# Microecological Interventions against Antibiotic-Induced Dysbiosis and Related Resistome Expansion

**Authors:** Yuxuan Shi, Huajun Li

PMC · DOI: 10.4014/jmb.2601.01009 · 2026-03-26

## TL;DR

This paper reviews how gut microbiota disruption from antibiotics promotes antibiotic resistance and explores microecological interventions to restore balance and reduce resistance spread.

## Contribution

The paper introduces a comprehensive framework integrating ecological and therapeutic approaches to combat antibiotic resistance through microecological interventions.

## Key findings

- Antibiotic-induced dysbiosis weakens gut barrier function and promotes antimicrobial resistance gene spread.
- Microbial metabolites influence resistance through mechanisms like biofilm formation and host-microbe interactions.
- Microecological interventions like probiotics and fecal transplants can restore microbial balance and reduce pathogen colonization.

## Abstract

Antibiotic exposure and the emergence of antimicrobial resistance are critical global health threats, with antibiotic-induced gut dysbiosis contributing to increased mortality, prolonged illness, and significant economic burden. This review introduces the complex interplay between antibiotic exposure, gut microbiota dysbiosis, and the dissemination of antimicrobial resistance genes, which collectively undermine intestinal barrier function and promote systemic inflammation. It also explores how microbial metabolites influence resistance mechanisms through metabolic regulation, alteration of bacterial communities, antibiotic biotransformation, biofilm formation, and host–microbe interactions. Microecological interventions—including probiotics, prebiotics, synbiotics, postbiotics, fecal microbiota transplantation, dietary modifications, and emerging strategies—have the potential to restore microbial homeostasis, enhance colonization resistance to invading pathogens, and mitigate the spread of resistant pathogens. By integrating ecological and therapeutic perspectives, these approaches offer a sustainable framework for combating antibiotic resistance and improving clinical outcomes.

## Full-text entities

- **Genes:** ABL2 (ABL proto-oncogene 2, non-receptor tyrosine kinase) [NCBI Gene 27] {aka ABLL, ARG}, Ocln (occludin) [NCBI Gene 18260] {aka Ocl}, Cldn4 (claudin 4) [NCBI Gene 12740] {aka Cep-r, Cpetr, Cpetr1}, AIP (AHR interacting HSP90 co-chaperone) [NCBI Gene 9049] {aka ARA9, FKBP16, FKBP37, PITA1, SMTPHN, XAP-2}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Tjp1 (tight junction protein 1) [NCBI Gene 21872] {aka ZO1}, Ifng (interferon gamma) [NCBI Gene 15978] {aka IFN-g, If2f, Ifg}, SERPINA2 (serpin family A member 2 (gene/pseudogene)) [NCBI Gene 390502] {aka ARGS, ATR, PIL, SERPINA2P, psiATR}
- **Diseases:** flatulence (MESH:D005414), abdominal cramps or pain (MESH:D015746), infection (MESH:D007239), IBD (MESH:D015212), opportunistic infections (MESH:D009894), IFIs (MESH:D000072742), bacterial infections (MESH:D001424), death (MESH:D003643), ulcerative colitis (MESH:D003093), Obesity (MESH:D009765), Crohn's disease (MESH:D003424), AAD (MESH:D004761), Candida infections (MESH:D002177), C. difficile (MESH:D003015), gram (MESH:D016908), bloodstream infections (MESH:D018805), Fungal Infections (MESH:D009181), constipation (MESH:D003248), bacteria (MESH:C000719206), MRSA (MESH:D013203), fever (MESH:D005334), diarrhea (MESH:D003967), mucosal (MESH:D052016), Invasive candidiasis (MESH:D058365), Dysbiosis (MESH:D064806), AMR (MESH:D060467), invasive (MESH:D009361), Inflammatory (MESH:D007249), gastrointestinal pathogens (MESH:D005767), edema (MESH:D004487), Klebsiella pneumoniae (MESH:D007710)
- **Chemicals:** AHLs (-), methicillin (MESH:D008712), cephalosporins (MESH:D002511), xylo-oligosaccharides (MESH:C570991), nitroimidazoles (MESH:D009593), lactic acid (MESH:D019344), carbon (MESH:D002244), fluoroquinolones (MESH:D024841), vancomycin (MESH:D014640), Prebiotics (MESH:D056692), LPS (MESH:D008070), ceftriaxone (MESH:D002443), tetracycline (MESH:D013752), carbohydrate (MESH:D002241), chitosan (MESH:D048271), ampicillin (MESH:D000667), butyrate (MESH:D002087), nitrogen (MESH:D009584), polysaccharides (MESH:D011134), acetate (MESH:D000085), carbapenems (MESH:D015780), fructooligosaccharides (MESH:C116580), propionate (MESH:D011422), SCFA (MESH:D005232), sugars (MESH:D000073893)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Akkermansia muciniphila (species) [taxon 239935], Bacillota (clostridial firmicutes, phylum) [taxon 1239], Staphylococcus aureus (species) [taxon 1280], Bdellovibrio sp. P (species) [taxon 191744], Mediterraneibacter gnavus (species) [taxon 33038], Acinetobacter baumannii (species) [taxon 470], Enterobacteriaceae (enterobacteria, family) [taxon 543], Pseudomonas aeruginosa (species) [taxon 287], Bacteroidia (class) [taxon 200643], Candida [taxon 1535326], Candidozyma auris (species) [taxon 498019], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Lachnoclostridium (genus) [taxon 1506553], Escherichia coli (E. coli, species) [taxon 562], Bacteriophage sp. (species) [taxon 38018], Klebsiella pneumoniae (species) [taxon 573], Lactobacillus (genus) [taxon 1578], Weissella (genus) [taxon 46255], Nakaseomyces glabratus (species) [taxon 5478], Homo sapiens (human, species) [taxon 9606], Sus scrofa (pig, species) [taxon 9823], Salmonella enterica (species) [taxon 28901], Pseudomonadota (proteobacteria, phylum) [taxon 1224], Escherichia coli O80:H26 (no rank) [taxon 2605620], Bifidobacterium longum (species) [taxon 216816], Candida albicans (species) [taxon 5476], Enterococcus faecium (species) [taxon 1352]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13036508/full.md

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Source: https://tomesphere.com/paper/PMC13036508