, 2007 and Nicod, 1999), which contribute to the recruitment of circulating cells into inflamed tissue. In addition, AMs
are pivotal cells in the resolution of the inflammatory process selleck kinase inhibitor as they are professional phagocytes of apoptotic cells, such as polymorphonuclear cells (Kennedy and DeLeo, 2009 and Soehnlein and Lindbom, 2010). Alveolar macrophages are phenotypically differentiated circulating monocytes, which are recruited from the blood to the lung in a steady state. During this process, the monocytes express adhesion molecules that bind to endothelial cell ligands, mediating the initial monocyte–endothelial interactions, and they migrate into lung tissue in response to chemoattractant mediators (Geissmann et al., 2010).
In the lung parenchyma, blood monocytes differentiate and proliferate and subsequently migrate into the alveolar space. During a host defence response, this scenario is exacerbated to provide higher levels of functional AMs in the bronchoalveolar lavage fluid (BALF; Landsman and Jung, 2007). Monocyte chemoattractant protein-1 (MCP-1 or CCL2), a member of the chemokine (C C motif) subfamily, is a potent mononuclear cell chemoattractant produced by different cell types including macrophages, monocytes and epithelial cells in response to oxidizing agents, cytokines, growth selleck inhibitor factors and endotoxins (Yadav et al., 2010). Although MCP-1 is constitutively produced, higher concentrations are observed during the inflammatory response. Monocyte chemoattractant protein-1 controls the monocyte/macrophage phenotype profile and monocyte traffic during inflammation by interacting with G-protein-coupled receptors; chemokine (C C motif) receptor 2 and the Duffy antigen receptor for chemokines (DARC) are expressed on leukocyte membranes (Deshmane Clomifene et al., 2009 and Yadav et al., 2010). In addition, it has been shown that in vivo
blockade of MCP-1 functions hampers alveolar tissue repair in virus-induced pneumonitis, therefore suggesting a pivotal role of MCP-1 during the resolution of inflammation ( Narasaraju et al., 2010). Recently, the role of HQ on MCP-1 production was observed. In vitro HQ exposure was found to inhibit MCP-1 secretion by human retinal pigment epithelial cells via a reduction of mRNA transcription. Moreover, cells obtained from age-related macular degeneration (AMD) patients also showed reduced levels of MCP-1. It has been suggested that HQ may be involved in AMD genesis since cigarette smoking is one of the biggest risk factors for the onset and severity of this degenerative disease ( Pons and Marin-Castaño, 2011). Epidemiological and experimental studies have shown that lung infections are more common in smokers than in non-smokers. However, the mechanisms involved in this increased susceptibility to infections are not yet known (Arcavi and Benowitz, 2004, Feng et al.