Probiotic-derived extracellular vesicles alleviate AFB1-induced intestinal injury by modulating the gut microbiota and AHR activation

  • J Nanobiotechnology. 2024 Nov 11;22(1):697. doi: 10.1186/s12951-024-02979-3.
Jinyan Li  1  2  3 ,  Mengdie Shi  1  2  3 ,  Yubo Wang  1  2  3 ,  Jinyan Liu  1  2  3 ,  Shuiping Liu  1  2  3 ,  Weili Kang  1  2  3 ,  Xianjiao Liu  1  2  3 ,  Xingxiang Chen  1  2  3 ,  Kehe Huang  1  2  3 ,  Yunhuan Liu  4  5  6
Affiliations
  • 1. College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, 210095, China.
  • 2. Institute of Animal Nutritional Health, Nanjing Agricultural University, Nanjing, Jiangsu, China.
  • 3. MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, China.
  • 4. College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, 210095, China. [email protected].
  • 5. Institute of Animal Nutritional Health, Nanjing Agricultural University, Nanjing, Jiangsu, China. [email protected].
  • 6. MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, China. [email protected].
PMID: 39529091 DOI: 10.1186/s12951-024-02979-3
Abstract

Background: Aflatoxin B1 (AFB1) is a mycotoxin that widely found in the environment and mouldy foods. AFB1 initially targets the intestine, and AFB1-induced intestinal injury cannot be ignored. Lactobacillus amylovorus (LA), a predominant species of Lactobacillus, plays a role in carbohydrate metabolism. Extracellular vesicles (EVs), small lipid membrane vesicles, are widely involved in diverse cellular processes. However, the mechanism by which Lactobacillus amylovorus-QC1H-derived EVs (LA.EVs) protect against AFB1-induced intestinal injury remains unclear.

Results: In our study, a new strain named Lactobacillus amylovorus-QC1H (LA-QC1H) was isolated from pig faeces. Then, EVs derived from LA-QC1H were extracted via ultracentrifugation. Our results showed that LA.EVs significantly alleviated AFB1-induced intestinal injury by inhibiting the production of proinflammatory cytokines, decreasing intestinal permeability and increasing the expression of tight junction proteins. Moreover, 16 S rRNA analysis revealed that LA.EVs modulated AFB1-induced gut dysbiosis in mice. However, LA.EVs did not exert beneficial effects in antibiotic-treated mice. LA.EVs treatment increased intestinal levels of indole-3-acetic acid (IAA) and activated intestinal Aryl Hydrocarbon Receptor (AHR)/interleukin-22 (IL-22) signalling in AFB1-exposed mice. Inhibition of intestinal AHR signalling markedly weakened the protective effect of LA.EVs in AFB1-exposed mice.

Conclusions: LA.EVs alleviated AFB1-induced intestinal injury by modulating the gut microbiota, activating the intestinal AHR/IL-22 signalling, reducing the inflammatory response and promoting intestinal barrier repair in mice.

Keywords
Lactobacillus amylovorus; Aflatoxin B1; Aryl hydrocarbon receptor; Extracellular vesicles; Gut microbiota.
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