High-fat diet-induced obesity affects alpha 7 nicotine acetylcholine receptor expressions in mouse lung myeloid cells

Ample evidence indicates that obesity causes dysfunctions in the lung. Previous studies also show that cholinergic anti-inflammatory pathways play crucial roles in obesity-induced chronic inflammation via α7 nicotinic acetylcholine receptor (α7nAChR) signaling. However, it remains unclear whether and how obesity affects the expressions of α7nAChR in myeloid cells in the lung. To address this question, we treated regular chow diet-fed mice or high-fat diet induced obese mice with lipopolysaccharide (LPS) or vehicle via endotracheal injections. By using a multicolor flow cytometry approach to analyze and characterize differential cell subpopulations and α7nAChR expressions, we find no detectable α7nAChR in granulocytes, monocytes and alveolar macrophages, and low expression levels of α7nAChR were detected in interstitial macrophages. Interestingly, we find that a challenge with LPS treatment significantly increased expression levels of α7nAChR in monocytes, alveolar and interstitial macrophages. Meanwhile, we observed that the expression levels of α7nAChR in alveolar and interstitial macrophages in high-fat diet induced obese mice were lower than regular chow diet-fed mice challenged by the LPS. Together, our findings indicate that obesity alters the expressions of α7nAChR in differential lung myeloid cells.