Abstract
Dysbiosis, an imbalance of intestinal flora, can cause serious conditions such as obesity, cancer, and psychoneurological disorders. One cause of dysbiosis is inflammation. Ulcerative enteritis is a side effect of non-steroidal anti-inflammatory drugs (NSAIDs). To counteract this side effect, we proposed the concurrent use of histamine H2 receptor antagonists (H2RA), and we examined the effect on the intestinal flora. We generated a murine model of NSAID-induced intestinal mucosal injury, and we administered oral H2RA to the mice. We collected stool samples, compared the composition of intestinal flora using terminal restriction fragment length polymorphism, and performed organic acid analysis using high-performance liquid chromatography. The intestinal flora analysis revealed that NSAID [indomethacin (IDM)] administration increased Erysipelotrichaceae and decreased Clostridiales but that both had improved with the concurrent administration of H2RA. Fecal levels of acetic, propionic, and n-butyric acids increased with IDM administration and decreased with the concurrent administration of H2RA. Although in NSAID-induced gastroenteritis the proportion of intestinal microorganisms changes, leading to the deterioration of the intestinal environment, concurrent administration of H2RA can normalize the intestinal flora.
Highlights
Dysbiosis refers to the state of disturbance in the balance of the microbial flora in the body, which allows illness to develop in the host and can cause collapse of the environment in the body established through coexistence to date [1]
Many publications have indicated a relationship between inflammation and bacterial flora because dysbiosis induces failure of immunological homeostasis and causes inflammatory bowel disease (IBD) [5,6], and the intestinal flora controls the secretion of inflammatory cytokines and inhibits the onset of diabetes [7]
While pump inhibitors (PPIs) have a more potent inhibitory action than H2-receptor antagonists (H2RA), they change the composition of the bacterial flora and potentially increase the risk of enteral infection [15,16]; it is perceived that H2RA can be used instead of PPI as an anti-inflammatory agent that is compatible with non-steroidal anti-inflammatory drugs (NSAIDs)
Summary
Dysbiosis (imbalance) refers to the state of disturbance in the balance of the microbial flora in the body, which allows illness to develop in the host and can cause collapse of the environment in the body established through coexistence to date [1]. Many publications have indicated a relationship between inflammation and bacterial flora because dysbiosis induces failure of immunological homeostasis and causes inflammatory bowel disease (IBD) [5,6], and the intestinal flora controls the secretion of inflammatory cytokines and inhibits the onset of diabetes [7]. While PPIs have a more potent inhibitory action than H2RA, they change the composition of the bacterial flora and potentially increase the risk of enteral infection [15,16]; it is perceived that H2RA can be used instead of PPI as an anti-inflammatory agent that is compatible with NSAIDs. Previously, our group reported that lafutidine, a second-generation H2RA, activated mucus-secreting cells [17,18] and could effectively prevent mucositis caused by cancer chemotherapy [19]. To evaluate the effect of H2RA against dysbiosis caused by enteritis, we analyzed the microbiome of a murine model of NSAID-induced mucosal injury
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