Williams Julie C, Lee Rebecca D, Doerschuk Claire M, Mackman Nigel
Division of Hematology and Oncology, Department of Medicine, McAllister Heart Institute, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035, USA.
J Signal Transduct. 2011;2011:415195. doi: 10.1155/2011/415195. Epub 2011 Dec 7.
Protease activated receptors (PAR) have been shown to play a role in inflammation. PAR-2 is expressed by numerous cells in the lung and has either proinflammatory, anti-inflammatory, or no effect depending on the model. Here, we examined the role of PAR-2 in a model of LPS-induced lung inflammation. We found that PAR-2-deficient mice had significantly less KC expression in bronchial lavage fluid compared with wild-type mice but there was no difference in MIP-2 or TNF-α expression. We also found that isolated alveolar and resident peritoneal macrophages lacking PAR-2 showed a similar deficit in KC after LPS stimulation without differences in MIP-2 or TNF-α. Infiltration of neutrophils and macrophages into the lung following LPS administration was not affected by an absence of PAR-2. Our results support the notion that PAR-2 plays a role in LPS activation of TLR4 signaling in macrophages.
蛋白酶激活受体（PAR）已被证明在炎症中起作用。PAR-2在肺中的许多细胞中表达，根据模型的不同，它具有促炎、抗炎或无作用。在此，我们研究了PAR-2在脂多糖（LPS）诱导的肺部炎症模型中的作用。我们发现，与野生型小鼠相比，PAR-2缺陷型小鼠支气管灌洗液中的KC表达明显较少，但MIP-2或TNF-α表达没有差异。我们还发现，缺乏PAR-2的分离肺泡巨噬细胞和驻留腹膜巨噬细胞在LPS刺激后KC表达有类似缺陷，而MIP-2或TNF-α没有差异。LPS给药后中性粒细胞和巨噬细胞向肺内的浸润不受PAR-2缺失的影响。我们的结果支持PAR-2在巨噬细胞中LPS激活TLR4信号通路中起作用这一观点。
