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. 2022 Mar 10;17(3):e0263762.
doi: 10.1371/journal.pone.0263762. eCollection 2022.

High cellulose dietary intake relieves asthma inflammation through the intestinal microbiome in a mouse model

Song Wen  1 , Guifang Yuan  1 , Cunya Li  2 , Yang Xiong  3   4 , Xuemei Zhong  5 , Xiaoyu Li  6
Affiliations

High cellulose dietary intake relieves asthma inflammation through the intestinal microbiome in a mouse model

Song Wen et al. PLoS One. .

Abstract

Numerous epidemiological studies have shown that a high dietary fiber intake is associated inversely with the incidence of asthma in the population. There have been many studies on the role of soluble dietary fiber, but the mechanism of action for insoluble dietary fiber, such as cellulose-the most widely existing dietary fiber, in asthma is still unclear. The current study investigated the outcomes of a high-cellulose diet in a mouse model of asthma and detected pathological manifestations within the lungs, changes in the intestinal microbiome, and changes in intestinal short-chain fatty acids (SCFAs) in mice. A high-cellulose diet can reduce lung inflammation and asthma symptoms in asthmatic mice. Furthermore, it dramatically changes the composition of the intestinal microbiome. At the family level, a new dominant fungus family Peptostreptococcaceae is produced, and at the genus level, the unique genus Romboutsla, [Ruminococcus]_torques_group was generated. These genera and families of bacteria are closely correlated with lipid metabolism in vivo. Many studies have proposed that the mechanism of dietary fiber regulating asthma may involve the intestinal microbiome producing SCFAs, but the current research shows that a high-cellulose diet cannot increase the content of SCFAs in the intestine. These data suggest that a high-cellulose diet decreases asthma symptoms by altering the composition of the intestinal microbiome, however, this mechanism is thought to be independent of SCFAs and may involve the regulation of lipid metabolism.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. High-fiber diet can reduce lung inflammation and related cytokine production.
A: The pulmonary inflammation in the AS group was significantly worse than that in the N group, but the situation was alleviated in the HF group. B: The IL-4 level in the AS group was significantly higher than that in the N group (P<0.05), while the IL-4 level in the HF group was significantly reduced (P<0.01). C: The IgE level in the AS group was higher than that in the N group (P<0.05), while the IL-4 level in the HF group was significantly reduced (P<0.05).
Fig 2
Fig 2. Fecal microbial composition analysis and beta-diversity analysis.
A, B: analysis of the fecal microbial composition of the three groups on the family level and genus level; B, C: PCA analysis is used to explore the correlation of the composition of the microbiome on the family level and genus level of each group; C, D: ANOSIM analysis compares differences between groups and within groups (C:P <0.001, D: P<0.001).
Fig 3
Fig 3. Significantly different species analysis on the family level and genus level.
A: Analysis of significantly different species at the family level; B: Analysis of significantly different species at the genus level (*, P < 0.05; **, P <0 .01; ***, P <0 .001).
Fig 4
Fig 4. Analysis of short-chain fatty acid content in feces.
A-H: Quantitative analysis of short-chain fatty acids in mouse feces.
See this image and copyright information in PMC

References

    1. Boonpiyathad T, Sozener ZC, Satitsuksanoa P, Akdis CA. Immunologic mechanisms in asthma. Semin Immunol. 2019;46:101333. Epub 2019/11/11. doi: 10.1016/j.smim.2019.101333 . - DOI - PubMed
    1. Huang HR, Zhong YQ, Wu JF. The association between IFN-γ and IL-4 genetic polymorphisms and childhood susceptibility to bronchial asthma. Gene. 2012;494(1):96–101. Epub 2011/12/07. doi: 10.1016/j.gene.2011.09.027 . - DOI - PubMed
    1. Humbert M, Menz G, Ying S, Corrigan CJ, Robinson DS, Durham SR, et al.. The immunopathology of extrinsic (atopic) and intrinsic (non-atopic) asthma: more similarities than differences. Immunol Today. 1999;20(11):528–33. Epub 1999/10/26. doi: 10.1016/s0167-5699(99)01535-2 . - DOI - PubMed
    1. O’Keefe SJ. The association between dietary fibre deficiency and high-income lifestyle-associated diseases: Burkitt’s hypothesis revisited. Lancet Gastroenterol Hepatol. 2019;4(12):984–96. Epub 2019/11/08. doi: 10.1016/S2468-1253(19)30257-2 ; PubMed Central PMCID: PMC6944853. - DOI - PMC - PubMed
    1. Wood LG, Garg ML, Smart JM, Scott HA, Barker D, Gibson PG. Manipulating antioxidant intake in asthma: a randomized controlled trial. Am J Clin Nutr. 2012;96(3):534–43. Epub 2012/08/03. doi: 10.3945/ajcn.111.032623 . - DOI - PubMed

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