Alveolar macrophages initiate the systemic microvascular inflammatory response to alveolar hypoxia

作者：Chao Jie; Wood John G; Gonzalez Norberto C^*

来源：Respiratory Physiology & Neurobiology, 2011, 178(3): 439-448.

DOI：10.1016/j.resp.2011.03.008

• Alveolar hypoxia
• Alveolar macrophages
• Systemic inflammation
• Mast cells
• MCP-1/CCL2

Alveolar hypoxia occurs as a result of a decrease in the environmental PO2, as in altitude, or in clinical conditions associated with a global or regional decrease in alveolar ventilation. Systemic effects, in most of which an inflammatory component has been identified, frequently accompany both acute and chronic forms of alveolar hypoxia. Experimentally, it has been shown that acute exposure to environmental hypoxia causes a widespread systemic inflammatory response in rats and mice.
Recent research has demonstrated that alveolar macrophages, in addition to their well known intrapulmonary functions, have systemic, extrapulmonary effects when activated, and indirect evidence suggest these cells may play a role in the systemic consequences of alveolar hypoxia.
This article reviews studies showing that the systemic inflammation of acute alveolar hypoxia observed in rats is not initiated by the low systemic tissue P-O2, but rather by a chemokine, Monocyte Chemoattractant Protein-1 (MCP-1, or CCL2) released by alveolar macrophages stimulated by hypoxia and transported by the circulation. Circulating MCP-1, in turn, activates perivascular mast cells to initiate the microvascular inflammatory cascade.
The research reviewed here highlights the extrapulmonary effects of alveolar macrophages and provides a possible mechanism for some of the systemic effects of alveolar hypoxia.

• 出版日期2011-9-30