Cladosporium cladosporioides ameliorates visceral hypersensitivity in irritable bowel syndrome-like mice by inhibiting dectin-1 signaling and mast cell activation

doi:10.3748/wjg.119605

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Study

Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.

World J Gastroenterol. Sep 14, 2026; 32(34): 119605
Published online Sep 14, 2026. doi: 10.3748/wjg.119605

Cladosporium cladosporioides ameliorates visceral hypersensitivity in irritable bowel syndrome-like mice by inhibiting dectin-1 signaling and mast cell activation

Hua-Hong Wang, Yan Chi, Hao-Nan Zheng, Shang-Qing Zhang, Cheng-Lin Guo

Cheng-Lin Guo, Shang-Qing Zhang, Yan Chi, Hua-Hong Wang, Department of Gastroenterology, Peking University First Hospital, Beijing 100034, China

Hao-Nan Zheng, Department of Gastroenterology, Peking University Third Hospital, Beijing 100191, China

Author contributions: Guo CL and Zhang SQ developed the methodology, conducted the investigation, and wrote the manuscript, they contributed equally to this manuscript and are co-first authors; Guo CL and Zheng HN interpreted the data and conducted formal analysis; Chi Y and Wang HH designed the research study, supervised the project, and reviewed the manuscript, they contributed equally to this manuscript and are co-corresponding authors; Chi Y obtained research funding. All authors have read and approved the final manuscript.

Supported by the Natural Science Foundation of Beijing Municipality, No. 7212110 (to Chi Y); Peking University First Hospital Youth Clinical Research Special Fund, No. 2018CR06 (to Chi Y); and Peking University First Hospital Interdisciplinary Clinical Research Special Fund, No. 2019CR42 (to Chi Y).

Institutional review board statement: The study was reviewed and approved by the Ethics Committee of the Peking University First Hospital (No. 2019-074), registered on Chinese Clinical Trials Registry (ChiCTR2400079961, Registered January 17, 2024).

Institutional animal care and use committee statement: The animal study protocol was approved by the Ethics Committee of Peking University First Hospital and followed the institutional guidelines for the care and use of laboratory animals (Ethics No. LA2021501).

Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.

ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.

Data sharing statement: The datasets generated and/or analysed during the current study are available in the NCBI Sequence Read Archive (SRA) repository under accession number PRJNA1107793 (https://dataview.ncbi.nlm.nih.gov/object/PRJNA1107793?reviewer=3kmk8bkp77msdl5hm1u7p0ooik) and PRJNA1107803 (https://dataview.ncbi.nlm.nih.gov/object/PRJNA1107803?reviewer=ocvfmgaml4re4694b6m1uksofp). Other analytic methods, including statistical codes, software information, and algorithms used in this study, and the study protocol and the deidentified individual participant data are available in Supplementary material.

Corresponding author: Yan Chi, MD, Associate Professor, Chief Physician, Department of Gastroenterology, Peking University First Hospital, No. 8 Xishiku Road, Xicheng District, Beijing 100034, China. chiyan@bjmu.edu.cn

Received: February 2, 2026
Revised: March 17, 2026
Accepted: April 24, 2026
Published online: September 14, 2026
Processing time: 199 Days and 14.4 Hours

Abstract

BACKGROUND

Gut mycobiota dysbiosis contributes to visceral hypersensitivity (VH) in irritable bowel syndrome (IBS); however, the roles of colony-specific fungi in IBS-VH development remain unclear.

AIM

To investigate the effects of mucosal mycobiota in IBS-VH pathogenesis in vitro and in vivo along with the underlying mechanisms.

METHODS

In this study, 36 patients with diarrhea-predominant IBS and 29 healthy controls were enrolled for screening of biomarker fungi using internal transcribed spacer region sequencing. The relationship between fungal abundance and VH in patients was assessed. A trinitrobenzene sulfonic acid (TNBS)-induced IBS mouse model was used to explore the effect of a specific fungal species on IBS-VH. Colonic inflammatory cytokine levels, activation of mast cells, and dectin-1 signaling were assayed. A human mast cell line (HMC-1) was used to investigate the underlying mechanisms in vitro.

RESULTS

The results showed that Cladosporium was a characteristic fungal genus in the colonic mucosa of patients with diarrhea-predominant IBS. Oral gavage of Cladosporium cladosporioides (C. cladosporioides) improved IBS-VH in mice. In terms of the mechanisms, application of C. cladosporioides reduced colonic mucosal inflammatory cytokine levels, inhibited the activation of mast cells, and downregulated dectin-1/nuclear factor kappa B (NF-κB) signaling in the TNBS-induced IBS mouse model. Studies in HMC-1 cells indicated that cotreatment with C. cladosporioides inhibited the dectin-1 agonist curdlan-induced activation of NF-κB signaling and upregulation of inflammatory cytokines.

CONCLUSION

Cladosporium, a characteristic colony-specific fungal genus enriched in IBS patients, improved TNBS-induced IBS-VH in mice by inhibiting dectin-1/NF-κB signaling and mast cell activation. C. cladosporioides is a promising fungal species that protects against the IBS-VH.

Keywords: Cladosporium; Mycobiota; Mast cell; Dectin-1; Visceral hypersensitivity

Core Tip: Gut mycobiota are linked to visceral hypersensitivity (VH) in irritable bowel syndrome (IBS); however, the specific role of fungi in IBS remains unexplored. This study explored the role of the gut mycobiota in VH associated with diarrhea-predominant IBS. We identified Cladosporium as a key fungal genus enriched in diarrhea-predominant IBS patients and demonstrated that Cladosporium cladosporioides (C. cladosporioides) alleviates IBS-VH in mice. Mechanistically, C. cladosporioides reduces inflammatory cytokine levels, inhibits mast cell activation, and downregulates dectin-1/nuclear factor kappa B signaling. These findings suggest C. cladosporioides as a potential therapeutic probiotic for IBS-VH, highlighting the role of this gut fungus in modulating IBS pathogenesis.