Vojtova Jana, Kamanova Jana, Sebo Peter
Institute of Microbiology of the Academy of Sciences, Videnska 1083, 142 20 Prague, Czech Republic.
Curr Opin Microbiol. 2006 Feb;9(1):69-75. doi: 10.1016/j.mib.2005.12.011. Epub 2006 Jan 6.
Bordetella that infect mammals produce a multifunctional repeat in toxin (RTX) adenylate cyclase toxin known as CyaA, an excellent example of bacterial sophistication in subverting host defense. Recent reports show that interaction of CyaA with tracheal epithelial cells aids adhesion of Bordetella to ciliated mucosa and induces production of the pro-inflammatory cytokine interleukin, IL-6. Myeloid phagocytes, attracted to the site of infection are the target of freshly secreted CyaA that binds to the alpha(M)beta2 integrin (CD11b/CD18), penetrates cells and promptly suppresses their bactericidal functions by converting cellular ATP to cAMP. Such uncontrolled cAMP signaling can also drive CD11b-expressing immature dendritic cells into a semi-mature state, possibly hijacking them to shape the local adaptive immune response towards tolerance of the pathogen.
感染哺乳动物的博德特氏菌会产生一种名为CyaA的多功能重复毒素（RTX）腺苷酸环化酶毒素，这是细菌在破坏宿主防御方面复杂性的一个典型例子。最近的报告表明，CyaA与气管上皮细胞的相互作用有助于博德特氏菌黏附于纤毛黏膜，并诱导促炎细胞因子白细胞介素IL-6的产生。被吸引到感染部位的髓系吞噬细胞是新分泌的CyaA的靶标，CyaA与α（M）β2整合素（CD11b/CD18）结合，穿透细胞，并通过将细胞ATP转化为cAMP迅速抑制其杀菌功能。这种不受控制的cAMP信号传导还可驱使表达CD11b的未成熟树突状细胞进入半成熟状态，可能借此操纵它们，使局部适应性免疫反应朝着对病原体的耐受性发展。
