Chitin

About: Chitin is a research topic. Over the lifetime, 6590 publications have been published within this topic receiving 253993 citations.

TLR-2 and IL-17A in chitin-induced macrophage activation and acute inflammation.

Abstract: Chitin is a ubiquitous polysaccharide in fungi, insects, and parasites. To test the hypothesis that chitin is an important immune modulator, we characterized the ability of chitin fragments to regulate murine macrophage cytokine production in vitro and induce acute inflammation in vivo. In this study, we show that chitin is a size-dependent stimulator of macrophage IL-17A production and IL-17AR expression and demonstrate that these responses are TLR-2 and MyD88-dependent. We further demonstrate that IL-17A pathway activation is an essential event in the stimulation of some but not all chitin-stimulated cytokines and that chitin uses a TLR-2, MyD88-, and IL-17A-dependent mechanism(s) to induce acute inflammation. These studies demonstrate that chitin is a size-dependent pathogen-associated molecular pattern that activates TLR-2 and MyD88 in a novel IL-17A/IL-17AR-based innate immunity pathway.

Developmentally regulated conversion of surface‐exposed chitin to chitosan in cell walls of plant pathogenic fungi

Abstract: Summary • Conversion of surface-exposed chitin to chitosan in cell walls of in vitro - and in vivo -differentiated infection structures of two rust fungi, the wheat stem rust fungus Puccinia graminis f. sp. tritici and the broad bean rust fungus Uromyces fabae , and of the causal agent of maize anthracnose, Colletotrichum graminicola , were studied. • Epi-fluorescence microscopy with the fluorescence-labeled lectin wheat germ agglutinin (WGA) revealed that surfaces of infection structures formed on the plant cuticle expose chitin, whereas surfaces of structures formed after invading the host do not. • To identify chitin modification by de- N -acetylation, we raised polyclonal antibodies specifically recognizing de- N -acetylated chitosan. These antibodies labeled only those infection structures that differentiate inside the plant, indicating that chitosan is exposed on cell wall surfaces post penetration. • Surface modification of the fungal cell walls by chitin de- N -acetylation is discussed as a fungal strategy to protect cell walls of pathogenic hyphae from enzymatic hydrolysis by host chitinases, and to avoid generation of an auto-catalytic defense response system in the invaded host tissue.