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

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...

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Bibliographic Details
Published in:	Mucosal immunology Vol. 9; no. 3; pp. 767 - 776
Main Authors:	Choteau, L, Parny, M, François, N, Bertin, B, Fumery, M, Dubuquoy, L, Takahashi, K, Colombel, J-F, Jouault, T, Poulain, D, Sendid, B, Jawhara, S
Format:	Journal Article
Language:	English
Published:	London Nature Publishing Group UK 01-05-2016 Elsevier Limited
Subjects:	631/250/255/1672 631/45/612/1235 692/699/1503/1581/1392/1388 Allergology Animals Antibodies Biomedicine Candida albicans - immunology Candidiasis - immunology Cells, Cultured Colitis Colitis - immunology Colonization Complement Pathway, Mannose-Binding Lectin Dextran Dextran Sulfate Digestive system Epithelium Female Gastroenterology Gastrointestinal tract Homeostasis Host-Pathogen Interactions Humans Immune system Immunity, Mucosal Immunoblotting Immunology Innate immunity Interleukin 23 Interleukin-17 - metabolism Intestinal Mucosa - immunology Intestinal Mucosa - metabolism Intestinal Mucosa - microbiology Intestine Kidneys Lectins Leukocytes Mannose Mannose-binding lectin Mannose-Binding Lectin - genetics Mannose-Binding Lectin - metabolism Mice Mice, Inbred C57BL Mice, Knockout Phagocytosis RNA-directed DNA polymerase Rodents Sodium sulfate Toll-Like Receptor 4 - metabolism Toll-like receptors
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1933-0219 1935-3456
DOI:	10.1038/mi.2015.100