Antibiotic-induced gut dysbiosis and barrier disruption and the potential protective strategies

Abstract

The oral antibiotic therapies administered widely to people and animals can cause gut dysbiosis and barrier disruption inevitably. Increasing attention has been directed toward antibiotic-induced gut dysbiosis, which involves a loss of diversity, changes in the abundances of certain taxa and consequent effects on their metabolic capacity, and the spread of antibiotic-resistant bacterial strains. Treatment with beta-lactam, glycopeptide, and macrolide antibiotics is associated with the depletion of beneficial commensal bacteria in the genera Bifidobacterium and Lactobacillus. The gut microbiota is a reservoir for antibiotic resistance genes, the prevalence of which increases sharply after antibiotic ingestion. The intestinal barrier, which comprises secretory, physical, and immunological barriers, is also a target of antibiotics. Antibiotic induced changes in the gut microbiota composition could induce weakening of the gut barrier through changes in mucin, cytokine, and antimicrobial peptide production by intestinal epithelial cells. Reports have indicated that dietary interventions involving prebiotics, probiotics, omega-3 fatty acids, and butyrate supplementation, as well as fecal microbiota transplantation, can alleviate antibiotic-induced gut dysbiosis and barrier injuries. This review summarizes the characteristics of antibiotic-associated gut dysbiosis and barrier disruption, as well as the strategies for alleviating this condition. This information is intended to provide a foundation for the exploration of safer, more efficient, and affordable strategies to prevent or relieve antibiotic-induced gut injuries.

Keywords:

• Antibiotic
• dietary supplementation
• FMT
• gut barrier disruption
• gut dysbiosis
• gut immunity
• probiotics

Author contributions

Conceptualization: L.L.Y., Q.X.Z., and W.C. Funding acquisition: L.L.Y., F.W.T., L.P.F., and W.C. Investigation: H.D. Project administration: H.D. and L.L.Y. Supervision: L.P.F. and W.C. Writing—original draft: H.D. and L.L.Y. Writing—review and editing: H..D., L.L.Y., and Q.X.Z.

Competing interests

The authors declare that they have no competing interests.

Additional information

Funding

This work was supported by the National Natural Science Foundation of Program (32001665, 31820103010, 31772090, 31871840, U1903205), Natural Science Foundation of Jiangsu Province (BK20180603), the Postdoctoral Science Foundation of China (2018M642166), BBSRC Newton Fund Joint Centre Award (BB/J004529/1), the National first-class discipline program of Food Science and Technology (JUFSTR20180102).