| Interleukin-7 (IL-7) treatment accelerates neutrophil recruitment through gamma delta T-cell IL-17 production in a murine model of sepsis. | |
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MedLine Citation:
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PMID: 20823197 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The sepsis syndrome represents an improper immune response to infection and is associated with unacceptably high rates of mortality and morbidity. The interactions between T cells and the innate immune system while combating sepsis are poorly understood. In this report, we observed that treatment with the potent, antiapoptotic cytokine interleukin-7 (IL-7) accelerated neutrophil recruitment and improved bacterial clearance. We first determined that T cells were necessary for the previously observed IL-7-mediated enhanced survival. Next, IL-7 increased Bcl-2 expression in T cells isolated from septic mice as early as 3 h following treatment. This treatment resulted in increased gamma interferon (IFN-γ) and IP-10 production within the septic peritoneum together with local and systemic increases of IL-17 in IL-7-treated mice. We further demonstrate that the increase in IL-17 was largely due to increased recruitment and production by γδ T cells, which express CXCR3. Consistent with increased IL-17 production, IL-7 treatment increased CXCL1/KC production, neutrophil recruitment, and bacterial clearance. Significantly, end-organ tissue injury was not significantly different between vehicle- and IL-7-treated mice. Collectively, these data illustrate that IL-7 can mediate the cross talk between Th1 and Th17 lymphocytes during sepsis such that neutrophil recruitment and bacterial clearance is improved while early tissue injury is not increased. All together, these observations may underlay novel potential therapeutic targets to improve the host immune response to sepsis. |
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Authors:
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Kevin R Kasten; Priya S Prakash; Jacqueline Unsinger; Holly S Goetzman; Lisa G England; Cindy M Cave; Aaron P Seitz; Cristina N Mazuski; Tony T Zhou; Michel Morre; Richard S Hotchkiss; David A Hildeman; Charles C Caldwell |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-09-07 |
Journal Detail:
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Title: Infection and immunity Volume: 78 ISSN: 1098-5522 ISO Abbreviation: Infect. Immun. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-19 Completed Date: 2010-11-12 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 0246127 Medline TA: Infect Immun Country: United States |
Other Details:
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Languages: eng Pagination: 4714-22 Citation Subset: IM |
Affiliation:
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Division of Research, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0558, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cytokines / immunology Disease Models, Animal Interleukin-17 / biosynthesis* Interleukin-7 / administration & dosage, therapeutic use* Lymphocyte Activation Male Mice Mice, Inbred C57BL Neutrophil Infiltration / immunology* Receptors, Antigen, T-Cell, gamma-delta / genetics, metabolism* Sepsis / immunology*, microbiology, mortality, therapy* T-Lymphocytes / immunology*, metabolism Treatment Outcome |
| Grant Support | |
ID/Acronym/Agency:
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AI057753/AI/NIAID NIH HHS; GM44118/GM/NIGMS NIH HHS; GM55194/GM/NIGMS NIH HHS; GM72760/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Interleukin-17; 0/Interleukin-7; 0/Receptors, Antigen, T-Cell, gamma-delta |
| Comments/Corrections | |
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