The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins.
The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins.
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DOI：
10.1007/s00011-012-0436-8
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发表时间：
2012-02
影响因子：
6.7
通讯作者：
Levinson, Arnold I.
中科院分区：
文献类型：
--
作者：
Anderson, Amy L.;Zheng, Yi;Song, Decheng;LaRosa, David;Van Rooijen, Nico;Kierstein, Gerold;Kierstein, Sonja;Haczku, Angela;Levinson, Arnold I.
To determine whether Finegoldia magna protein L (PL) causes lung inflammation and, if so, whether the response is dependent on its Ig-binding B cell superantigenic property. Pulmonary inflammatory reactions were analyzed at varying time points after intratracheal administration of PL to various strains of mice. PL caused peribronchial and perivascular inflammation that peaked at 18–24 hours. Polymorphonuclear cells (PMNs) began to accumulate in bronchoalveolar lavage fluid (BALF) of PL-challenged mice by 4 hours and accounted for >90% of leukocytes by 18–24 hours. Inflammation was marked by the appearance of MIP-2, KC, TNF-α, and IL-6 in the BALF with peak levels attained 4 hours after PL administration. PL-induced pulmonary inflammation was associated with increased airway hyperreactivity following inhalation of methacholine. The inflammatory reaction was unabated in mice lacking B cells and Igs. By contrast, PL-induced inflammation was abrogated in MyD88- deficient mice. PL-induced responses required alveolar macrophages. These results strongly suggest that PL-induced lung inflammation is dependent on an innate MyD88 dependent pathway rather than the Ig-binding properties of this microbial B cell superantigen. We propose that this pulmonary inflammatory reaction is caused by the interaction of PL with a Toll-like receptor expressed on alveolar macrophages.
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