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Animal Models

Exploring the interaction of obesity and allergy and the potential roles of gut microbiota in the development of this comorbidity in male mice

Abstract

Background

Plenty of epidemiological studies have focused on obesity and allergic diseases, less is known about the interaction of the comorbidity.

Objective

The present study was conducted to identify the relationship between obesity and allergy and to clarify the potential regulatory roles of gut microbiota in the development of comorbidity.

Methods

Four-week-old male BALB/c mice were used to establish the comorbidity model. The high-fat diet was used to induce obese mice, and ovalbumin was used to induce allergic mice. The post-obesity allergy mice and post-allergy obesity mice (n = 12/group) were used to clarify the effects of obesity on allergic reactions and those of allergy on metabolic function. Changes in gut microbiota, short-chain fatty acids (SCFAs), bile acids (BAs), the expression of the SCFAs and the BAs receptors were also detected.

Results

In the post-obesity allergy study, the serum Immunoglobulin E and the splenic CD4+CD25+FOXP3+ T cells (Tregs) in post-obesity allergic mice were higher than that in allergic mice. Post-obesity allergic mice had higher abundance of Alistipes, Parabacteroides, Rikenellaceae_RC9_gut_group, Colidextribacter, Muribaculum, Lachnospiraceae_NK4A136_group, and Erysipelatoclostridium but lower levels of SCFAs and expressions of GPR41 and 43. In the post-allergy obesity study, OVA-induced allergy alleviated fat accumulation and glycolipid metabolism disorder in obese mice. However, there was no significant difference in the gut microbiota and the SCFAs receptors between post-allergy obese mice and obese mice, except for BAs.

Conclusions

The post-obesity allergy model suggested that early obesity impaired allergic reaction and immune function, which aggravated the development of allergy via altering the composition of the gut microbiota and the contents and function of SCFAs. The post-allergy obesity study suggested that early allergy did not promote metabolic disorder, instead of alleviating the development of obesity, and BAs may contribute to this alleviation.

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Fig. 1: Obesity alters immune regulation in allergic mice.
Fig. 2: obesity alters gut microbiota and their metabolites in allergic mice.
Fig. 3: OVA-induced allergy alleviates the development of obesity.
Fig. 4: The effects of OVA-induced allergy on gut microbiota and their metabolites in obese mice.

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Data availability

Raw reads of 16S sequencing data is submitted to Sequence Read Archive (SRA) under the accession BioProject ID PRJNA1051783 in NCBI. The other original experimental data are presented in the Supplementary file.

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Acknowledgements

We appreciate the support of Public health and Preventive Medicine Provincial Experiment Teaching Center at Sichuan University and Food Safety Monitoring and Risk Assessment Key Laboratory of Sichuan Province.

Funding

This work was supported by the National Natural Science Foundation of China (Grant number 81973042), Natural Science Foundation of Sichuan Province (Grant number 2025ZNSFSC1782), Sichuan University Postdoctoral Interdisciplinary Innovation Fund (Grant number: JCXK2231) and China Postdoctoral Science Foundation (Grant number: 2022M712228).

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Contributions

FH, RC, ZM and XW designed the study. ZM, FJ and JL performed the study. ZM, XZ, YM, SS and WH analyzed the data. ZM and FJ draft the manuscript. XW and RC revised the manuscript.

Corresponding authors

Correspondence to Xiaona Wu or Ruyue Cheng.

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The authors declare no competing interests.

Ethics approval

This study was approved by the Ethics Committee of West China Medical Center, Sichuan University (No. K2021022) and all methods were performed in accordance with the relevant guidelines and regulations required by the Ethics Committee.

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Miao, Z., Jiang, F., Li, J. et al. Exploring the interaction of obesity and allergy and the potential roles of gut microbiota in the development of this comorbidity in male mice. Int J Obes (2026). https://doi.org/10.1038/s41366-026-02041-2

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