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Glycosaminoglycan profile in macrophages exposed to Candida albicans and interleukins
Author(s) -
Bodo Maria,
Blasi Elisabetta,
Becchetti Ennio,
Giammarioli Monica,
Conte Carmela,
Bellocchio Silvia,
Baroni Tiziano,
Bellucci Catia,
Bistoni Francesco
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.64.5.650
Subject(s) - glycosaminoglycan , hyaluronic acid , chondroitin sulfate , candida albicans , biology , heparan sulfate , extracellular matrix , macrophage , microbiology and biotechnology , extracellular , interleukin , hyaluronan synthase , cytokine , immunology , biochemistry , in vitro , anatomy
Glycosaminoglycans (GAG), are extracellular matrix macromolecules that affect the phagocytic properties of macrophages. In order to assess whether the interaction between macrophages and Candida albicans (iCa) provokes changes in the phenotype, we analyzed the GAG profiles in two macrophage lines, ANA‐1 (from murine bone‐marrow) and BV‐2 (from murine brain). We also investigated GAG modulation by interleukin‐1α (IL‐1α) and interleukin‐6 (IL‐6). During iCa treatment and even after the addition of ILs, ANA‐1 accumulated less total GAG compared to controls. IL‐1 treatment, combined with iCa exposure, induced a decrease in heparan sulfate and chondroitin sulfate chains, and an increase in the hyaluronic acid percentage. IL‐6 treatment, with or without iCa, decreased the hyaluronic acid/sulfated GAG ratio. The GAG pattern in BV‐2 appears to be different to ANA‐1 and iCa exposure does not induce any difference in total GAG. The inhibitory effect induced by ILs on GAG synthesis is less than that observed in ANA‐1 and the GAG elution profile is modulated to a lesser extent by treatment with ILs and/or iCa compared to the ANA‐1. We suggest that the observed changes in the expression of the individual GAG classes may be responsible for the macrophage functional heterogeneity. J. Leukoc. Biol. 64: 650–656; 1998.