Cell Wall Polysaccharides of &lt;i&gt;Candida albicans&lt;/i&gt; Induce Mast Cell Degranulation in the Gut

Sakurai, Akihiko; Yamaguchi, Natsu; Sonoyama, Kei

doi:10.12938/bmfh.31.67

Cited by 14 publications

(15 citation statements)

References 14 publications

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“…Our study shows that mast cells degranulated more intensely towards opsonized C. albicans cells. Both, the previous and our study oppose a third using a rat-derived RBL-2H3 cell line 37 , in which the authors could not identify degranulation. Thus, we assume that these diverging results stem from differences in mast cell origin and maturation and from the fact that humans are natural hosts for C. albicans , whereas rats are not.…”

Section: Discussioncontrasting

confidence: 80%

Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells

Lopes

Stylianou

Nilsson

et al. 2015

Sci Rep

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Immunosuppressed patients are frequently afflicted with severe mycoses caused by opportunistic fungal pathogens. Besides being a commensal, colonizing predominantly skin and mucosal surfaces, Candida albicans is the most common human fungal pathogen. Mast cells are present in tissues prone to fungal colonization being expectedly among the first immune cells to get into contact with C. albicans. However, mast cell-fungus interaction remains a neglected area of study. Here we show that human mast cells mounted specific responses towards C. albicans. Collectively, mast cell responses included the launch of initial, intermediate and late phase components determined by the secretion of granular proteins and cytokines. Initially mast cells reduced fungal viability and occasionally internalized yeasts. C. albicans could evade ingestion by intracellular growth leading to cellular death. Furthermore, secreted factors in the supernatants of infected cells recruited neutrophils, but not monocytes. Late stages were marked by the release of cytokines that are known to be anti-inflammatory suggesting a modulation of initial responses. C. albicans-infected mast cells formed extracellular DNA traps, which ensnared but did not kill the fungus. Our results suggest that mast cells serve as tissue sentinels modulating antifungal immune responses during C. albicans infection. Consequently, these findings open new doors for understanding fungal pathogenicity.

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Section: Discussioncontrasting

confidence: 80%

Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells

Lopes

Stylianou

Nilsson

et al. 2015

Sci Rep

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“…In C. albicans, these mannose-related proteoglycans purportedly display several immunomodulatory roles. These roles include the suppression of B and T lymphocytes (88) and the promotion of mast cell degranulation, a process that releases several mediators (e.g., histamine, serotonin, serine protease, and proteoglycans) that affect the gastrointestinal mucosal barrier (114). Interestingly, the pathogenesis of H. pylori-infected gastritis has been associated with mast cell degranulation (115,116) and regulatory T cells that actively suppress the T cell response (117)(118)(119).…”

Section: Studies Of H Pylori Biofilms and Immune Evasionmentioning

confidence: 99%

Helicobacter pylori Biofilm Formation and Its Potential Role in Pathogenesis

Hathroubi

Servetas

Windham

et al. 2018

Microbiol Mol Biol Rev

141

142

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Despite decades of effort, infections remain difficult to treat. Over half of the world's population is infected by, which is a major cause of duodenal and gastric ulcers as well as gastric cancer. During chronic infection, localizes within the gastric mucosal layer, including deep within invaginations called glands; thanks to its impressive ability to survive despite the harsh acidic environment, it can persist for the host's lifetime. This ability to survive and persist in the stomach is associated with urease production, chemotactic motility, and the ability to adapt to the fluctuating environment. Additionally, biofilm formation has recently been suggested to play a role in colonization. Biofilms are surface-associated communities of bacteria that are embedded in a hydrated matrix of extracellular polymeric substances. Biofilms pose a substantial health risk and are key contributors to many chronic and recurrent infections. This link between biofilm-associated bacteria and chronic infections likely results from an increased tolerance to conventional antibiotic treatments as well as immune system action. The role of this biofilm mode in antimicrobial treatment failure and survival has yet to be determined. Furthermore, relatively little is known about the biofilm structure or the genes associated with this mode of growth. In this review, therefore, we aim to highlight recent findings concerning biofilms and the molecular mechanism of their formation. Additionally, we discuss the potential roles of biofilms in the failure of antibiotic treatment and in infection recurrence.

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“…Fungi are associated with a wide spectrum of diseases in humans and animals, ranging from acute self‐limiting manifestations in immunocompetent individuals to allergy and severe life‐threatening infections in immunocompromised patients . Considering the harmful effects of mast cells in connection with allergic reactions, mast cell degranulation by the cell wall polysaccharides of Candida albicans , a commensal fungus of the skin and mucosal surfaces, was meant to contribute to sensitization against food antigens by affecting the mucosal barrier in mice . Controversy still exists as to whether gastrointestinal colonization by C. albicans contributes to atopic dermatitis aggravation.…”

Section: Mast Cells and Fungal Infectionsmentioning

confidence: 99%

“…effects of mast cells in connection with allergic reactions, mast cell degranulation by the cell wall polysaccharides of Candida albicans, a commensal fungus of the skin and mucosal surfaces,71 was meant to contribute to sensitization against food antigens by affecting the mucosal barrier in mice 72. Controversy still exists as to whether gastrointestinal colonization by C. albicans contributes to atopic dermatitis aggravation.…”

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confidence: 99%

The contribution of mast cells to bacterial and fungal infection immunity

Piliponsky

Romani

2018

Immunological Reviews

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Mast cells are hematopoietic progenitor-derived, granule-containing immune cells that are widely distributed in tissues that interact with the external environment, such as the skin and mucosal tissues. It is well-known that mast cells are significantly involved in IgE-mediated allergic reactions, but because of their location, it has also been long hypothesized that mast cells can act as sentinel cells that sense pathogens and initiate protective immune responses. Using mast cell or mast cell protease-deficient murine models, recent studies by our groups and others indicate that mast cells have pleiotropic regulatory roles in immunological responses against pathogens. In this review, we discuss studies that demonstrate that mast cells can either promote host resistance to infections caused by bacteria and fungi or contribute to dysregulated immune responses that can increase host morbidity and mortality. Overall, these studies indicate that mast cells can influence innate immune responses against bacterial and fungal infections via multiple mechanisms. Importantly, the contribution of mast cells to infection outcomes depends in part on the infection model, including the genetic approach used to assess the influence of mast cells on host immunity, hence highlighting the complexity of mast cell biology in the context of innate immune responses.

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Cell Wall Polysaccharides of <i>Candida albicans</i> Induce Mast Cell Degranulation in the Gut

Cited by 14 publications

References 14 publications

Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells

Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells

Helicobacter pylori Biofilm Formation and Its Potential Role in Pathogenesis

The contribution of mast cells to bacterial and fungal infection immunity

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