Interactions of Gut Microbiota, Endotoxemia, Immune Function, and Diet in Exertional Heatstroke

Table 4

Potential effects of the intestinal microbiota (IM) and dietary intake on immune function.

Intestinal lumen sites/processes	Bacterial effects on immune function	Influence of diet
Mucus layer	(i)  Block cell adhesion sites of pathogenic bacteria
	(ii) Site of competition for nutrients with pathogenic bacteria	X
	(iii) Affect function of mucosal immune cells/factors	X
	(iv) Alter bacterial diversity and abundance of specific phyla	X
Epithelial cell layer	(i)  Goblet cells secrete mucins (high molecular weight glycoproteins) which prevent entry of pathogens and noxious substances
	(ii) Paneth cells contain antimicrobial peptides
	(iii) Express heat shock proteins which reduce inflammation and injury	X
	(iv) Influence the function of lymphocytes, leukocytes (T-cells, macrophages, secretory immunoglobulin A), neutrophils, monocytes	X
Biochemical/metabolic processes	(i)  Produce antimicrobial substances that inhibit pathogenic bacteria
	(ii) Produce LPS, which affects systemic, liver, adipose tissue inflammation	X
	(iii) Modulate antibody production in response to large antigen load	X
	(iv) Degrade toxins and toxin receptors
	(v) Bacterial metabolites (e.g., SCFA) have pro- and anti-inflammatory effects	X

Due to its vast surface area, the human intestine houses the largest number of immune cells in the human body. Mucus layer is the first line of defense against physical and chemical injury caused by ingested food, microbes, and microbial products; heat shock protein expression increases. IM, intestinal microbiota; LPS, lipopolysaccharide, an endotoxin; SCFA, short-chain fatty acids. Sources: [52, 103, 130, 133, 154, 316, 327, 330–333].