RCAN1 deficiency protects against Salmonella intestinal infection by modulating JNK activation

Publication date: September 2016
Source:Molecular Immunology, Volume 77
Author(s): Qian-Qian Lei, Gui-Qiu Hu, Wei Chen, Shui-Xing Yu, Shuai Qi, Chong-Tao Du, Jing-Min Gu, Tong-Jun Lin, Yong-Jun Yang
ObjectiveRCAN1 (regulator of calcineurin 1) has been shown to be involved in various physiological and pathological processes. However, the biological implications of RCAN1 during gastrointestinal tract infection remain unclear. In this study, we tried to determine the role of RCAN1 in acute Salmonella infectious colitis.MethodsWild type and RCAN1-deficient mice or macrophages were used to characterize the impacts of RCAN1 on intestinal inflammation, inflammatory cytokines production, animal survival, and pathogen clearance following Salmonella challenge.ResultsHistologic and quantitative assessments showed increased inflammation and elevated proinflammatory cytokines production in RCAN1-deficient mice. The aberrant inflammatory response was recapitulated in primary bone marrow-derived macrophages. In addition, we reveal a novel regulatory role for RCAN1 in the proinflammatory JNK signaling both in vitro and in vivo. Further analysis showed that the increased inflammation in RCAN1-deficient mice contributed to pathogen clearance and host survival.ConclusionsThe present study demonstrates that RCAN1 deficiency protects against Salmonella intestinal infection by enhancing proinflammatory JNK signaling.



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