TLR2-Mediated Survival of Staphylococcus aureus in Macrophages: A Novel Bacterial Strategy against Host Innate Immunity

• DOI: 10.4049/jimmunol.178.8.4917
• Publication Date: 2014-04-18T22:55:39Z
• Authors: Ikuko Watanabe; Manami Ichiki; Akiko Shiratsuchi; Yoshinobu Nakanishi
• Keywords: Staphylococcus aureus; Macrophages; JNK Mitogen-Activated Protein Kinases; Nitric Oxide; Immunity, Innate; Toll-Like Receptor 2; 3. Good health; Mice, Inbred C57BL; Mice; 03 medical and health sciences; 0302 clinical medicine; Phagocytosis; Superoxides; Animals

Abstract TLR2 plays a role as pattern-recognition receptor in the innate immune response involving secreted proteins against microbial pathogens. To examine its possible involvement cellular response, we determined levels of engulfment and subsequent killing bacteria by macrophages prepared from TLR2-deficient wild-type mice. The level Staphylococcus aureus or Escherichia coli was almost same between TLR2-lacking macrophages. However, colony-forming ability engulfed S. aureus, but not E. coli, decreased to greater extent than control. incubation with caused activation JNK macrophages, pretreatment inhibitor increased rate again coli. In addition, number colonies formed JNK-dependent manner when were pretreated LPS. Furthermore, seemed inhibit generation superoxide, NO, These results collectively suggested that superoxide is reduced have through actions TLR2-activated JNK, resulting prolonged survival bacterium phagosomes. regulation did influence because this more resistant aureus. We propose novel bacterial strategy for hijacking an receptor.