Correlation of Surface Toll-Like Receptor 9 Expression with IL-17 Production in Neutrophils during Septic Peritonitis in Mice Induced by E. coli
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Published on: May 2, 2018
Yunjia Ren1, Li Hua2, Xiuping Meng3
1Department of Molecular Biology in College of Basic Medical Sciences and Institute of Pediatrics in First Hospital, Jilin University, Changchun 130021, China; Department of Endodontics, School and Hospital of Stomatology, Jilin University, Changchun 130021, China.
Abstract:
IL-17 is a proinflammatory cytokine produced by various immune cells. Polymorphonuclear neutrophils (PMNs) are the first line of defense in bacterial infection and express surface Toll-like receptor 9 (sTLR9). To study the relationship of sTLR9 and IL-17 in PMNs during bacterial infection, we infected mice with E. coli intraperitoneally to establish a septic peritonitis model for studying the PMNs response in peritoneal cavity. We found that PMNs and some of "giant cells" were massively accumulated in the peritoneal cavity of mice with fatal septic peritonitis induced by E. coli. Kinetically, the CD11b(+) PMNs were increased from 20-40% at 18 hours to >80% at 72 hours after infection. After E. coli infection, sTLR9 expression on CD11b(+) and CD11b(-) PMNs and macrophages in the PLCs were increased at early stage and deceased at late stage; IL-17 expression was also increased in CD11b(+) PMNs, CD11b(-) PMNs, macrophages, and CD3(+) T cells. Using experiments of in vitro blockage, qRT-PCR and cell sorting, we confirmed that PMNs in the PLCs did increase their IL-17 expression during E. coli infection. Interestingly, sTLR9(-)CD11b(+)Ly6G(+) PMNs, not sTLR9(+)CD11b(+)Ly6G(+) PMNs, were found to be able to increase their IL-17 expression. Together, the data may help understand novel roles of PMNs in septic peritonitis.
Insights
Polymorphonuclear neutrophils (PMNs) play a key role in bacterial infections. This study reveals that PMNs increase IL-17 expression, particularly those lacking surface Toll-like receptor 9 (sTLR9), during E. coli-induced septic peritonitis.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Proinflammatory cytokine IL-17 is crucial in immune responses.
- Polymorphonuclear neutrophils (PMNs) are vital in combating bacterial infections.
- PMNs express surface Toll-like receptor 9 (sTLR9), implicated in immune signaling.
Purpose of the Study:
- To investigate the interplay between sTLR9 and IL-17 production in PMNs during bacterial infection.
- To elucidate the role of PMNs in the context of E. coli-induced septic peritonitis.
Main Methods:
- Established a murine model of E. coli-induced septic peritonitis.
- Analyzed PMN accumulation and expression of sTLR9 and IL-17 using flow cytometry and qRT-PCR.
- Utilized in vitro blockage and cell sorting techniques to differentiate PMN subsets.
Main Results:
- Massive accumulation of PMNs and "giant cells" observed in the peritoneal cavity during fatal septic peritonitis.
- Increased expression of sTLR9 and IL-17 in peritoneal cells, including PMNs, macrophages, and T cells, post E. coli infection.
- Specifically, sTLR9-negative PMNs demonstrated increased IL-17 expression, unlike their sTLR9-positive counterparts.
Conclusions:
- PMNs significantly contribute to IL-17 production during E. coli septic peritonitis.
- The absence of sTLR9 on PMNs is associated with enhanced IL-17 expression.
- Findings suggest novel roles for PMNs in the pathogenesis of septic peritonitis.
