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β-Chemokines Are Induced by Mycobacterium tuberculosis and Inhibit Its Growth

机译：结核分枝杆菌诱导β-趋化因子并抑制其生长

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Chemokines (CK) are potent leukocyte activators and chemoattractants and aid in granuloma formation, functions critical for the immune response to Mycobacterium tuberculosis. We hypothesized that infection of alveolar macrophages (AM) with different strains of M. tuberculosis elicits distinct profiles of CK, which could be altered by human immunodeficiency virus (HIV) infection. RANTES, macrophage inflammatory protein-1α (MIP-1α), and MIP-1β were the major β-CK produced in response to M. tuberculosis infection. Virulent M. tuberculosis (H37Rv) induced significantly less MIP-1α than did the avirulent strain (H37Ra), while MIP-1β and RANTES production was comparable for both strains. MIP-1α and MIP-1β were induced by the membrane, but not cytosolic, fraction of M. tuberculosis. M. tuberculosis-induced CK secretion was partly dependent on tumor necrosis factor alpha (TNF-α). AM from HIV-infected individuals produced less TNF-α and MIP-1β than did normal AM in response to either M. tuberculosis strain. We tested the functional significance of decreased β-CK secretion by examining the ability of β-CK to suppress intracellular growth of M. tuberculosis. MIP-1β and RANTES suppressed intracellular growth of M. tuberculosis two- to threefold, a novel finding. Thus, β-CK contribute to the innate immune response to M. tuberculosis infection, and their diminution may promote the intracellular survival of M. tuberculosis.
机译：趋化因子（CK）是有效的白细胞激活剂和趋化因子，有助于肉芽肿的形成，对结核分枝杆菌的免疫反应至关重要。我们假设用不同的 M菌株感染肺泡巨噬细胞（AM）。结核引起了CK的独特变化，而人类免疫缺陷病毒（HIV）感染可能会改变CK的变化。 RANTES，巨噬细胞炎性蛋白-1α（MIP-1α）和MIP-1β是响应 M产生的主要β-CK。结核感染。毒力 M。结核病（H37Rv）诱导的MIP-1α明显低于无毒力菌株（H37Ra），而两种菌株的MIP-1β和RANTES产量却相当。 MIP-1α和MIP-1β是由 M的膜部分而非胞质诱导的。结核病。 M。结核诱导的CK分泌部分依赖于肿瘤坏死因子α（TNF-α）。来自HIV感染个体的AM对任一 M的反应产生的TNF-α和MIP-1β均少于正常AM。结核菌株。我们通过检查β-CK抑制细胞内 M生长的能力，测试了β-CK分泌减少的功能意义。结核病。 MIP-1β和RANTES抑制了 M的细胞内生长。结核病2-3倍，这是一个新颖的发现。因此，β-CK有助于对 M的先天免疫应答。结核感染及其减少可能促进 M的细胞内存活。结核病。

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