Differential chemokine response of human monocytes to yeast and hyphal forms of Candida albicans and its relation to the beta-1,6 glucan of the fungal cell wall.
Hyphae formation from yeast cells is a virulence trait enabling the human opportunistic pathogen Candida albicans to invade host tissues. Hyphal cells proved to be much less efficient than yeast cells in stimulating production of macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, interleukin-8 (IL-8), and particularly, monocyte chemotactic protein-1 (MCP-1) by human monocyte. This different stimulation did not depend on the monocyte inability to ingest the hyphae nor did it imply hyphal resistance to the extracellular killing by the monocytes. Purified hyphal and yeast cell walls reproduced the differences shown by the intact cells, and chemical-enzymatic dissection of cell wall components suggested that cell wall beta-1,6 rather than beta-1,3 glucan was the main chemokine inducer. Coherently, immunofluorescence studies with an anti beta-1,6 glucan serum showed that the surface expression of this polysaccharide was much lower on hyphae than on yeast cells. By minimizing chemokine induction, the formation of hyphal filaments might facilitate C. albicans escaping from host immunity.
Torosantucci
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Department of Bacteriology, Istituto Superiore di Sanità, Rome, Italy.
Chiani
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Cassone
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D000328:Adult; D002176:Candida albicans / Q000737:chemistry / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D002236:Carbohydrate Conformation; D002473:Cell Wall / Q000737:chemistry*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000096:biosynthesis / Q000235:genetics; D019742:Chemokines, CC / Q000096:biosynthesis* / Q000235:genetics; D019743:Chemokines, CXC / Q000096:biosynthesis* / Q000235:genetics; D003602:Cytotoxicity, Immunologic; D005786:Gene Expression Regulation / Q000187:drug effects; D005936:Glucans / Q000494:pharmacology*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis / Q000235:genetics; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D010587:Phagocytosis; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics; D014774:Virulence; D047071:beta-Glucans
D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D019742:Chemokines, CC; D019743:Chemokines, CXC; D005936:Glucans; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D047071:beta-Glucans; C064197:beta-1,6-glucan; C033363:beta-1,3-glucan