Toll-Like Receptor 4 Protects Against Clostridium perfringens Infection in Mice.
Toll-Like Receptor 4 Protects Against Clostridium perfringens Infection in Mice.
复制标题
DOI：
10.3389/fcimb.2021.633440
复制
发表时间：
2021
影响因子：
5.7
通讯作者：
Nagahama M
中科院分区：
文献类型：
--
作者：
Takehara M;Kobayashi K;Nagahama M
据报道，Toll样受体4（TLR 4）通过作为病原体识别受体主要感测来自革兰氏阴性菌的脂多糖（LPS）来保护免受革兰氏阴性菌的侵害。然而，TLR 4在革兰氏阳性菌感染中的作用还不太清楚。A型产气荚膜梭菌是一种革兰氏阳性细菌，可引起以严重肌坏死为特征的气性坏疽。以前的研究表明C.产气荚膜杆菌θ毒素是一种TLR 4激动剂，但TLR 4在C.产气荚膜杆菌感染尚不清楚。在这里，TLR 4缺陷型C3 H/HeJ小鼠感染C.与野生型C3 H/HeN小鼠相比，产气荚膜梭菌的存活率显著降低，活细菌计数增加，并且感染部位的肌原纤维破坏加速。这些结果表明TLR 4在C.产气荚膜杆菌在C中观察到炎性细胞因子如白细胞介素-1 β（IL-1β）、白细胞介素-6（IL-6）和粒细胞集落刺激因子（G-CSF）的水平显著升高。在C3 H/HeJ小鼠中，增加是有限的。通常，增加的G-CSF加速骨髓和脾脏中的粒细胞生成，以加剧中性粒细胞的产生，从而消除细菌。C.脾脏中性粒细胞数量增加。与未感染的小鼠相比，产气荚膜梭菌感染的C3 H/HeN小鼠中的增加较低，而C.产气荚膜杆菌感染的C3 H/HeJ小鼠。此外，DNA微阵列分析显示，TLR 4突变部分影响了C.产气荚膜杆菌感染总之，我们的研究结果表明，TLR 4对于消除C的先天能力至关重要。产气荚膜杆菌
Toll-like receptor 4 (TLR4) has been reported to protect against Gram-negative bacteria by acting as a pathogen recognition receptor that senses mainly lipopolysaccharide (LPS) from Gram-negative bacteria. However, the role of TLR4 in Gram-positive bacterial infection is less well understood. Clostridium perfringens type A is a Gram-positive bacterium that causes gas gangrene characterized by severe myonecrosis. It was previously demonstrated that C. perfringens θ-toxin is a TLR4 agonist, but the role of TLR4 in C. perfringens infection is unclear. Here, TLR4-defective C3H/HeJ mice infected with C. perfringens showed a remarkable decrease in survival rate, an increase in viable bacterial counts, and accelerated destruction of myofibrils at the infection site compared with wild-type C3H/HeN mice. These results demonstrate that TLR4 plays an important role in the elimination of C. perfringens. Remarkable increases in levels of inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and granulocyte colony-stimulating factor (G-CSF), were observed in C. perfringens-infected C3H/HeN mice, whereas the increases were limited in C3H/HeJ mice. Generally, increased G-CSF accelerates granulopoiesis in the bone marrow and the spleen to exacerbate neutrophil production, resulting in elimination of bacteria. The number of neutrophils in the spleen was increased in C. perfringens-infected C3H/HeN mice compared with non-infected mice, while the increase was lower in C. perfringens-infected C3H/HeJ mice. Furthermore, DNA microarray analysis revealed that the mutation in TLR4 partially affects host gene expression during C. perfringens infection. Together, our results illustrate that TLR4 is crucial for the innate ability to eliminate C. perfringens.
登录
查看更多内容
影响因子：
64.8
作者：
Hoebe, K;Georgel, P;Beutler, B
通讯作者：
Beutler, B
结核分枝杆菌感染中的模式识别受体和细胞因子 - 双刃剑？
影响因子：
--
作者：
Hossain MM;Norazmi MN
通讯作者：
Norazmi MN
影响因子：
3
作者：
Bryant, AE;Bayer, CR;Stevens, DL
通讯作者：
Stevens, DL
对医疗统计信息的自由使用的易于使用的软件“ EZR”的调查。
影响因子：
4.8
作者：
Kanda Y
通讯作者：
Kanda Y
影响因子：
30.3
作者：
Burberry A;Zeng MY;Ding L;Wicks I;Inohara N;Morrison SJ;Núñez G
通讯作者：
Núñez G