Effect of Cigarette Smoke on Gut Microbiota: State of Knowledge

Abstract

Cigarette smoke is a representative source of toxic chemical exposures to humans, and the adverse consequences of cigarette smoking are mediated by its effect on both neuronal and immune-inflammatory systems. Cigarette smoking also is a major risk factor for intestinal disorders, such as Crohn's disease and peptic ulcer. On the other hand, cigarette smoking is protective against developing ulcerative colitis. The effects of cigarette smoking on intestinal disorders include changes in intestinal irrigation and microbiome, increases in permeability of the mucosa, and impaired mucosal immune responses. However, the underlying mechanism linking cigarette smoking with intestinal microbiota dysbiosis is largely unknown. In this communication, we first review the current knowledge about the mechanistic interaction between cigarette smoke and intestinal microbiota dysbiosis, which include the likely actions of nicotine, aldehydes, polycyclic aromatic hydrocarbons, heavy metals, volatile organic compounds and toxic gases, and then reveal the potential mechanisms of the lung-gut cross talk and skin-gut cross talk in regulating the balance of intestinal microbiota and the interrelation of intestinal microbiota dysbiosis and systemic disorders.

Keywords: cigarette smoking; intestinal microbiota dysbiosis; lung–gut axis; skin-gut axis; systemic disorders.

FIGURE 1

Potential mechanisms of lung-gut cross talk include lung-originating T-cell and eosinophils mis-homing and increases the expression of cytochrome oxidase in lymphocytes. Cigarette smoke exposure may exert important roles in organ cross-talk by affecting these processes, and/or by causing DCs mis-homing in the lungs and gut. Systemic IL-6 combined with local TGF-β may drive cross-organ Th17-polarized inflammation. Systemic IL-13 may stimulate NK cell and macrophage responses in organ cross-talk. DCs = dendritic cells; IL-6 = Interleukin-6; TGF-β = Transforming growth factor-β; NK cell = Natural killer cell.

FIGURE 2

Potential mechanisms of skin-gut cross talk include increases in the number of intestinal MCs and skin-originating eosinophils mis-homing. Systemic IL-4 may activate the intestinal MCs to increase the permeability of the gut. Systemic IL-33 may increase the number of mucosal MCs in the small intestine via ILC2 activation. MCs = Mast cells; IL-4 = Interleukin-4; ILC2 = Type 2 innate lymphoid cells.

FIGURE 3

Proposed association of dysbiosis of intestinal microbiota with systemic disorders, which include the disorders related to liver, lung, heart, gut, skin, metabolic, immunity and CNS.