted to study whether these differences had an effect on the immune Response triggered in the ovary, with a focus on the Chemokine Response. We have studied the kinetics of viral gene expression and the sites of replication, confirming that great differences exist between the replication of the two viruses in the gonad. Next, we studied the levels of expression of several CXC and CC Chemokines in the ovary and found that while VHSV strongly triggered Chemokine transcription, IPNV had almost no effect. This lack of immune Response might be an advantage that permits its vertical transmission.