title: Chitin and Its Effects on Inflammatory and Immune Responses.
abstract: Chitin, a potential allergy-promoting pathogen-associated molecular pattern (PAMP), is a linear polymer composed of N-acetylglucosamine residues which are linked by β-(1,4)-glycosidic bonds. Mammalians are potential hosts for chitin-containing protozoa, fungi, arthropods, and nematodes; however, mammalians themselves do not synthetize chitin and thus it is considered as a potential target for recognition by mammalian immune system. Chitin is sensed primarily in the lungs or gut where it activates a variety of innate (eosinophils, macrophages) and adaptive immune cells (IL-4/IL-13 expressing T helper type-2 lymphocytes). Chitin induces cytokine production, leukocyte recruitment, and alternative macrophage activation. Intranasal or intraperitoneal administration of chitin (varying in size, degree of acetylation and purity) to mice has been applied as a routine approach to investigate chitin's priming effects on innate and adaptive immunity. Structural chitin present in microorganisms is actively degraded by host true chitinases, including acidic mammalian chitinases and chitotriosidase into smaller fragments that can be sensed by mammalian receptors such as FIBCD1, NKR-P1, and RegIIIc. Immune recognition of chitin also involves pattern recognition receptors, mainly via TLR-2 and Dectin-1, to activate immune cells to induce cytokine production and creation of an immune network that results in inflammatory and allergic responses. In this review, we will focus on various immunological aspects of the interaction between chitin and host immune system such as sensing, interactions with immune cells, chitinases as chitin degrading enzymes, and immunologic applications of chitin.
authors.affiliation: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, East Azerbayjan, Iran.|Department of Immunology, Tabriz University of Medical Sciences, Tabriz, East Azerbayjan, Iran.
authors.forename: Daniel
authors.initials: D
authors.lastname: Elieh Ali Komi
authors.affiliation: Section of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
authors.forename: Lokesh
authors.initials: L
authors.lastname: Sharma
authors.affiliation: Section of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA. Charles.delacruz@yale.edu.|Department of Microbial Pathogenesis, Yale School of Medicine, Cedar Street, New Haven, CT, TACS441D, USA. Charles.delacruz@yale.edu.
authors.forename: Charles S
authors.initials: CS
authors.lastname: Dela Cruz
mesh_terms: D056704:Adaptive Immunity; D000485:Allergens / Q000276:immunology*; D000818:Animals; D002686:Chitin / Q000276:immunology*; D002688:Chitinases / Q000378:metabolism; D003170:Complement Pathway, Alternative; D004804:Eosinophils / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D015847:Interleukin-4 / Q000378:metabolism; D007422:Intestines / Q000276:immunology*; D008168:Lung / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D000069452:Pathogen-Associated Molecular Pattern Molecules / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000485:Allergens; D000069452:Pathogen-Associated Molecular Pattern Molecules; D002686:Chitin; D015847:Interleukin-4; D002688:Chitinases
keywords: Adaptive immunity; Chitin; Chitinase; Immune system; Innate immunity