Hazlett Linda D
Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Ocul Immunol Inflamm. 2005 Apr-Jun;13(2-3):133-8. doi: 10.1080/09273940490912362.
Pseudomonas aeruginosa is a common organism associated with bacterial keratitis primarily resulting from contact lens usage. Advances in our understanding of host innate and adaptive immune responses to experimental infection have been achieved using animal models, including inbred mouse models that are classed as resistant (cornea heals) vs. susceptible (cornea perforates). Evidence has shown that sustained IL-12-driven IFN-gamma production in dominant Th1 responder strains such as C57BL/6 (B6) contributes to corneal destruction and perforation. In contrast, in Th2-responder BALB/c mice, IL-18-driven IFN-gamma production regulates bacterial killing with less corneal destruction. IL-1 and chemotactic cytokines (e.g., MIP-2) recruit PMN to the cornea. The critical role of these cells in the innate immune response and their regulation after bacterial infection has been established. The studies provide a better understanding of the regulatory mechanisms that operate in the cornea after P. aeruginosa challenge, determining susceptibility vs. resistance to disease, and are consistent with long-term goals of providing targets for better treatment of disease.
铜绿假单胞菌是一种与细菌性角膜炎相关的常见病原体，主要由佩戴隐形眼镜引起。利用动物模型，包括被分类为抗性（角膜愈合）与易感性（角膜穿孔）的近交系小鼠模型，我们在理解宿主对实验性感染的固有免疫和适应性免疫反应方面取得了进展。有证据表明，在占主导地位的Th1反应株如C57BL/6（B6）中，由IL-12驱动的持续IFN-γ产生会导致角膜破坏和穿孔。相比之下，在Th2反应的BALB/c小鼠中，由IL-18驱动的IFN-γ产生在调节细菌杀伤的同时，对角膜的破坏较小。IL-1和趋化细胞因子（如MIP-2）将中性粒细胞募集到角膜。这些细胞在固有免疫反应中的关键作用及其在细菌感染后的调节作用已得到证实。这些研究有助于更好地理解铜绿假单胞菌攻击后角膜中起作用的调节机制，确定对疾病的易感性与抗性，并且与为疾病提供更好治疗靶点的长期目标相一致。
