CD11b Deficiency Exacerbates Methicillin-Resistant<i>Staphylococcus aureus</i>-Induced Sepsis by Upregulating Inflammatory Responses of Macrophages
Hyunsub Sim, Daecheol Jeong, Hye‐In Kim, Seongwon Pak, Bikash Thapa, Hyung‐Joo Kwon, Keunwook Lee
Abstract
knockout mice was significantly higher than that of control mice, which is associated with increased production of TNF-α and IL-6. In response to MRSA, both bone marrow-derived macrophages and peritoneal macrophages lacking CD11b produced elevated amounts of pro-inflammatory cytokines and nitric oxide. Moreover, CD11b deficiency upregulated IL-4-induced expression of anti-inflammatory mediators such as IL-10 and arginase-1, and an immunomodulatory function of macrophages to restrain T cell activation. Biochemical and confocal microscopy data revealed that CD11b deficiency augmented the activation of NF-κB signaling and phosphorylation of Akt, which promotes the functional activation of macrophages with pro-inflammatory and immunoregulatory phenotypes, respectively. Overall, our experimental evidence suggests that CD11b is a critical modulator of macrophages in response to microbial infection.