Malassezia Is Associated with Crohn’s Disease and Exacerbates Colitis in Mouse Models

Limon, Jose J.; Tang, Jie; Li, Dalin; Wolf, Andrea J.; Michelsen, Kathrin S.; Funari, Vince; Gargus, Matthew; Nguyen, Christopher; Sharma, Purnima; Maymi, Viviana I.; Iliev, Iliyan D.; Skalski, Joseph H.; Brown, Jordan; Landers, Carol J.; Borneman, James; Braun, Jonathan; Targan, Stephan R.; McGovern, Dermot P.; Underhill, David

doi:10.1016/j.chom.2019.01.007

Cited by 287 publications

(314 citation statements)

References 53 publications

(80 reference statements)

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“…The abundance change of gut fungi is not only restricted to the faecal microbiome but also occurs in the diseased‐mucosa . A mucosa‐associated fungus called Malassezia restricta ( M restricta ) that normally presents in skin and gut mucosa was found in CD mucosa .…”

Section: Fungal Alterations In Faecal and Mucosa Samples In Ibdmentioning

confidence: 99%

“…This hypothesis is supported by exacerbated colitis progression when M restricta was colonised in wild type and germ‐free mice . Various C‐type lectin receptors, Mincle, CARD9 and Dectin‐2 have been found to be responsible for M restricta recognition, but the function of CARD9 S12N remains unknown, and it was found to be associated with several autoimmune diseases, such as IBD and asthma . CARD9 S12N can facilitate interleukin 5 (IL‐5) secretion in alveolar macrophages for a type II immune response but its central role in CD pathogenesis is not understood …”

Section: Fungal Alterations In Faecal and Mucosa Samples In Ibdmentioning

confidence: 99%

“…36,37 The abundance change of gut fungi is not only restricted to the faecal microbiome but also occurs in the diseased-mucosa. 38 A mucosa-associated fungus called Malassezia restricta (M restricta) that normally presents in skin and gut mucosa was found in CD mucosa. 38 M restricta has been found to worsen gut inflammation particularly in CD patients who have Caspase recruitment domain-containing protein (CARD)-9 S12N polymorphism, suggesting that CARD9 signalling is critical for M restricta sensing.…”

Section: Fung Al Alter Ati On S In Faec Al and Mucosa Sample S In Ib Dmentioning

confidence: 99%

“…38 M restricta has been found to worsen gut inflammation particularly in CD patients who have Caspase recruitment domain-containing protein (CARD)-9 S12N polymorphism, suggesting that CARD9 signalling is critical for M restricta sensing. 38 This hypothesis is supported by exacerbated colitis progression when M restricta was colonised in wild type and germ-free mice. 38 Various C-type lectin receptors, Mincle, CARD9 and Dectin-2 have been found to be responsible for M restricta recognition, [38][39][40] but the function of CARD9 S12N remains unknown, and it was found to be associated with several autoimmune diseases, such as IBD and asthma.…”

Section: Fung Al Alter Ati On S In Faec Al and Mucosa Sample S In Ib Dmentioning

confidence: 99%

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Review article: fungal alterations in inflammatory bowel diseases

Lam

Zuo

et al. 2019

Aliment Pharmacol Ther

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Summary Background Emerging data suggest that alterations in gut fungi may be associated with the pathogenesis of inflammatory bowel disease (IBD). In healthy individuals, gut commensal fungi act synergistically with other members of the microbiota to maintain homeostasis but their role in IBD is less clear. Aim To review the role of gut fungi and their trans‐kingdom interactions with bacteria in IBD Methods A literature search was conducted on Ovid and Pubmed to select relevant animal and human studies that have reported fungi and IBD. Results There is an increased total fungal load particularly of Candida and Malassezia species in the faeces and mucosa of Crohn's disease patients, and a lower fungal diversity in the faeces of ulcerative colitis patients. Caspase recruitment domain‐containing protein (CARD)‐9 polymorphism in Crohn's disease patients favours Malassezia colonisation that worsens gut inflammation. Diet high in carbohydrates increased the total abundance of Candida species, whereas protein‐rich diet had the opposite effect. Anti‐fungal therapies are mostly used to treat Candida albicans or Histoplasma capsulatum infections in IBD, whereas pilot studies of supplementing fungal probiotics Saccharomycopsis fibuligera, Saccharomyces boulardii and Saccharomyces cerevisiae CNCM I‐3856 strain showed therapeutic effects in IBD. Conclusions Gut fungi are altered in patients with Crohn's disease and ulcerative colitis. Modulation of the fungal microbiota can be considered as a therapeutic approach for IBD. Future research should focus on understanding how the fungal microbiota interacts with other components of the gut microbiota in association with the pathogenesis and development of IBD.

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Section: Fungal Alterations In Faecal and Mucosa Samples In Ibdmentioning

confidence: 99%

Section: Fungal Alterations In Faecal and Mucosa Samples In Ibdmentioning

confidence: 99%

Section: Fung Al Alter Ati On S In Faec Al and Mucosa Sample S In Ib Dmentioning

confidence: 99%

Section: Fung Al Alter Ati On S In Faec Al and Mucosa Sample S In Ib Dmentioning

confidence: 99%

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Review article: fungal alterations in inflammatory bowel diseases

Lam

Zuo

et al. 2019

Aliment Pharmacol Ther

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“…Fungal species other that Candida have also been associated with the pathogenesis of IBD. The skin-resident fungus Malassezia restricta is particularly abundant in the gut of IBD patients carrying the CARD9 risk allele [80]. This polymorphism is associated with increased proinflammatory response to M. restricta in vitro.…”

Section: Antifungal Innate Immunity In the Oral Mucosa And Gastrointementioning

confidence: 99%

Cellular and molecular mechanisms of antifungal innate immunity at epithelial barriers: The role of C‐type lectin receptors

2020

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Humans are constantly exposed to fungi, either in the form of commensals at epithelial barriers or as inhaled spores. Innate immune cells play a pivotal role in maintaining commensal relationships and preventing skin, mucosal, or systemic fungal infections due to the expression of pattern recognition receptors that recognize fungal cell wall components and modulate both their activation status and the ensuing adaptive immune response. Commensal fungi also play a critical role in the modulation of homeostasis and disease susceptibility at epithelial barriers. This review will outline cellular and molecular mechanisms of anti‐fungal innate immunity focusing on C‐type lectin receptors and their relevance in the context of host‐fungi interactions at skin and mucosal surfaces in murine experimental models as well as patients susceptible to fungal infections.

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