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Although laxatives or opioid antagonists can alleviate constipation, their efficacy is still insufficient (Tuteja et al., 2010). The disrupted GI motility may contribute to increased susceptibility to infections with gut origin considering that impaired peristalsis results in accumulation of residual food and bacteria in the gut lumen. Clinical studies imply that the early enteral feeding could enhance immune function and decrease the risk of infections in postoperative patients, so delayed enteral feeding because of opioid treatment and subsequent ileus may be responsible for increased risk of infection. Additionally, the opioid loperamide has been shown to shift microbiome taxonomic and metabolic profile, and these changes contribute to development of constipation in mice (Touw et al., 2014). As discussed previously, the dysbiosis in the gut microbiome plays a crucial role in GI homeostasis disruption and promotes pathogenesis of gut infectious diseases especially for HIV infection. Thus it will be interesting to investigate how opioids and/or opioid-induced GI motility disorder influence gut microbiome and the physiological consequence of this modulation. Despite the observation that opioid receptors are expressed on immune cells within the intestinal lamina propria, studies focusing on the effects of opioids on intestinal immune function and inflammation are relatively sparse. Researches using animal models show that both chronic morphine and morphine withdrawal can lower host defense to enteric bacteria such as Salmonella enterica, Acinetobacter baumannii, and Pseudomonas aeruginosa. Opioids can Selleckchem OTX015 induce bacterial translocation into the systemic system resulting in sepsis in mice (Hilburger et al., 1997; Ocasio et al., 2004; Feng et al., 2006; Breslow et al., 2011; Babrowski et al., 2012; Meng et al., 2013). In addition to bacterial translocation, morphine has been documented to increase pro-inflammatory cytokine production in rats and accelerate the progression of LPS-induced sepsis to septic shock (Roy et al., 1999; Greeneltch et al., 2004; Ocasio et al., 2004). In clinical studies, higher circulating morphine levels were observed in patients with sepsis, severe sepsis, and septic shock compared with healthy controls, implying the role of opioids in sepsis progression (Glattard et al., 2010). Overall, both clinical and laboratory studies provide evidence that besides the indirect effects mediated by GI peristalsis, other direct effects of opioids on epithelial cells and immune cells on intestinal lamina propria and GALTs also play important roles in impaired gut immune function. However, the mechanisms underlying compromised gut immune function and increased susceptibility to infections after opioid treatment have not been well studied.