TLR2 mediates the innate response of retinal Muller glia to Staphylococcus aureus.
TLR2 mediates the innate response of retinal Muller glia to Staphylococcus aureus.
复制标题
DOI：
10.4049/jimmunol.1100565
复制
发表时间：
2011-06-15
期刊：
影响因子：
--
通讯作者：
Kumar A
中科院分区：
文献类型：
--
作者：
Shamsuddin N;Kumar A
Muller cells, the principal glia of the retina, play several key roles in normal and various retinal diseases. To date, their direct involvement in retinal innate defense against bacterial pathogens has not been investigated. Here, we show that Muller cells express Toll-like receptor-2 (TLR2), a key sensor implicated in recognizing Gram-positive bacteria. We found that intravitreal injection of TLR2 agonist Pam3Cys (Pam3) and Staphylococcus(S) aureus activated Muller glia in C57BL/6 mouse retina. Similarly, Pam3 or S. aureus elicited the expression of TLR2 and activated the NF-κB and p38 MAPK signaling cascade. Concomitant with the activation of signaling pathways, transcriptional expression and secretion of various pro-inflammatory cytokines (IL-6, TNF-α, & IL-1β), chemokines (IL-8), and antimicrobial peptide (LL-37) were also induced in Muller glia. Importantly, the culture media derived from TLR2-activated Muller glia exhibited robust bactericidal activity against S. aureus. Furthermore, utilization of neutralizing antibody, siRNA, and pharmacological inhibitors revealed that Muller glial innate response to S. aureus is mediated via theTLR2-›NF-κB axis. Collectively, this study for the first time establishes that the retinal Muller glia senses pathogens via TLR2 and contributes directly to retinal innate defense via production of inflammatory mediators and antimicrobial peptides.
登录
查看更多内容
影响因子：
2
作者：
Callegan, Michelle C.;Cochran, Daniel C.;Stroman, David W.
通讯作者：
Stroman, David W.
影响因子：
3.7
作者：
Gao N;Kumar A;Jyot J;Yu FS
通讯作者：
Yu FS
影响因子：
3.1
作者：
Callegan, MC;Booth, MC;Gilmore, MS
通讯作者：
Gilmore, MS
影响因子：
4.2
作者：
Doshi, Rishi R.;Arevalo, J. Fernando;Cunningham, Emmett T., Jr.
通讯作者：
Cunningham, Emmett T., Jr.
影响因子：
4.7
作者：
Esen, N;Tanga, FY;Kielian, T
通讯作者：
Kielian, T