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Conference Paper: A possible role of IL-17 during Salmonella typhimurium infection

TitleA possible role of IL-17 during Salmonella typhimurium infection
Authors
Issue Date2015
PublisherIHMC 2015. The Conference programmes' website is located at http://www.ihmc2015.org/en/scientific-programme/abstractbook
Citation
The 5th International Human Microbiome Congress (IHMC 2015), Luxembourg, 31 March-2 April 2015. In Abstracts Book, 2015, p. 122-123 How to Cite?
AbstractInterleukin 17 is a crucial immunomodulator in various chronic immunological diseases and infectious diseases including inflammatory bowel disease and tuberculosis. The action of IL-17 in chronic disease could be detrimental through the overproduction of proinflammatory cytokines but IL-17 can also be protective during microbial infection by suppressing the overwhelmed immune responses. Therefore, the balance between the population of IL-17 producing cells (Th17) and other T cell subset plays an important role in maintaining the homeostatic of the immunity. Previous studies showed that the gut microbes and its colonies could enhance the Th17 cells differentiation and induce the production of IL-17 in intestine. During the pathogenic bacteria infection, such as Salmonella typhimurium infection, the colonies of the microbiota will be affected. These changes may activate the T cells and macrophages to produce proinflammatory cytokines to combat both the commensals and pathogenic bacteria. As IL-17 is crucial in both innate and mucosal immunity, we hypothesize that IL-17 could affect the immune cells to fight against the bacterial infection in intestine. Human macrophages were isolated and differentiated from peripheral blood mononuclear cell of healthy donors. In order to mimic the condition at the intestine that IL-17 is induced by commensals, the macrophages were primed with interleukin-17A for 3 days, followed by Salmonella typhimurium infection for 24 h. Culture supernatant was collected for enzyme-linked immunosorbant assay to quantify proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6. We observed that IL-17A-treated macrophages exhibited suppressed productions of TNF-α and IL-6 in response to Salmonella typhimurium infection. The reduction of cytokines production was not associated with cell death. These data suggested IL-17 primed macrophage could limit the proinflammatory cytokine production during pathogenic bacterial infection. As the microbiota could induce the Th17 differentiation, this could be a protective mechanism for commensal bacteria to fight against other bacterial infection in intestine.
DescriptionCongress Theme: Future Directions for Human Microbiome Research in Health and Disease
Session - Evidence for Cause and Effect in Microbiome Diseases: no. Evi-078#287
Persistent Identifierhttp://hdl.handle.net/10722/209363

 

DC FieldValueLanguage
dc.contributor.authorLing, WL-
dc.contributor.authorWang, LJ-
dc.contributor.authorChan, GCF-
dc.contributor.authorLi, JCB-
dc.date.accessioned2015-04-17T05:10:55Z-
dc.date.available2015-04-17T05:10:55Z-
dc.date.issued2015-
dc.identifier.citationThe 5th International Human Microbiome Congress (IHMC 2015), Luxembourg, 31 March-2 April 2015. In Abstracts Book, 2015, p. 122-123-
dc.identifier.urihttp://hdl.handle.net/10722/209363-
dc.descriptionCongress Theme: Future Directions for Human Microbiome Research in Health and Disease-
dc.descriptionSession - Evidence for Cause and Effect in Microbiome Diseases: no. Evi-078#287-
dc.description.abstractInterleukin 17 is a crucial immunomodulator in various chronic immunological diseases and infectious diseases including inflammatory bowel disease and tuberculosis. The action of IL-17 in chronic disease could be detrimental through the overproduction of proinflammatory cytokines but IL-17 can also be protective during microbial infection by suppressing the overwhelmed immune responses. Therefore, the balance between the population of IL-17 producing cells (Th17) and other T cell subset plays an important role in maintaining the homeostatic of the immunity. Previous studies showed that the gut microbes and its colonies could enhance the Th17 cells differentiation and induce the production of IL-17 in intestine. During the pathogenic bacteria infection, such as Salmonella typhimurium infection, the colonies of the microbiota will be affected. These changes may activate the T cells and macrophages to produce proinflammatory cytokines to combat both the commensals and pathogenic bacteria. As IL-17 is crucial in both innate and mucosal immunity, we hypothesize that IL-17 could affect the immune cells to fight against the bacterial infection in intestine. Human macrophages were isolated and differentiated from peripheral blood mononuclear cell of healthy donors. In order to mimic the condition at the intestine that IL-17 is induced by commensals, the macrophages were primed with interleukin-17A for 3 days, followed by Salmonella typhimurium infection for 24 h. Culture supernatant was collected for enzyme-linked immunosorbant assay to quantify proinflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6. We observed that IL-17A-treated macrophages exhibited suppressed productions of TNF-α and IL-6 in response to Salmonella typhimurium infection. The reduction of cytokines production was not associated with cell death. These data suggested IL-17 primed macrophage could limit the proinflammatory cytokine production during pathogenic bacterial infection. As the microbiota could induce the Th17 differentiation, this could be a protective mechanism for commensal bacteria to fight against other bacterial infection in intestine.-
dc.languageeng-
dc.publisherIHMC 2015. The Conference programmes' website is located at http://www.ihmc2015.org/en/scientific-programme/abstractbook-
dc.relation.ispartofInternational Human Microbiome Congress, IHMC 2015-
dc.titleA possible role of IL-17 during Salmonella typhimurium infection-
dc.typeConference_Paper-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.emailLi, JCB: jamesli@hku.hk-
dc.identifier.authorityChan, GCF=rp00431-
dc.identifier.authorityLi, JCB=rp00496-
dc.identifier.hkuros242939-
dc.identifier.spage122-
dc.identifier.epage123-
dc.publisher.placeLuxembourg-

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