Divergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response

Rahabi, Mouna; Jacquemin, Godefroy; Prat, Mélissa; Meunier, Étienne; Alaeddine, Mohamad; Bertrand, Bénédicte; Lefèvre, Lise; Benmoussa, Khaddouj; Batigne, Philippe; Aubouy, Agnès; Auwerx, Johan; Kirzin, Sylvain; Bonnet, Delphine; Danjoux, Marie; Pipy, Bernard; Alric, Laurent; Authier, Hélène; Coste, Agnès

doi:10.1016/j.celrep.2020.03.018

Cited by 44 publications

(30 citation statements)

References 45 publications

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Section: Dectin-1 Ko (Clec7a −/− ) Micesupporting

confidence: 87%

“…[58,111]. Indeed, our colleagues have failed to detect the presence of this fungal species in their facility [61], however, when colonization of C. tropicalis was induced, severe inflammation of the colon in dectin-1 KO mice was observed that is consistent with those of Rahabi and colleagues' report [112] (Figure 2). Taken together, these accumulating lines of evidence ascertained from dectin-1 KO mice suggest that beta-glucan-dependent modulation of fungal immunity and host resistance is rather a multilayered process that is constantly shaped by a panoply of factors including fungal strain and species, genetic background of mice, specific immune cell population, fungal load, ligand type and purity, etc.…”

Section: Dectin-1 Ko (Clec7a −/− ) Micesupporting

confidence: 87%

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Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models

Desamero

Chung

Kakuta

2021

IJMS

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Understanding the host anti-fungal immunity induced by beta-glucan has been one of the most challenging conundrums in the field of biomedical research. During the last couple of decades, insights on the role of beta-glucan in fungal disease progression, susceptibility, and resistance have been greatly augmented through the utility of various beta-glucan cognate receptor-deficient mouse models. Analysis of dectin-1 knockout mice has clarified the downstream signaling pathways and adaptive effector responses triggered by beta-glucan in anti-fungal immunity. On the other hand, assessment of CR3-deficient mice has elucidated the compelling action of beta-glucans in neutrophil-mediated fungal clearance, and the investigation of EphA2-deficient mice has highlighted its novel involvement in host sensing and defense to oral mucosal fungal infection. Based on these accounts, this review focuses on the recent discoveries made by these gene-targeted mice in beta-glucan research with particular emphasis on the multifaceted aspects of fungal immunity.

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Section: Dectin-1 Ko (Clec7a −/− ) Micesupporting

confidence: 87%

Section: Dectin-1 Ko (Clec7a −/− ) Micesupporting

confidence: 87%

Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models

Desamero

Chung

Kakuta

2021

IJMS

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“…Takagawa et al, 88 reported a more severe colitis followed by DSS treatment in transgenic mice overexpressing Lrrk2 , associated with NF‐κB activation induced by Dectin‐1 and pro‐inflammatory cytokines in lamina propria DCs. More recently, Rahabi et al, 89 evaluated the role of Dectin‐1 and mannose receptor (MR) in the intestinal inflammation in Dectin‐1−/− or MR−/− mice and concluded that the lack of Dectin‐1 attenuates the inflammatory responses, while the lack of MR exacerbates the inflammation responses in the gut in DSS‐induced colitis models. Therefore, disruption of the gut mycobiome balance of the gut towards overgrowth of pathogenic species such as C albicans may lead to overexpression of Dectin‐1 and an increase in the intestinal inflammation.…”

Section: Gut Fungi and The Immune Systemmentioning

confidence: 99%

Gut mycobiome: The probable determinative role of fungi in IBD patients

Beheshti-Maal

Shahrokh

Ansari

et al. 2021

Mycoses

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Inflammatory bowel disease (IBD) is a multi‐factorial autoimmune disorder that its causative agents are unknown. The gut microbiota comprises of bacteria, viruses, fungi and protozoa that its role in IBD has remained controversially. Bacteria constitute more than 99% of the gut microbiota composition, and the main core of the gut microbiota is composed from Bacteroidetes and Firmicutes. The gut microbiota plays an important role in training, development and haemostasis of the immune responses during the life. Fungi compose a very small portion of gut microbiota, but play determinative roles in homeostasis of the gut bacterial composition and the mucosal immune responses. An interkingdom correlation between bacteria and fungi has been suggested. For example, the presence of Salmonella enterica serovar Typhimurium reduces the viability and colonisation of C albicans. Alterations in the composition and function of the gut microbiota, which is known as dysbiosis, are a usual event in patients who suffer from IBD. Although the main reason for this alteration is not clear, the interaction between gut bacteria and gut fungi seems to be an important subject in IBD patients. This review covers new findings on the interaction between fungi and bacteria and the role of fungi in the pathophysiology of IBD.

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“…During intestinal inflammation, macrophages infiltrate the intestinal mucosa and contribute to inflammatory cytokine production [30,31]. To assess the role of H89 in the modulation of macrophage activation, we evaluated the expression of pro-inflammatory cytokines and innate immune receptors in macrophages pretreated with H89 and then exposed to LPS (Figure 2).…”

Section: H89 Modulates the Expression Of Pro-inflammatory Cytokines And Toll-like Receptors (Tlrs) In Macrophagesmentioning

confidence: 99%

“…Disruption of intestinal epithelial barrier function during gut inflammation promotes the migration of immune cells including macrophages [30,31]. The effect of H89 on the migration of macrophages to C. albicans through DSS-challenged Caco-2 cells was assessed (Figure 3).…”

Section: H89 Decreases Macrophage Migration To C Albicans Through Dss-challenged Caco-2 Cellsmentioning

confidence: 99%

H89 Treatment Reduces Intestinal Inflammation and Candida albicans Overgrowth in Mice

et al. 2020

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Deregulation of the dynamic crosstalk between the gut microbiota, intestinal epithelial cells, and immune cells is critically involved in the development of inflammatory bowel disease and the overgrowth of opportunistic pathogens, including the human opportunistic fungus Candida albicans. In the present study, we assessed the effect of N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, on the migration of macrophages to C. albicans through dextran sulphate sodium (DSS)-challenged Caco-2 cells. We also investigated the impact of H89 on intestinal inflammation and C. albicans clearance from the gut, and determined the diversity of the gut microbiota in a murine model of DSS-induced colitis. H89 reduced the migration of macrophages to C. albicans through DSS-challenged Caco-2 cells. In addition, H89 decreased C. albicans viability and diminished the expression of pro-inflammatory cytokines and innate immune receptors in macrophages and colonic epithelial Caco-2 cells. In mice with DSS-induced colitis, H89 attenuated the clinical and histological scores of inflammation and promoted the elimination of C. albicans from the gut. H89 administration to mice decreased the overgrowth of Escherichia coli and Enterococcus faecalis populations while Lactobacillus johnsonii populations increased significantly. Overall, H89 reduced intestinal inflammation and promoted the elimination of C. albicans from the gut.

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Divergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response

Cited by 44 publications

References 45 publications

Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models

Insights on the Functional Role of Beta-Glucans in Fungal Immunity Using Receptor-Deficient Mouse Models

Gut mycobiome: The probable determinative role of fungi in IBD patients

H89 Treatment Reduces Intestinal Inflammation and Candida albicans Overgrowth in Mice

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