Specifically, nicotine upregulated Siglec6 and Siglec15 (both have been shown to act to suppress inflammation via decreasing degranulation or blunting immune signaling) while vehicle chemicals had a more profound effect, upregulating HMOX1 (associated with protective effects against airway epithelial cell damage), IL-32 and IL-34 while decreasing expression of CCL2 (directs type 2 inflammatory cells to the sites of disease), IL-1A, IL-1B, LTC4S and MS4A2
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