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Review
. 2021 Oct 28;13(11):3839.
doi: 10.3390/nu13113839.

Intestinal Microbiota as a Contributor to Chronic Inflammation and Its Potential Modifications

Affiliations
Review

Intestinal Microbiota as a Contributor to Chronic Inflammation and Its Potential Modifications

Marta Potrykus et al. Nutrients. .

Abstract

The gut microbiota is a crucial factor in maintaining homeostasis. The presence of commensal microorganisms leads to the stimulation of the immune system and its maturation. In turn, dysbiosis with an impaired intestinal barrier leads to accelerated contact of microbiota with the host's immune cells. Microbial structural parts, i.e., pathogen-associated molecular patterns (PAMPs), such as flagellin (FLG), peptidoglycan (PGN), lipoteichoic acid (LTA), and lipopolysaccharide (LPS), induce inflammation via activation of pattern recognition receptors. Microbial metabolites can also develop chronic low-grade inflammation, which is the cause of many metabolic diseases. This article aims to systematize information on the influence of microbiota on chronic inflammation and the benefits of microbiota modification through dietary changes, prebiotics, and probiotic intake. Scientific research indicates that the modification of the microbiota in various disease states can reduce inflammation and improve the metabolic profile. However, since there is no pattern for a healthy microbiota, there is no optimal way to modify it. The methods of influencing microbiota should be adapted to the type of dysbiosis. Although there are studies on the microbiota and its effects on inflammation, this subject is still relatively unknown, and more research is needed in this area.

Keywords: diet; inflammation; intestinal epithelial barrier; microbiome; prebiotic; probiotic.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mechanism of LPS’ influence on inflammation and intestinal permeability. Aberrations: LPS—lipopolysaccharide; LBP—LPS-binding protein; CD14—cluster of differentiation 14; MD-2—myeloid differential factor 2; TLR4—toll-like receptor 4; MyD88—myeloid differentiation factor 88; NF-κB—nuclear factor kappa-light-chain-enhancer of activated B cells.
Figure 2
Figure 2
Origin and receptors of pathogen-associated molecular patterns. Aberrations: LTA—lipoteichoic acid; PGN—peptidoglykan; FLG—flagellin; LPS—lipopolisaccharide; TLR2/4/5 –toll-like receptors2/4/5; NOD—nucleotide-binding oligomerization domain.
Figure 3
Figure 3
Effect of nutritional interventions on specific bacteria. Abbreviations: PP—polyphenols; FOS—fructooligosaccharides; RS—resistant starch; GOS—galactooligosaccharides; GFD—gluten-free diet; CLA—conjugated linoleic acid; MD—Mediterranean diet; LPS—lipopolysaccharide; TNF-α—tumor necrosis factor α; IL-1ß—interleukin 1ß; IL-6—interleukin 6; CRP—C-reactive protein; IL-10—interleukin 10.

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