Bry Lynn, Brenner Michael B
Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Immunol. 2004 Jan 1;172(1):433-41. doi: 10.4049/jimmunol.172.1.433.
Citrobacter rodentium uses virulence factors similar to the enteropathogenic Escherichia coli to produce attaching and effacing lesions in the distal colon of mice. We used this infection model to determine components of adaptive immunity needed to survive infection. During acute infection, wild-type mice develop breaks across infected epithelial surfaces but resolve infection. Surprisingly, mice markedly deficient in mucosal lymphocyte populations from beta(7) integrin deficiency resolve infection, as do CD8alpha-/- or TCR-delta-/- mice. In contrast, CD4-/- or TCR-beta-/- mice develop polymicrobial sepsis and end-organ damage, and succumb during acute infection, despite epithelial damage similar to wild-type mice. B cell-deficient (MuMT-/-) or B and T cell-deficient (recombinase-activating gene 2-/-) mice develop severe pathology in colon and internal organs, and deteriorate rapidly during acute infection. Surviving mice develop robust Citrobacter-specific serum IgM responses during acute infection, whereas mice that succumb do not. However, CD4-/- mice receiving serum Igs from infected wild-type mice survive and clear the infection. Our data show that survival of apparently self-limited and luminal mucosal infections requires a systemic T cell-dependent Ab response against bacteria that enter through damaged mucosa. These findings have implications for understanding host defense against mucosal infections, including the pathogenesis of these diseases in immunocompromised populations.
鼠柠檬酸杆菌利用与肠致病性大肠杆菌相似的毒力因子,在小鼠远端结肠产生紧密黏附并抹平损伤。我们利用这种感染模型来确定感染存活所需的适应性免疫成分。在急性感染期间,野生型小鼠在感染的上皮表面出现破损,但感染得以解决。令人惊讶的是,由于β7整合素缺陷而导致黏膜淋巴细胞群体明显缺乏的小鼠能够解决感染,CD8α-/-或TCR-δ-/-小鼠也是如此。相比之下,CD4-/-或TCR-β-/-小鼠会发生多种微生物败血症和终末器官损伤,并在急性感染期间死亡,尽管其上皮损伤与野生型小鼠相似。B细胞缺陷(MuMT-/-)或B细胞和T细胞缺陷(重组激活基因2-/-)的小鼠在结肠和内脏器官中出现严重病变,并在急性感染期间迅速恶化。存活的小鼠在急性感染期间会产生强大的柠檬酸杆菌特异性血清IgM反应,而死亡的小鼠则不会。然而,接受感染的野生型小鼠血清Ig的CD4-/-小鼠能够存活并清除感染。我们的数据表明,明显自限性的管腔内黏膜感染的存活需要针对通过受损黏膜进入的细菌产生全身性T细胞依赖性抗体反应。这些发现对于理解宿主对黏膜感染的防御,包括免疫受损人群中这些疾病的发病机制具有重要意义。