Recognition of Candida albicans by Dectin-1 induces mast cell activation

Nieto-Patlán, Alejandro; Campillo-Navarro, Marcia; Rodríguez‐Cortés, Octavio; Muñoz-Cruz, Samira; Wong‐Baeza, Isabel; Estrada‐Parra, Sergio; Estrada-Garcı́a, Iris; Serafín‐López, Jeanet; Chacón‐Salinas, Rommel

doi:10.1016/j.imbio.2015.05.005

Cited by 46 publications

(37 citation statements)

References 56 publications

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“…19,[21][22][23][24] In addition, it was shown that fungi/fungal antigens are activators of mast cells. 25,26 Together this led us to assess the possible role of fungi (i.e. the mycobiome) in abdominal pain in a cohort of IBS patients and an animal model for IBS.…”

Section: Introductionmentioning

confidence: 99%

Intestinal Fungal Dysbiosis Is Associated With Visceral Hypersensitivity in Patients With Irritable Bowel Syndrome and Rats

et al. 2017

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Section: Introductionmentioning

confidence: 99%

Intestinal Fungal Dysbiosis Is Associated With Visceral Hypersensitivity in Patients With Irritable Bowel Syndrome and Rats

et al. 2017

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“…These data indicate Didox suppresses newly-synthesized cytokines and chemokines that comprise the late phase of the mast cell response. To measure rapid degranulation, we assessed changes in surface expression of CD107a and CD63, markers which we and others have used previously [23–26]. We typically see that upon cross linking, the percent of CD107 positive cells increases as well as the mean fluorescence intensity (MFI) of CD63, as CD63 is constitutively expressed on BMMC while CD107a is not.…”

Section: Resultsmentioning

confidence: 99%

Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IgE-mediated mast cell activation through attenuation of NFκB and AP-1 transcription

McLeod

Caslin

Spence

et al. 2017

Cellular Immunology

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Mast cell activation via the high-affinity IgE receptor (FcεRI) elicits production of inflammatory mediators central to allergic disease. As a synthetic antioxidant and a potent ribonucleotide reductase (RNR) inhibitor, Didox (3,4-dihyroxybenzohydroxamic acid) has been tested in clinical trials for cancer and is an attractive therapeutic for inflammatory disease. We found that Didox treatment of mouse bone marrow-derived mast cells (BMMC) reduced IgE-stimulated degranulation and cytokine production, including IL-6, IL-13, TNF and MIP-1a (CCL3). These effects were consistent using BMMC of different genetic backgrounds and peritoneal mast cells. While the RNR inhibitor hydroxyurea had little or no effect on IgE-mediated function, high concentrations of the antioxidant N-acetylcysteine mimicked Didox-mediated suppression. Furthermore, Didox increased expression of the antioxidant genes superoxide dismutase and catalase, and suppressed DCFH-DA fluorescence, indicating reduced reactive oxygen species production. Didox effects were not due to changes in FcεRI expression or cell viability, suggesting it inhibits signaling required for inflammatory cytokine production. In support of this, we found that Didox reduced FcεRI-mediated AP-1 and NFκB transcriptional activity. Finally, Didox suppressed mast cell-dependent, IgE-mediated passive systemic anaphylaxis in vivo. These data demonstrate the potential use for Didox as a means of antagonizing mast cell responses in allergic disease.

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“…More recently, Nieto‐Patlán et al. have shown that both yeasts and hyphae of C. albicans can induce BMCMCs degranulation, production of TNF‐α, IL‐6, IL‐10, CCL3, CCL4, and ROS as well as NO involving TLR2 and dectin‐1 . Moreover, MC seems to be able to phagocytose C. albicans .…”

Section: Do Mcs Contribute To the Pathogenic Effects Of Candida Albicmentioning

confidence: 99%

The complex role of mast cells in fungal infections

Jiao

Luo

Zhao

et al. 2019

Experimental Dermatology

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In addition to their critical role in allergic disorders, mast cells (MCs) are well recognized for their protective effector functions during bacteria and parasite infections. This review describes recent advancements of our understanding of the complex role of MCs in fungal infections. Specifically, we outline key features of the contribution of MCs to infections with six fungal pathogens, namely Sporothrix, Paracoccidioides, Aspergillus, Malassezia, Candida and Dermatophytes. Evidence from studies of these pathogens suggests that MCs can function as positive regulators that detect and contain fungi at the site of infection. However, it appears that the inflammation induced by MCs following fungal infections may not always and only be beneficial to the host. MC responses during fungal infections may primarily benefit the pathogen by facilitating its spreading and contributing to a greater severity of fungal infections. This review also highlights key drivers of MCs activation and effector mechanisms that have been identified for the multidimensional function of MCs in fungal diseases and in allergic diseases combined with fungal infection.

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Recognition of Candida albicans by Dectin-1 induces mast cell activation

Cited by 46 publications

References 56 publications

Intestinal Fungal Dysbiosis Is Associated With Visceral Hypersensitivity in Patients With Irritable Bowel Syndrome and Rats

Intestinal Fungal Dysbiosis Is Associated With Visceral Hypersensitivity in Patients With Irritable Bowel Syndrome and Rats

Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IgE-mediated mast cell activation through attenuation of NFκB and AP-1 transcription

The complex role of mast cells in fungal infections

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