Abstract
Cigarette smoking (CS) is the cause of several organ and apparatus diseases. The effects of smoke in the gut are partially known. Accumulating evidence has shown a relationship between smoking and inflammatory bowel disease, prompting us to investigate the mechanisms of action of smoking in animal models. Despite the role played by neuropeptides in gut inflammation, there are no reports on their role in animal models of smoking exposure. The hormone relaxin has shown anti-inflammatory properties in the intestine, and it might represent a putative therapy to prevent gut damage caused by smoking. Presently, we investigate the effects of chronic smoke exposure on inflammation, mucosal secretion, and vasoactive intestinal peptide (VIP) and substance P (SP) expressions in the ileum and colon of guinea pigs. We also verify the ability of relaxin to counter the smoke-induced effects. Smoke impacted plasma carbon monoxide (CO). In the ileum, it induced inflammatory infiltrates, fibrosis, and acidic mucin production; reduced the blood vessel area; decreased c-kit-positive mast cells and VIP-positive neurons; and increased the SP-positive nerve fibers. In the colon, it reduced the blood vessel area and the goblet cell area and decreased c-kit-positive mast cells, VIP-positive neurons, and SP-positive nerve fibers. Relaxin prevented most of the smoking-induced changes in the ileum, while it was less effective in the colon. This study shows the diverse sensitivity to CS between the ileum and the colon and demonstrates that both VIP and SP are affected by smoking. The efficacy of relaxin proposes this hormone as a potential anti-inflammatory therapeutic to counteract gut damage in humans affected by inflammatory bowel diseases.
Highlights
Thirty years of scientific research have proven cigarette smoking (CS) as the main cause of lung cancer (Schwartz and Cote, 2016), as a promoter of pathologies of the respiratory and cardiovascular systems (Rigotti and Clair, 2013) and as one of the major risk factors for neuro-inflammatory and neurovascular disorders by supporting oxidative stress and inflammation (Aseervatham et al, 2017).Smoke-Induced Gut Damage, Relaxin RoleCS is involved in several malignancies and intestinal inflammatory disorders such as Crohn’s disease (CD) (Verschuere et al, 2012a).investigation on the role played by CS in the gastrointestinal (GI) tract is limited
The animals were weighed at the beginning and at the end of the exposition, and statistical evaluation of the data showed no significant difference (p > 0.10)
All the animals exposed to chronic CS, independently of the RLX-2 treatment, had significantly elevated carbon monoxide (CO) levels (CS group, 37.9 ± 3.2 ppm; CS+RLX-2 group, 32.1 ± 3.1 ppm) compared with the control group (6.4 ± 0.8 ppm: p < 0.001 versus the other groups)
Summary
Thirty years of scientific research have proven cigarette smoking (CS) as the main cause of lung cancer (Schwartz and Cote, 2016), as a promoter of pathologies of the respiratory and cardiovascular systems (Rigotti and Clair, 2013) and as one of the major risk factors for neuro-inflammatory and neurovascular disorders by supporting oxidative stress and inflammation (Aseervatham et al, 2017).Smoke-Induced Gut Damage, Relaxin RoleCS is involved in several malignancies and intestinal inflammatory disorders such as Crohn’s disease (CD) (Verschuere et al, 2012a).investigation on the role played by CS in the gastrointestinal (GI) tract is limited. Chronic smoke exposure caused an increase in apoptosis of the follicle-associated epithelium (Verschuere et al, 2012b; Allais et al, 2016; Allais et al, 2017), an increase in pro-inflammatory cytokines (Eliakim and Karmeli, 2003), and an excessive nitric oxide (NO) production (Allais et al, 2017). At variance with the ileum, the colon seems less sensitive to smoke irritants, as demonstrated by the failure of inflammatory cell recruitment in rats (Eliakim and Karmeli, 2003), the reduction of pro-inflammatory cytokines (Benson and Shepherd, 2011; Allais et al, 2017), and the changes in the CD4/CD8 ratio in mice (Daniluk et al, 2017)
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