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Background <p>Plenty of epidemiological studies have focused on obesity and allergic diseases, less is known about the interaction of the comorbidity.</p> Objective <p>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.</p> Methods <p>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 (<i>n</i> = 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.</p> Results <p>In the post-obesity allergy study, the serum Immunoglobulin E and the splenic CD4<sup>+</sup>CD25<sup>+</sup>FOXP3<sup>+</sup> T cells (Tregs) in post-obesity allergic mice were higher than that in allergic mice. Post-obesity allergic mice had higher abundance of <i>Alistipes</i>, <i>Parabacteroides</i>, <i>Rikenellaceae_RC9_gut_group</i>, <i>Colidextribacter</i>, <i>Muribaculum</i>, <i>Lachnospiraceae_NK4A136_group</i>, and <i>Erysipelatoclostridium</i> 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.</p> Conclusions <p>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.</p> <p></p>

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

  • 期刊论文

  • 发表日期：

    2026年3月14日

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  • Zhonghua Miao,
  • Fengling Jiang,
  • Jinxing Li,
  • Simou Wu,
  • Xuguang Zhang,
  • Yuejian Mao,
  • Shengpeng Su,
  • Weiwei Han,
  • Fang He,
  • Xiaona Wu,
  • Ruyue Cheng

摘要

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.