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(Firmicutes) while showing depletion of the Proteobacteria populations [177, 178]. This is further proven by a study conducted on 317 patients showing 92% of patients showed complete recovery from CDI, out of which 89% exhibited full recovery after the first treatment. Only approximately 4% of patients experienced a relapse in symptoms after the FMT [177, 178]. It is mentioned from the studies above that FMT as adjunctive therapy to antibiotic treatment would be an avenue that merits further investigation.

      Aside from typical colonoscopic lavage, there is increasing interest in oral delivery of encapsulated FMT. Compared to colonoscopy, oral FMT administration is considered non‐invasive, less resource intensive, easily administered, and more accessible to patients [179]. A meta‐analysis has identified that a single FMT capsule infusion has an average colonization efficiency of 80%, whereas multiple infusions showed 92% efficiency [180]. In a randomized clinical trial, orally administered FMT showed minimal difference compared to FMT lavage to prevent recurrent infection over 12 weeks [181]. Current studies are geared toward developing smart oral delivery methods to facilitate the targeted release of the microbes. Preliminary studies of FMT capsules with a targeted colonic release(FMTcr) showed better therapeutic effects compared to FMT capsules with the gastric release (FMTgr) [182].

      1.3.1.2 Prebiotic‐, Diet‐, and Probiotic‐Mediated Prevention of Pathogenic Infections

      As discussed in the earlier subchapter 1.2, a perturbation in the gut ecosystem increases the risk of microbiome dysbiosis, significantly increasing the hosts' vulnerability to infection [163, 183]. Thus, other measures have been taken to re‐establish homeostatic balance and restore the host health. In the following, we will discuss the use of prebiotics, diet, and probiotic means of balancing the gut microbiome.

      Adjusting the dietary consumption of lipids was further found to encourage the growth of certain microbial groups by altering hepatic lipid and bile metabolism, thus indirectly changing the microbiome and their corresponding metabolites [163]. Fatty acids can alter pathogen virulence, survival, and growth; thus, clinical applications of fatty acid in infection treatment are carried out [186]. Scientists studying various dietary lipid sources influence the host's pathological response to Citrobacter rodentium infection, where olive oil showed one of the best chemoprotective properties [187].

      1.3.2 Inflammatory Disease

      In the event of microbiome dysbiosis, inflammation occurs resulting from the immune system attempting to remedy the situation [188]. There are increasing evidences suggesting the link of diet, microbiota imbalance, and the pathogenesis of the inflammatory disease. The nutritional composition may trigger inflammation through direct interactions with the mucosal tissues and indirect interactions by altering the microbiota composition [164, 189–192]. We will discuss IBD as a case study on the effect of diet on IBD pathogenesis.

      Patients suffering from IBD experience due to long‐term incidences of tissue inflammation on the dorsal end of the GI tract [193] that can be divided into Crohn's disease (CD) and UC. The dietary habits of individuals can either prevent or increase the risk of developing IBD [193]. A westernized diet abundant in fat and protein increases the risk of developing IBD [194], while fiber‐rich diet was found to lower the risk of developing IBD in rats [195, 196]. As discussed in Section 1.2, a fatty and protein‐rich diet was found to enrich Proteobacteria and deplete Firmicutes and Bacteroidetes involved in the biosynthesis of butyrate production [197–199]. These reduced levels of SCFAs in the large intestine are primarily attributed to preventing bowel inflammation [200, 201]. The use of FMT to enrich butyrate‐producing microbes was found to recover the microbiome balance and alleviate IBD symptoms.

      Other nutritional elements such as amino acids, fibers, vitamins, and fatty acids can influence IBD pathogenesis. Some studies showed that glutamine‐ and arginine‐supplemented diet conferred improved protection against dextran sulfate sodium (DSS)‐induced colitis in a murine model [210, 211]. Prebiotic fibers can attenuate IBD symptoms in mice model [195, 212] through regulating intestinal bacterial composition and synthesis of anti‐inflammatory by‐products, such as SCFAs [193, 213, 214].

      1.3.3 Cancer

      Many studies concluded that the microbiota plays a role in cancer pathogenesis in humans. It is further demonstrated that the dietary nutritional content facilitates the behavior of the microbiome. Prebiotics‐containing fiber (soluble and insoluble) helps to move the bowel by bulking up the intestinal lumen and absorbing carcinogens such as nitrosamines, thus limiting the contact time of the carcinogens to the GI epithelium tissue. These fibers also house the SCFA‐producing microbes, enriching the Gram‐positive anaerobic Firmicutes population and providing the substance for microbial fermentation [215–218]. The two most abundant butyrate‐producing Firmicutes in the human colon are E. rectale/Roseburia spp. and F. prausnitzii. E. rectale/Roseburia spp. belongs to the Clostridium coccoides (or Clostridial cluster XIVa) cluster, and F. prausnitzii belongs to the C. leptum (or Clostridial cluster IV) cluster [219–222].

      The SCFA butyrate can prevent gut tissue inflammation and suppress cancer cell motility by deactivating Akt/ERK signaling pathway of histone deacetylase in colorectal cancer and lymphoma cancer [223]. Butyrate also exerts its anticancer activity by interfering with the mitochondrial and exogenous apoptotic pathways through regulating oncogenic signaling molecules through microRNAs and methylation [224, 225]. On top of generating butyrate, these bacteria can produce other metabolites such as lactic acid and formic acid that can further exert anticancer activities [226].

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