tailieunhanh - Báo cáo y học: " Alveolar hypoxia, alveolar macrophages, and systemic inflammation"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:"" Alveolar hypoxia, alveolar macrophages, and systemic inflammation. | Respiratory Research BioMed Central Review Alveolar hypoxia alveolar macrophages and systemic inflammation Jie Chao John G Wood and Norberto C Gonzalez Open Access Address Department of Molecular and Integrative Physiology University of Kansas Medical Center Kansas City KS 66160 USA Email Jie Chao - jchao@ John G Wood - jwood2@ Norberto C Gonzalez - ngonzale@ Corresponding author Published 22 June 2009 Received 2 April 2009 Respiratory Research 2009 10 54 doi 1465-9921-10-54 Accepted 22 June 2009 This article is available from http content 10 1 54 2009 Chao et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Diseases featuring abnormally low alveolar PO2 are frequently accompanied by systemic effects. The common presence of an underlying inflammatory component suggests that inflammation may contribute to the pathogenesis of the systemic effects of alveolar hypoxia. While the role of alveolar macrophages in the immune and defense functions of the lung has been long known recent evidence indicates that activation of alveolar macrophages causes inflammatory disturbances in the systemic microcirculation. The purpose of this review is to describe observations in experimental animals showing that alveolar macrophages initiate a systemic inflammatory response to alveolar hypoxia. Evidence obtained in intact animals and in primary cell cultures indicate that alveolar macrophages activated by hypoxia release a mediator s into the circulation. This mediator activates perivascular mast cells and initiates a widespread systemic inflammation. The inflammatory cascade includes activation of the local renin-angiotensin system and results in increased leukocyte-endothelial