The host’s natural defensive mechanism is largely comprised of lysozyme (1,4-N-acetyl- muramidase). In the human small intestine and ascending colon, paneth cells generate this

Gut dysbiosis is the loss of the microbial population’s equilibrium in the gut. In this condi­tion, the population of commensal microorganisms declines while the number of pathogenic microbes increases. Dysbiosis results in immunological dysregulation and proinflammatory effects that are associated to a variety of disease states, such as autoimmune illnesses, type 2 diabetes, CVDs, and fatty liver (Martinez et al., 2021). Mucosal immunity, genetic, and environmental variables tightly control the gut microbiota’s homeostasis (Lee et al., 2011; Swidsinski et al., 2007; Yatsunenko et al., 2012). Gut dysbiosis and its associated factors, such as small intestinal bacterial overgrowth, rise in pathogen population, increase in endo­toxin levels, rise in microbial energy harvesting capacity , mucosal inflammation, and so on work together to cause a leaky gut. Commensal microorganisms can protect the integrity of the intestinal barrier by secreting antibacterial compounds like bacteriocins and creating short-chain fatty acids (SCFAs) with anti-inflammatory characteristics like butyrate from dietary fibers. Gut dysbiosis induces increased bacterial metabolites like LPS, toxins, and so on which causes mild to severe inflammations in the intestinal epithelium leading to an impaired intestinal barrier. The unfavorable synthesis of zonulin, a protein crucial for regulating TJs and eventually leading to the disintegration of gut barrier, is another way that gut dysbiosis can manifest as a leaky gut disorder (Fasano, 2020).