IL-10 suppresses bactericidal response of macrophages against Salmonella Typhimurium

• Published in: The journal of microbiology Vol. 49; no. 6; pp. 1050 - 1053
• Main Authors: Lee, K.S., Konkuk University, Seoul, Republic of Korea, Jeong, E.S., Konkuk University, Seoul, Republic of Korea, Heo, S.H., Konkuk University, Seoul, Republic of Korea, Seo, J.H., Konkuk University, Seoul, Republic of Korea, Jeong, D.G., Konkuk University, Seoul, Republic of Korea, Choi, Y.K., Konkuk University, Seoul, Republic of Korea
• Format: Journal Article
• Language: English
• Published: Heidelberg The Microbiological Society of Korea 01.12.2011; Springer Nature B.V; 한국미생물학회
• Subjects: AKT protein; Animals; Bacteria; Bcl-x protein; Biomedical and Life Sciences; Cell Line; Cell survival; cyclin D1; Cyclooxygenase-2; Down-Regulation - drug effects; Humans; IL-10; Infection; Interleukin 10; Interleukin-10 - immunology; Life Sciences; MACROFAGOS; MACROPHAGE; MACROPHAGES; Macrophages - immunology; Macrophages - microbiology; Mice; Microbiology; mRNA; Phosphorylation; Replication; SALMONELLA; Salmonella Infections - immunology; Salmonella Infections - microbiology; Salmonella typhimurium; Salmonella typhimurium - immunology; Salmonella typhimurium - physiology; Tumor necrosis factor- alpha; 생물학; macrophage; IL-10
• ISSN: 1225-8873; 1976-3794
• DOI: 10.1007/s12275-011-1043-z

We report, herein, an attempt to determine whether an IL-10-induced immunological state affects the response of macrophages against Salmonella Typhimurium (ST). Pretreatment with mrIL-10 induced the intracellular invasion of ST into macrophages in a dose-dependent manner. It also activated AKT phosphorylation, cyclin D1, Bcl-X∧L, and COX-2 upon ST infection, which may correlate with Salmonella's survival within the macrophages. However, I-κB phosphorylation was shown to be inhibited, along with the expression of TNF-α and MIP-2α mRNA. Therefore, IL-10 not only suppresses the bactericidal response of macrophages against ST, but also ultimately causes infected macrophages to function as hosts for ST replication.