免疫复合物炎症的神经源性放大。

Neurogenic amplification of immune complex inflammation.

作者信息

Bozic C R, Lu B, Höpken U E, Gerard C, Gerard N P

机构信息

Perlmutter Laboratory, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.

出版信息

Science. 1996 Sep 20;273(5282):1722-5. doi: 10.1126/science.273.5282.1722.

DOI:10.1126/science.273.5282.1722

PMID:8781237

Abstract

The formation of intrapulmonary immune complexes in mice generates a vigorous inflammatory response characterized by microvascular permeability and polymorphonuclear neutrophil influx. Gene-targeted disruption of the substance P receptor (NK-1R) protected the lung from immune complex injury, as did disruption of the C5a anaphylatoxin receptor. Immunoreactive substance P was measurable in fluids lining the lung at time points before neutrophil influx and may thus be involved in an early step in the inflammatory response to immune complexes in the lung.

摘要

小鼠肺内免疫复合物的形成会引发强烈的炎症反应，其特征为微血管通透性增加和多形核中性粒细胞流入。对P物质受体（NK-1R）进行基因靶向破坏可保护肺免受免疫复合物损伤，对C5a过敏毒素受体进行破坏也有同样效果。在中性粒细胞流入之前的时间点，可在肺内衬液中检测到免疫反应性P物质，因此它可能参与了肺对免疫复合物炎症反应的早期步骤。