Genetic Association Analysis of the Functional c.714T&gt;G Polymorphism and Mucosal Expression of Dectin-1 in Inflammatory Bowel Disease

Vries, Hilbert S. de; Plantinga, Theo S.; Krieken, J. Han van; Stienstra, Rinke; Bodegraven, Ad A. van; Festen, Eleonora A. M.; Weersma, Rinse K.; Crusius, J.B.A.; Linskens, Ronald K.; Joosten, Leo A. B.; Netea, Mihai G.; Jong, Dirk J. de

doi:10.1371/journal.pone.0007818

Cited by 39 publications

(30 citation statements)

References 26 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This suggests that colitis in Clec7a −/− mice is not aggravated by a typical fungal infection, but that other aspects of host–fungal interactions affecting the mycobiota might be involved. Consistent with the mouse models, patients carrying a two-marker CLEC7A haplotype developed more severe refractory ulcerative colitis supporting a possible role of dectin-1 in severity 16 , but not susceptibility to intestinal disease 87 . Furthermore, dectin-1 deficiency is also associated with increased colonization of Candida spp.…”

Section: Mucosal Immunity To Fungisupporting

confidence: 65%

Fungal dysbiosis: immunity and interactions at mucosal barriers

2017

View full text Add to dashboard Cite

Fungi and mammals share a co-evolutionary history and are involved in a complex web of interactions. Studies focused on commensal bacteria suggest that pathologic changes in the microbiota, historically termed as ‘dysbiosis’, are at the root of many inflammatory diseases of non-infectious origin. Yet, the importance of dysbiosis in the fungal community— the mycobiota — was only recently acknowledged to have a pathological role as novel findings suggest that mycobiota disruption can have detrimental effects on host immunity. Fungal dysbiosis and homeostasis are dynamic processes that are probably more common than actual fungal infections, and therefore constantly shape the immune response. In this Review, we summarize specific patterns associated with fungal dysbiosis, and discuss how mucosal immunity has evolved to distinguish fungal infection from dysbiosis and how it responds to these different conditions. We propose that gut microbiota dysbiosis is a collective feature of complex interactions between prokaryotic and eukaryotic microbial communities that can affect immunity and influence health and disease.

show abstract

Section: Mucosal Immunity To Fungisupporting

confidence: 65%

Fungal dysbiosis: immunity and interactions at mucosal barriers

2017

View full text Add to dashboard Cite

show abstract

“…Actually, we showed that the proportion of L. salivarius was reduced in intestinal flora of IBD patients, suggesting a protective role of this commensal species. In this context, it was reported that Dectin-1 expression is upregulated in IBD patients (de Vries et al, 2009), and fecal calprotectin is one good marker of IBD (Foell et al, 2009). On the other hand, two single-nucleotide polymorphisms in CLEC7A are associated with medically refractory UC, in which fungal infection may play a pathogenic role (Iliev et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Dectin-1 Signaling Ameliorates Colitis by Inducing Lactobacillus-Mediated Regulatory T Cell Expansion in the Intestine

Tang

Kamiya

Liu

et al. 2015

Cell Host & Microbe

227

199

View full text Add to dashboard Cite

Dectin-1, the receptor for β-glucans, protects the host against fungal infection; however, its role in intestinal immunity is incompletely understood. We found that Dectin-1-deficient (Clec7a(-/-)) mice were refractory to both dextran sodium sulfate (DSS)- and CD45RB(high)CD4(+) T cell-induced colitis, and that this resistance was associated with an increase in regulatory T (Treg) cells. The proportion of lactobacilli, especially Lactobacillus murinus, in the commensal microflora was increased in Clec7a(-/-) mouse colons, and accompanied by a decrease in antimicrobial peptides induced by Dectin-1 signaling. L. murinus colonization increased Treg cells in the colon. Oral administration of laminarin, a Dectin-1 antagonist, suppressed the development of DSS-colitis, associated with an increase of L. murinus and Treg cells. Human patients with inflammatory bowel disease were found to have a decreased proportion of closely related Lactobacillus species. These observations suggest that Dectin-1 regulates the homeostasis of intestinal immunity by controlling Treg cell differentiation through modification of microbiota.

show abstract

“…albicans is a common commensal of the intestinal tract, and it was reported to increase the severity of intestinal inflammation in murine models of colitis (10,11). The b-glucan receptor dectin-1 is involved in this effect, and polymorphisms in this receptor have been associated with the severity of ulcerative colitis (11) but not with the susceptibility to ulcerative colitis or Crohn's disease (36). Little is known about the mechanisms through which C. albicans may influence autoinflammatory diseases, such as Crohn's disease.…”

Section: Discussionmentioning

confidence: 99%

Candida albicans Primes TLR Cytokine Responses through a Dectin-1/Raf-1–Mediated Pathway

Ifrim¹,

Joosten²,

Kullberg³

et al. 2013

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

The immune system is essential to maintain homeostasis with resident microbial populations, ensuring that the symbiotic host–microbial relationship is maintained. In parallel, commensal microbes significantly shape mammalian immunity at the host mucosal surface, as well as systemically. Candida albicans is an opportunistic pathogen that lives as a commensal on skin and mucosa of healthy individuals. Little is known about its capacity to modulate responses toward other microorganisms, such as colonizing bacteria (e.g., intestinal microorganisms). The aim of this study was to assess the cytokine production of PBMCs induced by commensal bacteria when these cells were primed by C. albicans. We show that C. albicans and β-1,3-glucan induce priming of human primary mononuclear cells and this leads to enhanced cytokine production upon in vitro stimulation with TLR ligands and bacterial commensals. This priming requires the β-1,3-glucan receptor dectin-1 and the noncanonical Raf-1 pathway. In addition, although purified mannans cannot solely mediate the priming, the presence of mannosyl residues in the cell wall of C. albicans is nevertheless required. In conclusion, C. albicans is able to modify cytokine responses to TLR ligands and colonizing bacteria, which is likely to impact the inflammatory reaction during mucosal diseases.

show abstract

Genetic Association Analysis of the Functional c.714T>G Polymorphism and Mucosal Expression of Dectin-1 in Inflammatory Bowel Disease

Cited by 39 publications

References 26 publications

Fungal dysbiosis: immunity and interactions at mucosal barriers

Fungal dysbiosis: immunity and interactions at mucosal barriers

Inhibition of Dectin-1 Signaling Ameliorates Colitis by Inducing Lactobacillus-Mediated Regulatory T Cell Expansion in the Intestine

Candida albicans Primes TLR Cytokine Responses through a Dectin-1/Raf-1–Mediated Pathway

Contact Info

Product

Resources

About