Interleukin 6 Promotes Brucella abortus Clearance by Controlling Bactericidal Activity of Macrophages and CD8(+) T Cell Differentiationopen access
- Authors
- Huynh Tan Hop; Tran Xuan Ngoc Huy; Reyes, Alisha Wehdnesday Bernardo; Arayan, Lauren Togonon; Vu, Son Hai; Min, WonGi; Lee, Hu Jang; Kang, Chang Keun; Kim, Dong Hee; Tark, Dong Seob; Kim, Suk
- Issue Date
- Nov-2019
- Publisher
- AMER SOC MICROBIOLOGY
- Keywords
- B. abortus; IL-6; cytotoxic T cells; lysosomal enzymes; SOCS3
- Citation
- INFECTION AND IMMUNITY, v.87, no.11
- Indexed
- SCIE
SCOPUS
- Journal Title
- INFECTION AND IMMUNITY
- Volume
- 87
- Number
- 11
- URI
- https://scholarworks.bwise.kr/gnu/handle/sw.gnu/8536
- DOI
- 10.1128/IAI.00431-19
- ISSN
- 0019-9567
- Abstract
- To date, the implications of interleukin 6 (IL-6) for immune responses in the context of Brucella infection are still unknown. In the present study, we found that Brucella abortus infection induced marked production of IL-6 in mice that was important for sufficient differentiation of CD8(+) T cells, a key factor in Brucella clearance. Blocking IL-6 signaling also significantly induced serum IL-4 and IL-10, together with a decreased gamma interferon (IFN-gamma) level, suggesting that IL-6 is essential for priming the T-helper (Th) 1 cell immune response during Brucella infection. The IL-6 pathway also activated the bactericidal activity of primary and cultured macrophages. Bacterial killing was markedly abrogated when IL-6 signaling was suppressed, and this phenomenon was mainly associated with decreased activity of lysosome-mediated killing. Interestingly, suppressor of cytokine signaling 3 (SOCS3) was important for regulating the IL-6-dependent anti-Brucella activity through the JAK/STAT pathway. During early infection, in the absence of SOCS3, IL-6 exhibited anti-inflammatory effects and lysosome-mediated killing inhibition; however, the increase in SOCS3 successfully shifted functional IL-6 toward proinflammatory brucellacidal activity in the late stage. Our data clearly indicate that IL-6 contributes to host resistance against B. abortus infection by controlling brucellacidal activity in macrophages and priming cellular immune responses.
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Collections - College of Medicine > Department of Medicine > Journal Articles
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