Taxonomic group: fungi / Ascomycota
(Phylum: Ascomycota)
NCBI PubMed ID: 29712728Publication DOI: 10.1128/IAI.00944-17Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: Steele C <chadsteele
uab.edu>
Institutions: Department of Medicine, University of Alabama at Birmingham, Birmingham, USA, Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, USA, Inflammation and Immunity, Pfizer Worldwide R&D, Massachusetts, USA
Chitin is a polysaccharide that provides structure and rigidity to the cell walls of fungi and insects. Mammals possess multiple chitinases, which function to degrade chitin, thereby supporting a role for chitinases in immune defense. However, chitin degradation has been implicated in the pathogenesis of asthma. Here, we determined the impact of acidic mammalian chitinase (AMCase) (Chia) deficiency on host defense during acute exposure to the fungal pathogen Aspergillus fumigatus as well as its contribution to A. fumigatus-associated allergic asthma. We demonstrate that chitin in the fungal cell wall was detected at low levels in A. fumigatus conidia, which emerged at the highest level during hyphal transition. In response to acute A. fumigatus challenge, Chia-/- mice unexpectedly demonstrated lower A. fumigatus lung burdens at 2 days postchallenge. The lower fungal burden correlated with decreased lung interleukin-33 (IL-33) levels yet increased IL-1β and prostaglandin E2 (PGE2) production, a phenotype that we reported previously to promote the induction of IL-17A and IL-22. During chronic A. fumigatus exposure, AMCase deficiency resulted in lower dynamic and airway lung resistance than in wild-type mice. Improved lung physiology correlated with attenuated levels of the proallergic chemokines CCL17 and CCL22. Surprisingly, examination of inflammatory responses during chronic exposure revealed attenuated IL-17A and IL-22 responses, but not type 2 responses, in the absence of AMCase. Collectively, these data suggest that AMCase functions as a negative regulator of immune responses during acute fungal exposure and is a contributor to fungal asthma severity, putatively via the induction of proinflammatory responses.
Aspergillus fumigatus, asthma/allergy, lung defense
Structure type: structural motif or average structure
Location inside paper: p.2, paragraph 3
Trivial name: chitin
Compound class: cell wall polysaccharide, glucan
Contained glycoepitopes: IEDB_135813,IEDB_137340,IEDB_141807,IEDB_151531,IEDB_153212,IEDB_241099,IEDB_423114,IEDB_423150,SB_74,SB_85
Methods: biological assays, fluorescent staining of cell-wall
Biological activity: causes immune response during fungal infection
Related record ID(s): 48634, 48636, 48650, 48651, 48652, 48689, 48691, 48715, 48752, 48757, 48764, 48769, 48785, 48794, 48795, 48801, 48804, 48828, 48853, 48859, 48872, 48900, 48901, 48902, 48984
NCBI Taxonomy refs (TaxIDs): 746128Reference(s) to other database(s): GTC:G97099AY
Show glycosyltransferases
There is only one chemically distinct structure:
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