Major outer membrane protein Omp25 of Brucella suis is involved in inhibition of tumor necrosis factor alpha production during infection of human macrophages

摘要: Brucella spp. can establish themselves and cause disease in humans animals. The mechanisms by which evade the antibacterial defenses of their host, however, remain largely unknown. We have previously reported that live brucellae failed to induce tumor necrosis factor alpha (TNF-alpha) production upon human macrophage infection. This inhibition is associated with a nonidentified protein released into culture medium. Outer membrane proteins (OMPs) gram-negative bacteria been shown modulate functions, including cytokine production. Thus, we analyzed effects two major OMPs (Omp25 Omp31) suis 1330 (wild-type [WT] B. suis) on TNF-alpha For this purpose, omp25 omp31 null mutants (Deltaomp25 Deltaomp31 suis, respectively) were constructed for ability activate macrophages secrete TNF-alpha. showed that, contrast WT or Deltaomp25 induced when phagocytosed macrophages. complementation (Deltaomp25-omp25 mutant) significantly reversed effect: Deltaomp25-omp25 suis-infected secreted less than did infected mutant. Furthermore, pretreatment an anti-Omp25 monoclonal antibody directed against epitope exposed at surface resulted substancial during These observations demonstrated Omp25 involved negative regulation infection