Protective role of IL-1β against post-arthroplasty Staphylococcus aureus infection.
Protective role of IL-1β against post-arthroplasty Staphylococcus aureus infection.
复制标题
DOI：
10.1002/jor.21414
复制
发表时间：
2011-10
影响因子：
2.8
通讯作者：
Miller, Lloyd S.
中科院分区：
文献类型：
--
作者：
Bernthal, Nicholas M.;Pribaz, Jonathan R.;Stavrakis, Alexandra I.;Billi, Fabrizio;Cho, John S.;Ramos, Romela Irene;Francis, Kevin P.;Iwakura, Yoichiro;Miller, Lloyd S.
MyD 88是IL-1 R和TLR家族成员用于启动下游信号传导和促进免疫应答的衔接分子。鉴于IL-1β在S.金黄色葡萄球菌感染和TLR 2被S.金黄色葡萄球菌脂肽，我们假设IL-1β和TLR 2有助于MyD 88依赖性的保护性免疫应答，以对抗关节成形术后的S。金黄色葡萄球菌感染为了验证这一假设，我们使用了一个关节成形术后S。金黄色葡萄球菌感染，以比较IL-1β缺陷型、TLR 2缺陷型和野生型小鼠中的细菌负荷、生物膜形成和中性粒细胞募集。通过使用体内生物发光成像，我们发现IL-1β缺陷小鼠的细菌负荷在感染后1天高出26倍，并且在第42天保持比野生型小鼠高3至10倍。相比之下，TLR 2缺陷小鼠的细菌负荷与野生型小鼠没有差异。此外，与野生型小鼠相比，从IL-1β缺陷小鼠中收获的植入物具有更多的生物膜形成和14倍的粘附细菌。最后，与野生型小鼠相比，IL-1β缺陷型小鼠感染术后关节的中性粒细胞募集减少约50%。总之，这些发现表明IL-1β诱导中性粒细胞募集以帮助控制细菌负荷和随后的手术后关节中生物膜形成的机制。
MyD88 is an adapter molecule that is used by both IL-1R and TLR family members to initiate downstream signaling and promote immune responses. Given that IL-1β is induced after S. aureus infections and TLR2 is activated by S. aureus lipopeptides, we hypothesized that IL-1β and TLR2 contribute to MyD88-dependent protective immune responses against post-arthroplasty S. aureus infections. To test this hypothesis, we used a mouse model of a post-arthroplasty S. aureus infection to compare the bacterial burden, biofilm formation and neutrophil recruitment in IL-1β-deficient, TLR2-deficient and wildtype mice. By using in vivo bioluminescence imaging, we found that the bacterial burden in IL-1β-deficient mice was 26-fold higher at 1 day after infection and remained 3- to 10-fold greater than wildtype mice through day 42. In contrast, the bacterial burden in TLR2-deficient mice did not differ from wildtype mice. In addition, implants harvested from IL-1β-deficient mice had more biofilm formation and 14-fold higher adherent bacteria compared with those from wildtype mice. Finally, IL-1β-deficient mice had ~50% decreased neutrophil recruitment to the infected postoperative joints than wildtype mice. Taken together, these findings suggest a mechanism by which IL-1β induces neutrophil recruitment to help control the bacterial burden and the ensuing biofilm formation in a post-surgical joint.
登录
查看更多内容
DOI：
10.1006/clin.1996.4276
发表时间：
1997-01-01
期刊：
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY
影响因子：
--
作者：
Kimura, M;Matsukawa, A;Yoshinaga, M
通讯作者：
Yoshinaga, M
影响因子：
64.8
作者：
Hoebe, K;Georgel, P;Beutler, B
通讯作者：
Beutler, B
MyD88 缺陷人类的化脓性细菌感染。
影响因子：
56.9
作者：
von Bernuth, Horst;Picard, Capucine;Jin, Zhongbo;Pankla, Rungnapa;Xiao, Hui;Ku, Cheng-Lung;Chrabieh, Maya;Ben Mustapha, Imen;Ghandil, Pegah;Camcioglu, Yildiz;Vasconcelos, Julia;Sirvent, Nicolas;Guedes, Margarida;Vitor, Artur Bonito;Herrero-Mata, Maria Jose;Arostegui, Juan Ignacio;Rodrigo, Carlos;Alsina, Laia;Ruiz-Ortiz, Estibaliz;Juan, Manel;Fortuny, Claudia;Yague, Jordi;Anton, Jordi;Pascal, Mariona;Chang, Huey-Hsuan;Janniere, Lucile;Rose, Yoann;Garty, Ben-Zion;Chapel, Helen;Issekutz, Andrew;Marodi, Laszlo;Rodriguez-Gallego, Carlos;Banchereau, Jacques;Abel, Laurent;Li, Xiaoxia;Chaussabel, Damien;Puel, Anne;Casanova, Jean-Laurent
通讯作者：
Casanova, Jean-Laurent
影响因子：
4.2
作者：
Salgado, Cassandra D.;Dash, Sangita;Marculescu, Camelia E.
通讯作者：
Marculescu, Camelia E.
影响因子：
32.4
作者：
Miller, LS;O'Connell, RM;Modlin, RL
通讯作者：
Modlin, RL