Accumulation of gamma/delta T cells in the lungs and their roles in neutrophil-mediated host defense against pneumococcal infection
Accumulation of gamma/delta T cells in the lungs and their roles in neutrophil-mediated host defense against pneumococcal infection
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DOI：
10.1016/j.micinf.2006.11.015
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发表时间：
2007-03-01
影响因子：
5.8
通讯作者：
Kawakami, Kazuyoshi
中科院分区：
文献类型：
--
作者：
Nakasone, Chikara;Yamamoto, Natsuo;Kawakami, Kazuyoshi
本研究旨在阐明V γ 4（+）γ δ T细胞（肺γ δ T细胞的主要亚群）在宿主防御肺炎链球菌感染中的作用。在感染后3、6和12 h，肺中完整γ δ T细胞（鉴定为CD 3（+）和TCR-δ（+）细胞）和V γ 4（+）γ δ T细胞（鉴定为CD 3（+）和TCR-V γ 4（+）细胞）的比例和数量增加。与对照野生型（WT）小鼠相比，TCR-V γ 4（-/-）小鼠中感染小鼠的存活率和肺部细菌清除率严重受损。TCR-V γ 4（-/-）小鼠中受损的宿主保护与肺中中性粒细胞的减弱募集密切相关。与WT小鼠相比，TCR-V γ 4（-/-）小鼠感染组织中MIP-2和TNF-α的合成显著减少。在用活细菌刺激的肺白细胞的TNF-α合成中注意到类似的结果，但MIP-2的合成不清楚。我们的研究结果表明，V γ 4（+）γ δ T细胞在嗜中性粒细胞介导的宿主防御S。通过促进肺中TNF-α和可能的MIP-2的合成来治疗肺炎感染。(c)2006年爱思唯尔马森SAS。All rights reserved.
The present study was designed to elucidate the role of V gamma 4(+) gamma delta T cells, a major subset of pulmonary gamma delta T cells, in host defense against infection with Streptococcus pneumoniae. The proportion and number of whole gamma delta T cells, identified as CD3(+) and TCR-delta(+) cells, and V gamma 4(+) gamma delta T cells, identified as CD3(+) and TCR-V gamma 4(+) cells, increased in the lungs at 3, 6 and 12 h post-infection. Survival of infected mice and lung bacterial clearance were severely impaired in TCR-V gamma 4(-/-) mice compared with control wild-type (WT) mice. The impaired host protection in TCR-V gamma 4(-/-) mice correlated well with attenuated recruitment of neutrophils in lungs. MIP-2 and TNF-alpha synthesis in the infected tissues was significantly reduced in TCR-V gamma 4(-/-) mice compared with WT mice. Similar results were noted in the synthesis of TNF-alpha, but not clearly of MIP-2, by lung leukocytes stimulated with live bacteria. Our results demonstrate that V gamma 4(+) gamma delta T cells play an important role in the neutrophil-mediated host defense against S. pneumoniae infection by promoting the synthesis of TNF-alpha and possibly of MIP-2 in the lungs. (c) 2006 Elsevier Masson SAS. All rights reserved.