Nevertheless, investigation on the role played by CS in the gastrointestinal (GI) tract is limited. The experimental data available are often hardly comparable, mainly because of the different modalities of smoke exposure applied (active/passive smoking), the different smoke components studied [nicotine, carbon monoxide (CO), or whole cigarette], and the diverse administration methods used (oral, intraperitoneal, or subcutaneous). However, a region-specific modulation of the gut immune system has been reported after exposure to smoke. In the murine ileum, 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).
This dual pattern of the responses of the small and large bowels to smoke was also observed in animal models of colitis (Galeazzi et al., 1999; Eliakim et al., 2001; Guo et al., 2001; Benson and Shepherd, 2011) and in human inflammatory bowel diseases (IBDs) (Berkowitz et al., 2018; Ananthakrishnan, 2013; Ananthakrishnan, 2015; Papoutsopoulou et al., 2020).
Smoke 2011 Scaricare Activator 64 Bits Italiano
In this background, the hormone relaxin (RLX) emerges as an interesting putative therapy to preventing intestinal alterations caused by exposure to smoke. In fact, the human relaxin-2 (RLX-2) or serelaxin (Hossain and Wade, 2014) has shown anti-inflammatory and anti-apoptotic properties in both in vitro and in vivo animal models (Samuel et al., 2007). Moreover, RLX-2 has been shown to be protective in a guinea pig model of chronic exposure to CS, limiting vascular damage, lung inflammation, and fibrosis (Pini et al., 2016a; Pini et al., 2016b). In the gut, in vitro exposure to porcine RLX and in vivo porcine RLX chronic treatment caused muscle relaxation due to a region-specific modulation of the expressions of different NO synthase isoforms (Baccari et al., 2007; Vannucchi et al., 2011; Baccari et al., 2012). No data are available on the effect of RLX in the gut exposed to smoking. 2ff7e9595c
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