Role of mannose-binding lectin in intestinal homeostasis and fungal elimination

Abstract

Mannose-binding lectin (MBL) is a soluble lectin of the innate immune system that is produced by the liver and secreted into the circulation where it activates the lectin complement pathway, enhances phagocytosis of microorganisms by leukocytes, and modulates inflammation. MBL can recognize patterns on the surface of different pathogens, including Candida albicans. Our aims were to investigate whether MBL is expressed in the gut epithelium and to examine its effect on the modulation of intestinal inflammation and C. albicans elimination. Using reverse transcriptase-PCR, MBL transcripts were highly expressed in different parts of the mouse gut. MBL expression was also detected by immunoblotting and immunolocalization in response to C. albicans colonization of the gut; the highest expression of MBL was detected in the stomach. Blocking MBL by administering mannans to mice increased C. albicans colonization. MBL-deficient mice had a higher level of colonization than wild-type mice. Dextran sodium sulfate-induced colitis promoted C. albicans dissemination to the kidneys and lungs of MBL-deficient mice. MBL-deficient mice exhibited elevated expression of interleukin (IL)-17, IL-23, dectin-1, and Toll-like receptor-4. This study shows that MBL expression is induced in the gut in response to C. albicans sensing and is required for intestinal homeostasis and host defense against C. albicans.

Complement Activation by Giardia duodenalis Parasites through the Lectin Pathway Contributes to Mast Cell Responses and Parasite Control

“…Similarly, in a model of colitis-associated cancer induced by dextran sodium sulfate (DSS) along with azoxymethane, C3-deficient mice had reduced IL-17A production in myeloid cell populations and were therefore less susceptible to tumor development (48). In contrast, MBL-deficient mice had enhanced intestinal IL-17A and IL-23 mRNA levels in a DSS colitis model (49). The differential effects of complement in these two models may reflect differences in the time points analyzed (day 60 versus day 14), differences in the specific mouse mutants analyzed, or other differences between mouse colonies.…”

Pioglitazone-mediated reversal of elevated glucose metabolism in the airway epithelium of mouse lung adenocarcinomas

“…We also checked public databases to see the effect of pioglitazone on the expression of these 14 glycose metabolism genes in other epithelial cell populations. There is only one publicly available gene expression data set (GSE68852) studying the effects of pioglitazone treatment on the transcriptomic profile of intestinal epithelial cells (Caco-2 cells) (19). We compared our results with those of that study and found that only 2 of the 14 validated lung brushing glucose metabolism genes were downregulated in the Caco-2 cells by pioglitazone treatment; these were NUP107 (fold change = -1.4, P = 0.01) and VCAN (fold change = -1.9, P = 3.5 × 10 -5 ).…”

The Correlation of CD206, CD209, and Disease Severity in Behçet’s Disease with Arthritis

“…Several chronic inflammatory diseases, such as colitis, Crohn's disease, Kawasaki disease, and rheumatoid arthritis (RA), have been reported to be significantly associated with CD206, CD209, and Dectin-1 [6–8]. However, in BD, the correlation of CLR has not been published at all except mannose-binding lectin, one kind of soluble protein of CLR [9].…”