Taxonomic group: fungi / Ascomycota
(Phylum: Ascomycota)
Host organism: Rattus
Organ / tissue: cell wall
NCBI PubMed ID: 25916991Publication DOI: 10.1128/IAI.00196-15Journal NLM ID: 0246127Publisher: American Society for Microbiology
Correspondence: limper.andrew
mayo.edu
Institutions: Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, USA, University of Iceland School of Health Sciences, Reykjavík, Iceland
Inflammation is a major cause of respiratory impairment during Pneumocystis pneumonia. Studies support a significant role for cell wall β-glucans in stimulating inflammatory responses. Fungal β-glucans are comprised of d-glucose homopolymers containing β-1,3-linked glucose backbones with β-1,6-linked glucose side chains. Prior studies in Pneumocystis carinii have characterized β-1,3 glucan components of the organism. However, recent investigations in other organisms support important roles for β-1,6 glucans, predominantly in mediating host cellular activation. Accordingly, we sought to characterize β-1,6 glucans in the cell wall of Pneumocystis and to establish their activity in lung cell inflammation. Immune staining revealed specific β-1,6 localization in P. carinii cyst walls. Homology-based cloning facilitated characterization of a functional P. carinii kre6 (Pckre6) β-1,6 glucan synthase in Pneumocystis that, when expressed in kre6-deficient Saccharomyces cerevisiae, restored cell wall stability. Recently synthesized β-1,6 glucan synthase inhibitors decreased the ability of isolated P. carinii preparations to generate β-1,6 carbohydrate. In addition, isolated β-1,6 glucan fractions from Pneumocystis elicited vigorous tumor necrosis factor α (TNF-α) responses from macrophages. These inflammatory responses were significantly dampened by inhibition of host cell plasma membrane microdomain function. Together, these studies indicate that β-1,6 glucans are present in the P. carinii cell wall and contribute to lung cell inflammatory activation during infection
cell wall, β-Glucans, Pneumocystis carinii, lung cell inflammation
Structure type: homopolymer
Location inside paper: abstract, p. 2817, left column, paragraph 2
Trivial name: pustulan, β-1,6-glucan, β-1,6-D-glucan, β(1-6)-D-glucan, β-(1,6)-glucan, lasiodiplodan, pustulan, β-(1,6)-glucan, lasiodiplodan, β-(1,6)-glucan, β-(1,6)-glucan, lasiodiplodan, pustulan, β-1,6-glucan, β-(1,6)-glucan, pustulan, β-(1→6)-glucan PCPS, water-soluble glucan (PS-I)
Compound class: EPS, O-polysaccharide, cell wall polysaccharide, glycoprotein, glucan, polysaccharide, cell wall glucoprotein
Contained glycoepitopes: IEDB_135614,IEDB_141806,IEDB_142488,IEDB_146664,IEDB_241101,IEDB_983931,SB_192
Methods: DNA techniques, dot immunoblotting, biological assays, enzymatic digestion, extraction, centrifugation
Biological activity: glucan induces host innate immune response by the cytokines interleukin-1β (IL-1β), IL-6, IL-8, and TNF-α production
Enzymes that release or process the structure: PcKre6-like β-1,6glucan synthase
Related record ID(s): 7724, 8325, 42140, 43301, 43379, 44888, 44927, 44939, 45578, 47843, 48303, 48366, 48412, 48423, 48443, 49291, 101372, 124916, 138263, 143680, 143682, 149870
NCBI Taxonomy refs (TaxIDs): 4754,
136370Reference(s) to other database(s): GTC:G26777BZ, GlycomeDB:
863, CCSD:
50854, CBank-STR:4234
Show glycosyltransferases
There is only one chemically distinct structure:
Found 
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