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首页> 外文期刊>Infection and immunity >Chemokine Gene Expression during Pneumocystis carinii-Driven Pulmonary Inflammation
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Chemokine Gene Expression during Pneumocystis carinii-Driven Pulmonary Inflammation

机译：卡氏肺孢子菌驱动的肺炎症过程中趋化因子基因表达

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Severe combined immunodeficient (SCID) mice lack functional lymphocytes and therefore develop Pneumocystis cariniipneumonia. However, when infected SCID mice are immunologically reconstituted with congenic spleen cells, a protective inflammatory cascade is initiated. Proinflammatory cytokines are produced, and lymphocytes and macrophages are recruited specifically to alveolar sites of infection. Importantly, uninfected regions of the lung remain free from inflammatory involvement, suggesting that there are specific mechanisms that limit inflammation in the infected lung. Therefore, to determine whether chemokines are involved in targeting the P. carinii-driven inflammatory response, steady-state mRNA levels of several chemokines were measured in the lungs of both reconstituted and nonreconstituted P. carinii-infected SCID mice. Despite significant organism burdens in the lungs of 8- and 10-week-old SCID mice, there was no evidence of elevated chemokine gene expression, which is consistent with the lack of an inflammatory response in these animals. However, when 8-week-old infected SCID mice were immunologically reconstituted, signs of focal pulmonary inflammation were observed, and levels of RANTES, MCP-1, lymphotactin, MIP-1α, MIP-1β, and MIP-2 mRNAs were all significantly elevated. Chemokine mRNA abundance was elevated at day 10 postreconstitution (PR), was maximal at day 12 PR, and returned to baseline by day 22 PR. In situ hybridization demonstrated that during the peak of inflammation, RANTES gene expression was localized to sites of inflammatory cell infiltration and P. carinii infection. Thus, these observations indicate that chemokines play a role in the focal targeting of inflammatory cell recruitment to sites of P. carinii infection after the passive transfer of lymphocytes to the host.
机译：严重的联合免疫缺陷（SCID）小鼠缺乏功能性淋巴细胞，因此会发展出卡氏肺孢子虫肺炎。但是，当感染的SCID小鼠用同基因脾细胞免疫重建后，就会启动保护性炎症级联反应。产生促炎性细胞因子，并专门募集淋巴细胞和巨噬细胞至感染的肺泡部位。重要的是，肺的未感染区域保持不受炎症侵害，这表明存在限制感染肺中炎症的特定机制。因此，确定趋化因子是否参与靶向 P。在卡琳氏菌引起的炎症反应中，在重构的和未重构的 P的肺中测量了几种趋化因子的稳态mRNA水平。感染了Carinii 的SCID小鼠。尽管在8周龄和10周龄的SCID小鼠的肺中存在大量生物负荷，但没有证据表明趋化因子基因表达升高，这与这些动物缺乏炎症反应是一致的。但是，当对8周龄感染的SCID小鼠进行免疫重建后，观察到局灶性肺部炎症的迹象，并且RANTES，MCP-1，淋巴肌动蛋白，MIP-1α，MIP-1β和MIP-2 mRNA的水平均显着升高高架。趋化因子mRNA丰度在重建后第10天（PR）升高，在第12天PR达到最大值，并在第22天PR恢复到基线。原位杂交表明，在炎症高峰期，RANTES基因表达位于炎症细胞浸润和 P的位点。卡林氏菌感染。因此，这些观察结果表明趋化因子在炎性细胞募集到 P位点的靶向中发挥作用。淋巴细胞被动转移至宿主后发生卡林氏感染。

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