Muscarinic receptor subtype-deficient mice have been used to examine cigarette smoke-induced airway inflammation, with the conclusion that signaling through the M3 receptor was broadly pro-inflammatory, characterized by elevated neutrophils, macrophages, and lymphocytes in the airways and a corresponding increase in the expression of CXCL-1, CCL2, and IL-6, whereas signaling through the M1 and M2 mAChRs was generally anti-inflammatory, characterized by a reduction in cellular infiltration and chemokine levels (43). This evidence concerns the gene CCL2 and inflammatory response.