In vitro modulation of human keratinocyte pro- and anti-inflammatory cytokine production by the capsule of Malassezia species

Abstract Malassezia spp. are commensal, cutaneous fungi that are implicated in seborrhoeic dermatitis. We hypothesize that the lipid-rich capsule of Malassezia spp. masks the organism from host detection, and depletion of this layer elicits an inflammatory response. To test this, preparations of cap...

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Veröffentlicht in:FEMS immunology and medical microbiology 2008-11, Vol.54 (2), p.203-214
Hauptverfasser: Thomas, Daniel S., Ingham, Eileen, Bojar, Richard A., Holland, Keith T.
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Ingham, Eileen
Bojar, Richard A.
Holland, Keith T.
description Abstract Malassezia spp. are commensal, cutaneous fungi that are implicated in seborrhoeic dermatitis. We hypothesize that the lipid-rich capsule of Malassezia spp. masks the organism from host detection, and depletion of this layer elicits an inflammatory response. To test this, preparations of capsulated or acapsular [10% (v/v) Triton X-100 treated], viable and nonviable, exponential or stationary phase Malassezia furfur, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia slooffiae and Malassezia sympodialis, were incubated with normal human keratinocytes. Proinflammatory (IL-6, IL-8, IL-1α and tumour necrosis factor-α) and anti-inflammatory cytokine (IL-10) release and intracellular IL-10 concentrations were quantified using enzyme-linked immunosorbent assays. Capsulated Malassezia yeasts stimulated limited or no production of inflammatory cytokines, and increased intracellular IL-10 (P
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We hypothesize that the lipid-rich capsule of Malassezia spp. masks the organism from host detection, and depletion of this layer elicits an inflammatory response. To test this, preparations of capsulated or acapsular [10% (v/v) Triton X-100 treated], viable and nonviable, exponential or stationary phase Malassezia furfur, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia slooffiae and Malassezia sympodialis, were incubated with normal human keratinocytes. Proinflammatory (IL-6, IL-8, IL-1α and tumour necrosis factor-α) and anti-inflammatory cytokine (IL-10) release and intracellular IL-10 concentrations were quantified using enzyme-linked immunosorbent assays. Capsulated Malassezia yeasts stimulated limited or no production of inflammatory cytokines, and increased intracellular IL-10 (P&lt;0.05). Removal of the capsule of many Malassezia preparations caused a significantly increased production of IL-6, IL-8 and IL-1α, and a decrease in intracellular IL-10. Notably, acapsular viable, stationary phase M. globosa caused a 66-fold increase in IL-8 production (P&lt;0.001) and acapsular nonviable, stationary phase M. furfur caused a 38-fold increase in IL-6 production (P&lt;0.001) and a 12-fold decrease in intracellular IL-10 (P&lt;0.001). These results support the hypothesis that the lipid layer of Malassezia spp. modulates cytokine production by keratinocytes. 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We hypothesize that the lipid-rich capsule of Malassezia spp. masks the organism from host detection, and depletion of this layer elicits an inflammatory response. To test this, preparations of capsulated or acapsular [10% (v/v) Triton X-100 treated], viable and nonviable, exponential or stationary phase Malassezia furfur, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia slooffiae and Malassezia sympodialis, were incubated with normal human keratinocytes. Proinflammatory (IL-6, IL-8, IL-1α and tumour necrosis factor-α) and anti-inflammatory cytokine (IL-10) release and intracellular IL-10 concentrations were quantified using enzyme-linked immunosorbent assays. Capsulated Malassezia yeasts stimulated limited or no production of inflammatory cytokines, and increased intracellular IL-10 (P&lt;0.05). Removal of the capsule of many Malassezia preparations caused a significantly increased production of IL-6, IL-8 and IL-1α, and a decrease in intracellular IL-10. 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Psychology</subject><subject>Fungi</subject><subject>Humans</subject><subject>Immunoassays</subject><subject>immunoevasion</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Interleukins - biosynthesis</subject><subject>Intracellular</subject><subject>Keratinocytes</subject><subject>Keratinocytes - cytology</subject><subject>Keratinocytes - metabolism</subject><subject>Lipids</subject><subject>Lipids - physiology</subject><subject>Malassezia</subject><subject>Malassezia - physiology</subject><subject>Malassezia furfur</subject><subject>Malassezia sympodialis</subject><subject>Masks</subject><subject>Microbiology</subject><subject>Microscopy, Electron, Transmission</subject><subject>Miscellaneous</subject><subject>Mycology</subject><subject>Pathogenesis</subject><subject>seborrheic dermatitis</subject><subject>Skin - microbiology</subject><subject>Stationary phase</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><subject>Yeast</subject><subject>Yeasts</subject><issn>0928-8244</issn><issn>1574-695X</issn><issn>2049-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV9r1TAYxoMo7jj9ChIQvWtN0_wFb2Q4PbDhzS68C2maspy1SU3auQr77kvPOUxQRAMhL3l_z5M3PADACpVVXu93ZUU5KZik30qMkCgRIkyUd0_A5rHxFGyQxKIQmJAT8CKlHcqUROg5OKkEp5hhtAH3Ww9v3RQDHEI793pywcPQwet50B7e2JhvfDDLZOEYQwG1b_OeXOF81-th0FOIC8z9cOP8nmlnszdpFjhdW2j0mOberp6Xutcp2Z9OwzRa42x6CZ51uk_21fE8BVfnn67OvhQXXz9vzz5eFIZIKQpsSS26RlpKKGqEZA3iDW21Rpzx2mLMreg6UrVIEtGSTkrDGW45QZLzVten4N3BNo_3fbZpUoNLxva99jbMSTEpWM1J9U-wkjUWlIgMvvkN3IU5-vwHhWvEMJeUr3biQJkYUoq2U2N0g46LqpBag1Q7teal1rzUGqTaB6nusvT18YG5GWz7S3hMLgNvj4BORvdd1N649MhhxKlkgmbuw4H74Xq7_PcA6nx7mYssrw_yMI9_ERd_Tv8AePjJmA</recordid><startdate>200811</startdate><enddate>200811</enddate><creator>Thomas, Daniel S.</creator><creator>Ingham, Eileen</creator><creator>Bojar, Richard A.</creator><creator>Holland, Keith T.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>200811</creationdate><title>In vitro modulation of human keratinocyte pro- and anti-inflammatory cytokine production by the capsule of Malassezia species</title><author>Thomas, Daniel S. ; Ingham, Eileen ; Bojar, Richard A. ; Holland, Keith T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4998-2e438fb9e5450b896b07b5daa07673e227e8ff41d0948d4f99c762d740977da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Analysis of Variance</topic><topic>Biological and medical sciences</topic><topic>capsule</topic><topic>Cell Survival</topic><topic>Cell Wall - physiology</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Depletion</topic><topic>Dermatitis</topic><topic>Dermatomycoses - microbiology</topic><topic>Fundamental and applied biological sciences. 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We hypothesize that the lipid-rich capsule of Malassezia spp. masks the organism from host detection, and depletion of this layer elicits an inflammatory response. To test this, preparations of capsulated or acapsular [10% (v/v) Triton X-100 treated], viable and nonviable, exponential or stationary phase Malassezia furfur, Malassezia globosa, Malassezia obtusa, Malassezia restricta, Malassezia slooffiae and Malassezia sympodialis, were incubated with normal human keratinocytes. Proinflammatory (IL-6, IL-8, IL-1α and tumour necrosis factor-α) and anti-inflammatory cytokine (IL-10) release and intracellular IL-10 concentrations were quantified using enzyme-linked immunosorbent assays. Capsulated Malassezia yeasts stimulated limited or no production of inflammatory cytokines, and increased intracellular IL-10 (P&lt;0.05). Removal of the capsule of many Malassezia preparations caused a significantly increased production of IL-6, IL-8 and IL-1α, and a decrease in intracellular IL-10. Notably, acapsular viable, stationary phase M. globosa caused a 66-fold increase in IL-8 production (P&lt;0.001) and acapsular nonviable, stationary phase M. furfur caused a 38-fold increase in IL-6 production (P&lt;0.001) and a 12-fold decrease in intracellular IL-10 (P&lt;0.001). These results support the hypothesis that the lipid layer of Malassezia spp. modulates cytokine production by keratinocytes. This has implications in the pathogenesis of seborrhoeic dermatitis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18752620</pmid><doi>10.1111/j.1574-695X.2008.00468.x</doi><tpages>12</tpages></addata></record>
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source MEDLINE; Access via Wiley Online Library; Oxford University Press Journals All Titles (1996-Current)
subjects Analysis of Variance
Biological and medical sciences
capsule
Cell Survival
Cell Wall - physiology
Cells, Cultured
Cytokines
Depletion
Dermatitis
Dermatomycoses - microbiology
Fundamental and applied biological sciences. Psychology
Fungi
Humans
Immunoassays
immunoevasion
Inflammation
Inflammatory response
Interleukin 10
Interleukin 6
Interleukin 8
Interleukins - biosynthesis
Intracellular
Keratinocytes
Keratinocytes - cytology
Keratinocytes - metabolism
Lipids
Lipids - physiology
Malassezia
Malassezia - physiology
Malassezia furfur
Malassezia sympodialis
Masks
Microbiology
Microscopy, Electron, Transmission
Miscellaneous
Mycology
Pathogenesis
seborrheic dermatitis
Skin - microbiology
Stationary phase
Tumor Necrosis Factor-alpha - biosynthesis
Tumor necrosis factor-α
Tumors
Yeast
Yeasts
title In vitro modulation of human keratinocyte pro- and anti-inflammatory cytokine production by the capsule of Malassezia species
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