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Alveolar macrophages lack CCR2 expression and do not migrate to CCL2

DOI: 10.1186/1476-9255-4-19

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We examined the expression of these receptors in human peripheral blood monocytes and alveolar macrophages using microarray analysis, reverse-transcriptase PCR, flow cytometry and migration analyses.In contrast to peripheral blood monocytes, alveolar macrophages did not express the CCL2 receptor, CCR2, and did not migrate toward CCL2. In contrast, monocytes and freshly isolated resident alveolar macrophages both migrated towards CCL3. However, up to 6-fold more monocytes migrated toward equivalent concentrations of CCL3 than did alveolar macrophages from the same donor. While peripheral blood monocytes expressed the CCL3 receptor, CCR1, alveolar macrophages expressed the alternate CCL3 receptor, CCR5. The addition of anti-CCR5 blocking antibodies completely abrogated CCL3-induced migration in alveolar macrophages, but did not affect the migration of peripheral blood monocytes.These data support the specificity of CCL2 to selectively drive monocyte, but not alveolar macrophage recruitment to the lung and CCR5 as the primary macrophage receptor for CCL3.Peripheral blood monocytes and alveolar macrophages are similar in function, both physiologically and pathophysiologically. Because monocytes are precursors to tissue macrophages, these cells are often referenced interchangeably. However, these cells have independent functions and are differentially regulated. We hypothesized that differences in receptor expression on each cell type distinguished functional chemokine responsiveness between monocytes and alveolar macrophages.To delineate the mechanism regulating peripheral blood monocyte and alveolar macrophage recruitment to the lung, the response of these cells to CCL2 was examined. CCL2, a C-C chemokine, regulates monocyte chemotaxis [1,2], a property shared by several chemokines having adjacent cysteine residues in the N-terminus [3]. Although several chemokines influence monocyte trafficking, CCL2 appears to be critical, as mice deficient in CCL2 have decreased rec


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