2015年7月28日，我院熊思东教授在International Journal of Medical Microbiology杂志发表了题为“Signaling lymphocyte-activation molecule SLAMF1 augments mycobacteria BCG-induced inflammatory response and facilitates bacterial clearance” 的研究论文，该论文发现SLAMF1增强结核分枝杆菌BCG诱导的炎症反应并促进细菌的清除。
研究生宋腾飞和董春升副教授为该论文的共同第一作者。熊思东教授为该论文的通讯作者。该项研究由国家十二五规划科技重点项目(2013ZX10003007，2012ZX10003006-008)，国家重点基础研究发展计划(2013CB530501，2013CB531502)，江苏省高校优势学科建设工程(PAPD)，江苏省创新团队等基金资助。
文章摘要：
Tuberculosis, which is caused by intracellular mycobacterium Mycobacterium tuberculosis(Mtb), remains one of the most serious global public health concerns. The mechanisms by which innate immunity regulates the inflammatory responses and affects mycobacterial infection remain unclear. In this study, signalingly mphocyte-activation molecule family 1 (SLAMF1) was significantly upregulated in Mycobacterium bovis Bacille Calmette–Guérin (BCG)-infected RAW264.7 cells. Overexpression of SLAMF1 significantly increased the production of inflammatory factors TNF-α and IL-1β, as well as chemokine MCP-1, both in vitro and in vivo upon mycobacteria BCG infection. By contrast, knockdown of SLAMF1 significantly decreased the production of TNF-α, IL-1β, and MCP-1. Western blot analysis indicated that the NF-κB signaling pathway may contribute to the elevated inflammatory response promoted by SLAMF1, as evidenced by higher levels of phosphorylated p65 and IκBα detected with SLAMF1 overe-xpression. Furthermore,SLAMF1 upregulation facilitated bacterial clearance in infected RAW264.7 cells and in the lungs of infected mice. In conclusion, we demonstrated that BCG infection significantly upregulated SLAMF1, which enhanced inflammatory response by activating the NF-κB signaling pathway and facilitated bacterial clearance in BCG-infected RAW264.7 cells and mice.