Exposure to heat-inactivated Trichophyton rubrum resulting in a limited immune response of human keratinocytes
Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effective...
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| Vydáno v: | Chinese medical journal Ročník 126; číslo 2; s. 215 - 219 |
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China
Department of Dermatology and Venereology, Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, China
01.01.2013
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| ISSN: | 0366-6999, 2542-5641, 2542-5641 |
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| Abstract | Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors （CLR） and toll-like receptors （TLR） are the two major pattern recognition receptors （PRRs） that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae （l×106 and 1.5×105 colony-forming unit （CFU） in 2 ml medium, respectively） for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns （PAMPs） and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction （RT-PCR）. Meanwhile, surface toll-like receptor （TLR） 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter （FACS） 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2, 4 and 6, Dectinl and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 （IP-10） and monocyte chemotactic protein-1 （MCP-1） of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-I. Conclusion The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. |
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| AbstractList | Trichophyton rubrum (T. rubrum) represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors (CLR) and toll-like receptors (TLR) are the two major pattern recognition receptors (PRRs) that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively.BACKGROUNDTrichophyton rubrum (T. rubrum) represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors (CLR) and toll-like receptors (TLR) are the two major pattern recognition receptors (PRRs) that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively.HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae (1×10(6) and 1.5×10(5) colony-forming unit (CFU) in 2 ml medium, respectively) for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns (PAMPs) and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, surface toll-like receptor (TLR) 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter (FACS) 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment.METHODSHaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae (1×10(6) and 1.5×10(5) colony-forming unit (CFU) in 2 ml medium, respectively) for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns (PAMPs) and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, surface toll-like receptor (TLR) 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter (FACS) 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment.HaCaT cells constitutively expressed mRNA of membrane-bound TLR1, 2, 4 and 6, Dectin1 and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 (IP-10) and monocyte chemotactic protein-1 (MCP-1) of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-1.RESULTSHaCaT cells constitutively expressed mRNA of membrane-bound TLR1, 2, 4 and 6, Dectin1 and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 (IP-10) and monocyte chemotactic protein-1 (MCP-1) of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-1.The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion.CONCLUSIONThe cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors （CLR） and toll-like receptors （TLR） are the two major pattern recognition receptors （PRRs） that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae （l×106 and 1.5×105 colony-forming unit （CFU） in 2 ml medium, respectively） for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns （PAMPs） and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction （RT-PCR）. Meanwhile, surface toll-like receptor （TLR） 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter （FACS） 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2, 4 and 6, Dectinl and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 （IP-10） and monocyte chemotactic protein-1 （MCP-1） of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-I. Conclusion The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. Trichophyton rubrum (T. rubrum) represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors (CLR) and toll-like receptors (TLR) are the two major pattern recognition receptors (PRRs) that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae (1×10(6) and 1.5×10(5) colony-forming unit (CFU) in 2 ml medium, respectively) for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns (PAMPs) and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction (RT-PCR). Meanwhile, surface toll-like receptor (TLR) 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter (FACS) 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. HaCaT cells constitutively expressed mRNA of membrane-bound TLR1, 2, 4 and 6, Dectin1 and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 (IP-10) and monocyte chemotactic protein-1 (MCP-1) of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-1. The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. Background Trichophyton rubrum (T.rubrum) represents the most important agent of dermatophytosis in humans.T.rubrum infection causes slight inflammation,and tends to be chronic and recurrent.It is suggested that it may result from the failure of epithelial cells to recognize T.rubrum effectively and initiate effective immune responses.The C-type lectin receptors (CLR) and toll-like receptors (TLR) are the two major pattern recognition receptors (PRRs) that recognize fungal components.Therefore,the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T.rubrum conidia and hyphae,respectively.Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T.rubrum conidia and hyphae (1×106 and 1.5×10s colony-forming unit (CFU) in 2 ml medium,respectively) for 6,12 and 24 hours.The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns (PAMPs) and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction (RT-PCR).Meanwhile,surface toll-like receptor (TLR) 2,TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter (FACS) 24 hours after treatment.The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment.Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2,4 and 6,Dectin1 and DC-SIGN,but not Dectin-2 or Mincle.Heat-killed T.rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells.Heat-inactivated T.rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1,and suppressed the secretions of interferon-inducible protein-10 (IP-10) and monocyte chemotactic protein-1 (MCP-1) of HaCaT cells,while heat-killed T.rubrum hyphae significantly induced the secretions of IP-10 and MCP-1.Conclusion The cell-wall antigens of T.rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. |
| Author | HUANG Xiao-qiang YI Jin-ling YINSong-chao CHEN Rong-zhang LI Mei-rong GONG Ziojian LAI Wei CHEN Jian |
| AuthorAffiliation | Department of Dermatology and Venereology, Third AffiliatedHospital of Sun Yat-sen University, Guangzhou, Guangdong510630, China |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23324266$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1016_j_micpath_2015_04_002 crossref_primary_10_4103_0366_6999_172573 crossref_primary_10_1111_myc_13021 crossref_primary_10_3389_fphar_2024_1434136 crossref_primary_10_3390_ijms23147934 crossref_primary_10_1111_exd_14870 crossref_primary_10_4103_0366_6999_169106 crossref_primary_10_4049_jimmunol_1601665 crossref_primary_10_3390_jof8111151 crossref_primary_10_3389_fimmu_2022_1063443 |
| Cites_doi | 10.1128/IAI.01282-10 10.1111/j.1574-695X.2008.00378.x 10.1111/j.1365-3164.2009.00819.x 10.2340/0001555572273276 10.2217/fmb.09.51 10.1056/NEJMoa0901053 10.1111/1523-1747.ep12470582 10.1074/jbc.M606542200 10.1084/jem.20082818 10.3389/fimmu.2012.00079 10.1038/ni1408 10.1097/00008480-200108000-00008 10.1016/j.immuni.2011.05.001 10.4049/jimmunol.0802113 10.3109/13693780802641425 10.1016/j.immuni.2010.05.001 10.1002/eji.200838687 10.1093/glycob/cwn046 10.1016/0167-5699(94)90152-X 10.1086/340511 10.1111/j.1462-5822.2005.00505.x |
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| Notes | Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to be chronic and recurrent. It is suggested that it may result from the failure of epithelial cells to recognize T. rubrum effectively and initiate effective immune responses. The C-type lectin receptors （CLR） and toll-like receptors （TLR） are the two major pattern recognition receptors （PRRs） that recognize fungal components. Therefore, the purpose of the study was to analyze the expression of those PRRs and the cytokines in HaCaT cells stimulated with heat-inactivated T. rubrum conidia and hyphae, respectively. Methods HaCaT cells were unstimulated or stimulated with heat-inactivated T. rubrum conidia and hyphae （l×106 and 1.5×105 colony-forming unit （CFU） in 2 ml medium, respectively） for 6, 12 and 24 hours. The mRNA expression of PRRs involved in recognizing fungal pathogen-associated molecular patterns （PAMPs） and signaling molecules were measured by quantitative reverse transcription polymerase chain reaction （RT-PCR）. Meanwhile, surface toll-like receptor （TLR） 2, TLR4 and Dectin-1 were analyzed by fluorescence-activated cell sorter （FACS） 24 hours after treatment. The cytokines were detected in cell culture supernatants of HaCaT cells in 12 and 24 hours after treatment. Results HaCaT cells constitutively expressed mRNA of membrane-bound TLR1,2, 4 and 6, Dectinl and DC-SIGN, but not Dectin-2 or Mincle. Heat-killed T. rubrum did not significantly upregulate gene transcriptions of the PRRs of HaCaT cells. Heat-inactivated T. rubrum conidia significantly reduced the surface expression of TLR2 and Dectin-1, and suppressed the secretions of interferon-inducible protein-10 （IP-10） and monocyte chemotactic protein-1 （MCP-1） of HaCaT cells, while heat-killed T. rubrum hyphae significantly induced the secretions of IP-10 and MCP-I. Conclusion The cell-wall antigens of T. rubrum fail to activate transcriptional expression of PRRs and induce a lower immune response of HaCaT cells by limited cytokines secretion. human keratinocytes; Trichophyton rubrum, pattern recognition receptors, immune response HUANG Xiao-qiang, YI Jin-ling, YIN Song-chao, CHEN Rong-zhang, LI Mei-rong, GONG Zi-jian, LAI Wei and CHEN Jian 11-2154/R ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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| Snippet | Background Trichophyton rubrum （T. rubrum） represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation,... Trichophyton rubrum (T. rubrum) represents the most important agent of dermatophytosis in humans. T. rubrum infection causes slight inflammation, and tends to... Background Trichophyton rubrum (T.rubrum) represents the most important agent of dermatophytosis in humans.T.rubrum infection causes slight inflammation,and... |
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| SubjectTerms | Cells, Cultured Cytokines - biosynthesis HaCaT细胞 Humans Keratinocytes - immunology Lectins, C-Type - genetics Lectins, C-Type - physiology Receptors, Pattern Recognition - genetics Receptors, Pattern Recognition - physiology RNA, Messenger - analysis Toll-Like Receptor 2 - physiology Toll样受体 Trichophyton - immunology 免疫反应 单核细胞趋化蛋白1 毛癣菌 热灭活 角质形成细胞 逆转录聚合酶链反应 |
| Title | Exposure to heat-inactivated Trichophyton rubrum resulting in a limited immune response of human keratinocytes |
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