Esophagitis caused by<i>Candida guilliermondii</i>in diabetes mellitus: first reported case

Macêdo, Danielle Patrícia Cerqueira; Oliveira, Neiva Tinti de; Farias, Alessandro Santos; Silva, Vanessa K A; Wilheim, Ana Botler; Couto, Fabíola Maria Marques do; Neves, Rejane Pereira

doi:10.3109/13693780903582614

Cited by 5 publications

(4 citation statements)

References 21 publications

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“…However, our data underscore that insulin resistant mice are more susceptible to sustained GI Candida colonization than lean mice. These findings are in line with increased susceptibility to candidiasis in patients with metabolic dysregulation [9] . This discrepancy between the ex vivo and in vivo data is attributed to the fact that the in vivo Candida elimination involves both opsonin-dependent and independent host defence mechanisms, while in our ex vivo experimental conditions, only the elimination of non-opsonized C. albicans is implicated.…”

Section: Discussionsupporting

confidence: 80%

PPARγ Ligands Switched High Fat Diet-Induced Macrophage M2b Polarization toward M2a Thereby Improving Intestinal Candida Elimination

et al. 2010

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Obesity is associated with a chronic low-grade inflammation that predisposes to insulin resistance and the development of type 2 diabetes. In this metabolic context, gastrointestinal (GI) candidiasis is common. We recently demonstrated that the PPARγ ligand rosiglitazone promotes the clearance of Candida albicans through the activation of alternative M2 macrophage polarization. Here, we evaluated the impact of high fat diet (HFD)-induced obesity and the effect of rosiglitazone (PPARγ ligand) or WY14643 (PPARα ligand) both on the phenotypic M1/M2 polarization of peritoneal and cecal tissue macrophages and on the outcome of GI candidiasis. We demonstrated that the peritoneal macrophages and the cell types present in the cecal tissue from HF fed mice present a M2b polarization (TNF-αhigh, IL-10high, MR, Dectin-1). Interestingly, rosiglitazone induces a phenotypic M2b-to-M2a (TNF-αlow, IL-10low, MRhigh, Dectin-1high) switch of peritoneal macrophages and of the cells present in the cecal tissue. The incapacity of WY14643 to switch this polarization toward M2a state, strongly suggests the specific involvement of PPARγ in this mechanism. We showed that in insulin resistant mice, M2b polarization of macrophages present on the site of infection is associated with an increased susceptibility to GI candidiasis, whereas M2a polarization after rosiglitazone treatment favours the GI fungal elimination independently of reduced blood glucose. In conclusion, our data demonstrate a dual benefit of PPARγ ligands because they promote mucosal defence mechanisms against GI candidiasis through M2a macrophage polarization while regulating blood glucose level.

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Section: Discussionsupporting

confidence: 80%

PPARγ Ligands Switched High Fat Diet-Induced Macrophage M2b Polarization toward M2a Thereby Improving Intestinal Candida Elimination

et al. 2010

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“…Altogether, the above data show that a HFD, irrespective of the presence of carbohydrate, induces a strong specific decrease in the number of Th17 cells within the SILP which may lead to the onset of metabolic disease. It is noteworthy that T2D patients are more sensitive than normal to intestinal infections with pathogens like Candida guilliermondii, further suggesting that they may have impaired Th17 cells (Khovidhunkit et al, 2009;Lutsey et al, 2009;Macê do et al, 2010). Consistent with this observation in human subjects, it was shown that HFD-fed rodents were more prone to Candida albicans infection than controls (Lefè vre et al, 2010).…”

Section: Hfd-induced T2d Impairs Intestinal Immunitymentioning

confidence: 87%

The Gut Microbiota Regulates Intestinal CD4 T Cells Expressing RORγt and Controls Metabolic Disease

et al. 2015

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A high-fat diet (HFD) induces metabolic disease and low-grade metabolic inflammation in response to changes in the intestinal microbiota through as-yet-unknown mechanisms. Here, we show that a HFD-derived ileum microbiota is responsible for a decrease in Th17 cells of the lamina propria in axenic colonized mice. The HFD also changed the expression profiles of intestinal antigen-presenting cells and their ability to generate Th17 cells in vitro. Consistent with these data, the metabolic phenotype was mimicked in RORγt-deficient mice, which lack IL17 and IL22 function, and in the adoptive transfer experiment of T cells from RORγt-deficient mice into Rag1-deficient mice. We conclude that the microbiota of the ileum regulates Th17 cell homeostasis in the small intestine and determines the outcome of metabolic disease.

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“…It is the most common cause of esophageal infections. There are numerous Candida species, including Candida tropicalis and Candia guilliermondii , that have been linked with esophageal infection, but C. albicans account for the great majority of these infections [ 3 ]. Although EC rarely occurs without a clear underlying cause, even in immunocompetent hosts, a predisposing factor should be assumed [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Severe Esophageal Stricture Caused by Esophageal Candidiasis in a Non-HIV Patient

Abdelfattah,

Mahgoub

2023

Cureus

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Esophageal candidiasis (EC) is a common opportunistic infection in immunocompromised individuals, often encountered in situations such as untreated HIV/AIDS or following organ transplantation with immunosuppressant usage. While the main manifestation of esophageal candidiasis is mucosal inflammation, its progression and severe cases may lead to esophageal complications like dysphagia, odynophagia, and weight loss. One of the rare complications is esophageal stricture (ES). Few cases have been reported in the literature to date. Esophageal candidiasis can lead to the formation of ES through chronic inflammation, tissue damage, fibrosis, scarring, and ultimately narrowing of the esophageal lumen. Patients with ES often present with dysphagia, odynophagia, and other symptoms related to impaired swallowing. Esophageal strictures related to EC could seriously affect the patient’s quality of life. Malnutrition and weight loss can be easily encountered in those cases. So, prompt diagnosis and appropriate antifungal therapy are important. Management should include addressing the stricture through endoscopic dilation interventions. Timely recognition of this complication is crucial for improving patient outcomes and quality of life. We present the case of a 46-year-old male with EC complicated by severe ES, dysphagia, and weight loss of more than 30 lbs. The diagnosis was made based on the histopathological examination of the esophageal biopsies.

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Esophagitis caused byCandida guilliermondiiin diabetes mellitus: first reported case

Cited by 5 publications

References 21 publications

PPARγ Ligands Switched High Fat Diet-Induced Macrophage M2b Polarization toward M2a Thereby Improving Intestinal Candida Elimination

PPARγ Ligands Switched High Fat Diet-Induced Macrophage M2b Polarization toward M2a Thereby Improving Intestinal Candida Elimination

The Gut Microbiota Regulates Intestinal CD4 T Cells Expressing RORγt and Controls Metabolic Disease

Severe Esophageal Stricture Caused by Esophageal Candidiasis in a Non-HIV Patient

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