Fig. 1.

A schematic model for how nicotine exposure augments risk of COVID‐19 entry into the human host lung. (A) Pulmonary and immune responses to COVID‐19 infection in epithelial cells of smokers (right) and nonsmokers (left). (B) Cellular mechanisms of nicotinic receptor activity that promotes COVID‐19 entry and proliferation in epithelial cells through co‐expression of ACE2. Nicotine activation of nicotinic receptors can lead to enhanced protease activation, cell death (apoptosis), and inflammatory signaling through mechanisms that converge on ACE2 regulation and signaling.