Source:http://linkedlifedata.com/resource/pubmed/id/20722932
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-8-20
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pubmed:abstractText |
The association between vitamin D deficiency and asthma epidemic has been recognized. Tumor necrosis factor (TNF)-alpha and chemokines play important roles in pathogenesis of asthma. However, whether vitamin D has immunoregulatory function on TNF-alpha and chemokines expression in human monocytes is still unknown. The human monocytic cell line, THP-1 cells and human primary monocytes were pretreated with various concentration of 1alpha,25-(OH)(2)D(3) for 2 h before stimulation with lipopolysaccharide (LPS). Supernatants were collected 24 or 48 h after LPS stimulation. The levels of TNF-alpha, interferon-inducible protein 10 (IP-10)/CXCL10 (the Th1-related chemokine), macrophage-derived chemokine (MDC)/ CCL22 (the Th2-related chemokine), and interleukin 8 (IL-8)/CXCL8 (the neutrophil chemoattractant) were measured by ELISA. 1alpha,25-(OH)(2)D(3) could significantly suppress TNF-alpha and IP-10 expression in LPS-stimulated THP-1 and human primary monocytes. However, 1alpha,25-(OH)(2)D(3), especially in higher concentration, could significantly enhance MDC expression. 1alpha,25-(OH)(2)D(3) had no significant effects on IL-8 expression. We found 1alpha,25-(OH)(2)D(3) could significantly suppress TNF-alpha and Th1-related chemokine IP-10, which both play important roles in pathogenesis of severe refractory asthma and autoimmune diseases. However, 1alpha,25-(OH)(2)D(3) enhanced Th2-related chemokine MDC, which may result in Th2 inflammatory cell recruitment and thus adversely affect asthmatic patients. Although vitamin D has potential utility in the treatment of asthma and autoimmune diseases, excessive use of vitamin D may not be suitable in patients with Th2 allergic diseases.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCL22 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCL10 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Calcitriol,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL22,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/Cholecalciferol,
http://linkedlifedata.com/resource/pubmed/chemical/IL8 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1750-3841
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
75
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H200-4
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pubmed:meshHeading |
pubmed-meshheading:20722932-Asthma,
pubmed-meshheading:20722932-Autoimmune Diseases,
pubmed-meshheading:20722932-Calcitriol,
pubmed-meshheading:20722932-Cell Line,
pubmed-meshheading:20722932-Cells, Cultured,
pubmed-meshheading:20722932-Chemokine CCL22,
pubmed-meshheading:20722932-Chemokine CXCL10,
pubmed-meshheading:20722932-Chemokines,
pubmed-meshheading:20722932-Cholecalciferol,
pubmed-meshheading:20722932-Down-Regulation,
pubmed-meshheading:20722932-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20722932-Humans,
pubmed-meshheading:20722932-Interleukin-8,
pubmed-meshheading:20722932-Lipopolysaccharides,
pubmed-meshheading:20722932-Monocytes,
pubmed-meshheading:20722932-Osmolar Concentration,
pubmed-meshheading:20722932-Time Factors,
pubmed-meshheading:20722932-Tumor Necrosis Factor-alpha,
pubmed-meshheading:20722932-Up-Regulation,
pubmed-meshheading:20722932-Vitamin D Deficiency
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pubmed:year |
2010
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pubmed:articleTitle |
Effects of vitamin D3 on expression of tumor necrosis factor-alpha and chemokines by monocytes.
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pubmed:affiliation |
Dept. of Pediatrics, Kaohsiung Medical Univ. Hospital, Kaohsiung, Taiwan.
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pubmed:publicationType |
Journal Article
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