Fungi prevent intestinal healing

doi:10.1126/science.abg6017

GSTDTAP > 气候变化

DOI	10.1126/science.abg6017
	Fungi prevent intestinal healing
	Tyson Chiaro; June L. Round
	2021-03-12
发表期刊	Science
出版年	2021
英文摘要	Chronic intestinal diseases, such as inflammatory bowel disease (IBD), are associated with continual tissue damage that must be repaired. Mucosal restoration is a coordinated process that can be influenced by extrinsic factors, including the commensal bacterial community ([ 1 ][1]–[ 3 ][2]). However, individuals with intestinal disease often receive antibiotics during their care, disrupting these beneficial bacteria. Although fungi comprise a relatively small proportion of the microbial community, they can take over mucosal niches because they are not targeted by antibiotics ([ 4 ][3]). On page 1154 of this issue, Jain et al. ([ 5 ][4]) find that the yeast Debaryomyces hansenii , which is commonly used in the food industry, can colonize wounds in antibiotic-treated mice and is present in the inflamed tissue of individuals with IBD. This colonization enhances inflammation by blocking the signaling required for wound healing. Thus, disruption of commensal bacteria can open niches for fungi that exacerbate disease. ![Figure][5] The yeast Debaryomyces hansenii prevents intestinal wound healing During homeostasis, anaerobic organisms, such as Akkermansia muciniphila , seed the wound bed and, together with bacterial metabolites, such as deoxycholate, promote wound healing. Antibiotic therapy or loss of bacteria owing to chronic inflammation in inflammatory bowel disease can lead to the colonization of wounds in the epithelial lining with environmental organisms such as the yeast Debaryomyces hansenii . This stimulates a type I interferon (IFN) response in macrophages, which leads to production of C-C motif chemokine 5 (CCL5) and chronic inflammation that prevents wound healing. GRAPHIC: MELISSA THOMAS BAUM/ SCIENCE The intestinal microbiota is a consortium of microorganisms, including bacteria, archaea, fungi, and viruses. Many investigations have identified a role for bacterial members of the microbiota in IBD ([ 6 ][6]). Clinical evidence suggests that fungi may also influence IBD, including the presence of serum antibodies to fungal cell surface moieties in patients with certain types of IBD. Additionally, mutations in the gene that encodes the pattern recognition receptor DECTIN-1 (dendritic cell–associated C-type lectin 1), which recognizes fungal cell walls, or the downstream inflammatory signaling molecule CARD9 (caspase recruitment domain–containing protein 9) are commonly found in IBD patients ([ 7 ][7]). Furthermore, investigations in animal models have demonstrated that common gut fungi, such as Saccharomyces cerevisiae or Candida tropicalis , can influence IBD severity ([ 8 ][8]–[ 10 ][9]). However, a role for fungi during intestinal epithelial healing has never been evaluated. IBD is characterized by chronic intestinal inflammation, loss of intestinal barrier integrity, and epithelial damage, requiring constant repair of the mucosa. To study the injury process, Jain et al. used forceps to remove areas of the colonic mucosa during endoscopy in mice. As opposed to chemical or infectious models of intestinal injury, this method allows for spatial and temporal control of the wound. Mucosal healing occurs in three discrete and coordinated stages: barrier reestablishment involving neutrophil infiltration, extensive proliferation, and then tissue remodeling. Preventing any of these stages leads to chronic inflammation and a failure to reform the epithelium. Studies have identified a beneficial role for commensal bacteria during mucosal healing ([ 1 ][1]–[ 3 ][2]). In a healthy gut, shortly after tissue injury, neutrophils are recruited to the injured tissue, creating an anaerobic environment that allows specific bacterial members to seed the wound bed. In particular, Akkermansia muciniphila colonizes the injured tissue and influences signaling in epithelial cells to enhance proliferation and wound closure ([ 1 ][1]). Additionally, bacterial metabolites, such as deoxycholate, affect epithelial signaling to coordinate tissue remodeling ([ 3 ][2]). Thus, mucosal wound healing requires signaling from specific commensal bacteria to occur properly. During inflammatory flares associated with IBD, antibiotics are often used to prevent potentially harmful bacteria accessing the bloodstream. Jain et al. found that antibiotic treatment during the biopsy injury model prevented tissue repair. However, known microbiota-dependent pathways were not involved in this phenotype, leading the authors to test other hypotheses. Fungal out-growth is a frequent side effect of antibiotic use ([ 4 ][3]), and Jain et al. observed D. hansenii colonization of the injured tissue in antibiotictreated mice. Treatment with the antifungal agent amphotericin B improved tissue regeneration. Introduction of D. hansenii , but not S. cerevisiae , by oral gavage into non–antibiotic-treated, conventionally raised animals was sufficient to impair the wound healing process. The same species of yeast was also detected in inflamed colonic tissue from two geographically distinct populations of patients with Crohn's disease, a type of IBD. Therefore, D. hansenii can specifically infect intestinal wounds in mice and humans with IBD and restrict the wound healing process in mice. Jain et al. found that macrophages were increased within the wound bed of animals infected with D. hansenii . Moreover, expression of the chemokine CCL5 (C-C motif chemokine 5) was enriched in macrophages isolated from the wound bed. CCL5 promotes inflammation by recruiting other immune cells to the tissue, and its expression is increased in individuals with IBD ([ 11 ][10], [ 12 ][11]). Wound healing was not impaired by D. hansenii colonization in mice in which Ccl5 was deleted. Culture of macrophages with D. hansenii followed by RNA sequencing revealed that activation of the type I interferon–CCL5 pathway in macrophages prevents wound healing (see the figure). D. hansenii is likely not a common resident of the gut, because it was isolated from all samples obtained from individuals with IBD but from only 1 of 10 healthy donors. D. hansenii is an environmental yeast that is distinctive in its ability to tolerate high-salt and pH conditions and is often used in cheese and meat production ([ 13 ][12]). It is possible that the ability of D. hansenii to persist in extreme environments also allows it to survive within inflamed tissue. This suggests that certain dietary recommendations could be made for patients with IBD to prevent colonization with D. hansenii , but this would need to be established with clinical trials. Additionally, use of antibiotics in individuals with chronic intestinal disease should be evaluated more carefully. The study of Jain et al. demonstrates that the loss of commensal microbes can open up niches for potentially harmful opportunistic organisms. Although CCL5 represents an attractive drug target that is currently being explored in IBD patients ([ 14 ][13]), it is one of many factors that is dysregulated during disease. Because commensal microbes can influence multiple host pathways that include preventing inflammation ([ 15 ][14]), colonization of pathogens, and promoting wound healing, specific cocktails of commensal bacteria might prove to be better therapeutic agents that act on several levels to protect from disease. 1. [↵][15]1. A. Alam et al ., Nat. Microbiol. 1, 15021 (2016). [OpenUrl][16] 2. 1. A. Alam et al ., Mucosal Immunol. 7, 645 (2014). [OpenUrl][17][CrossRef][18][PubMed][19] 3. [↵][20]1. U. Jain et al ., Cell Host Microbe 24, 353 (2018). 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领域	气候变化 ; 资源环境
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引用统计
文献类型	期刊论文
条目标识符	http://119.78.100.173/C666/handle/2XK7JSWQ/318681
专题	气候变化资源环境科学
推荐引用方式 GB/T 7714	Tyson Chiaro,June L. Round. Fungi prevent intestinal healing[J]. Science,2021.
APA	Tyson Chiaro,&June L. Round.(2021).Fungi prevent intestinal healing.Science.
MLA	Tyson Chiaro,et al."Fungi prevent intestinal healing".Science (2021).