Role of probiotics in prevention and treatment of enteric infections: a comprehensive review

Abstract

Microorganisms that inhabits human digestive tract affect global health and enteric disorders. Previous studies have documented the effectiveness and mode of action of probiotics and classified as human-friendly biota and a competitor to enteric pathogens. Statistical studies reported more than 1.5 billion cases of gastrointestinal infections caused by enteric pathogens and their long-term exposure can lead to mental retardation, temporary or permanent physical weakness, and leaving the patient susceptible for opportunistic pathogens, which can cause fatality. We reviewed previous literature providing evidence about therapeutic approaches regarding probiotics to cure enteric infections efficiently by producing inhibitory substances, immune system modulation, improved barrier function. The therapeutic effects of probiotics have shown success against many foodborne pathogens and their therapeutic effectiveness has been exponentially increased using genetically engineered probiotics. The bioengineered probiotic strains are expected to provide a better and alternative approach than traditional antibiotic therapy against enteric pathogens, but the novelty of these strains also raise doubts about the possible untapped side effects, for which there is a need for further studies to eliminate the concerns relating to the use and safety of probiotics. Many such developments and optimization of the classical techniques will revolutionize the treatments for enteric infections.

Keywords: Bacterial strains; Enteric infections; Probiotics; Regulation of gut barrier; Therapeutic approach.

Fig. 1

Effects of metabolites of probiotics on gut. Indole 3-propionic acid has the ability to bind to PXR thus upregulating the expression of tight junction protein. The indole-3-lactic acid activates AhRs of the gut epithelium and promotes the expression of IL-22. Isolated from LGG, the soluble proteins P40 and P75 can activate EGFR and subsequently control the expression of APRIL into the epithel and, therefore, stimulate cell secretion of lgA via B-cells. Besides, P40 and p75 maintain gut homeostasis by activating EGFR–PIK3–Akt signaling pathway to. Furthermore, these two proteins prevent tight junctional disruption of the pathways that rely on protein kinase-C. Butyrate can bind to the GPCR, like GPR41, GPR109A, and GPR43, and induce colonic epithel to produce IL-18. Butyrate also motivates gut epithelia O₂ intakes to preserve HIF stability and to enhance the expression of HIF target genes that prevent barrier protective disease. Moreover, probiotic-based bacteriocins serve as colonizing peptides to enable producers to gain a competitive edge over other strains and to occupy niches in the intestines. Alternatively, bacteriocins has the ability to act as a killer peptide, which specifically prevents pathogen adhesion of the mucus layer and strengthens the first intestinal barrier (Liu et al. 2020)

Fig. 2

Immune system modulation using probiotics: Probiotics’ immunomodulatory acts. Specific pathways: probiotics’ role in the humoral immune system and cell-mediated responses. Relevant mechanisms: improvement of the role of the epithelial barrier, competitive removal of epithelial bacteria, specific microenvironment modifications, and elimination of the intestines inflammation (Tan et al. 2015)

Fig. 3

Regulation of Intestinal barrier mechanism using probiotics (Wan et al. 2016)

Fig. 4

Regulation of innate defence mechanism using probiotics (Wan et al. 2016)

Fig. 5

Regulation of Adaptive immune system using probiotics (Wan et al. 2016)

Fig. 6

Schematic diagram of the different pathways for probiotic-mediated pathogen control. At (1), probiotics may attenuate their physical and chemical surroundings (epithelial cell receptors, mucus, nutrients, pH, peristaltism, and tight junctions). At (2), probiotic supplements may yield biological molecules like antibiotics, bacteriocins, or peroxide-containing antimicrobial characteristics. At (3), probiotics can cause immune regulation, either by interfering with dendritic cells, which can, in effect, alter the segregation of naive T lymphocytes to Th1, 2, or Treg cells, corresponding to unique inductions of cytokines or by humoral response via IgA-based cells and their secretive IgAs (Travers et al. 2011b)