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High cellulose diet aggravates food allergy through gut homeostasis disruption

ABSTRACT: This study investigated the impact of a high cellulose diet (HCD) on intestinal homeostasis and food allergy development in BALB/c mice. While soluble fibers are known to mitigate FA via short-chain fatty acid (SCFA) production, the role of insoluble fibers like cellulose remains unclear. Mice fed HCD exhibited gut dysbiosis, characterized by increased Proteobacteria, decreased tight junction protein expression, and intestinal barrier impairment, despite unchanged SCFA levels. RNA sequencing revealed HCD-induced upregulation of immune pathways, including the positive regulation of B and T cells differentiation and antigen receptor-mediated signaling pathway. Following ovalbumin (OVA) sensitization, HCD-fed mice displayed exacerbated allergic symptoms, including elevated OVA-specific IgE, IgG, histamine, and mMCP-1 levels. Gut microbiota analysis highlighted enrichment of potentially pathogenic taxa in HCD+OVA groups. Fecal microbiota transplantation (FMT) from HCD donors to antibiotic-treated recipients showed severe food allergy responses, confirming microbiota-mediated effects. These findings demonstrate that HCD exacerbates food allergy through gut microbial dysbiosis, intestinal barrier disruption, and intestinal immune disorder.

ORGANISM(S): Mus musculus

PROVIDER: GSE299687 | GEO | 2025/06/17

REPOSITORIES: GEO

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Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.

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High cellulose diet aggravates food allergy through gut homeostasis disruption

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