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Granulocyte Colony‐Stimulating Factor (G‐CSF) and Granulocyte Macrophage Colony‐Stimulating Factor (GM‐CSF) in Behçet's Disease
Author(s) -
Takahama Hideto,
Itoh Rie,
InoueKomatsu Chiyuki,
Furusawa Shuichi,
Takahashi Hisashi,
Mizoguchi Masako
Publication year - 1994
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1994.tb01792.x
Subject(s) - granulocyte colony stimulating factor , granulocyte , colony stimulating factor , immunology , granulocyte macrophage colony stimulating factor , haematopoiesis , pathogenesis , hematopoietic growth factor , peripheral blood mononuclear cell , in vivo , chemotaxis , macrophage colony stimulating factor , medicine , cytokine , endocrinology , in vitro , biology , macrophage , chemotherapy , receptor , stem cell , biochemistry , microbiology and biotechnology , genetics
Increases in the number and activity of peripheral polymorphonuclear neutrophils (PMNs) is often found in Behçet's disease (BD), indicating that PMN may play an important role in the pathogenesis of this disorder. It has recently been reported that G‐CSF and GM‐CSF, a family of hematopoietic growth factors, enhance PMN activity. To explore the role of these two CSFs in BD, we first examined the chemotactic response of PMNs to these CSFs by performing a polarization assay. PMN response to G‐CSF in BD patients was lower than that in controls, while PMN response to GM‐CSF was similar in patients and controls. However, PMNs from BD patients showed an enhanced chemotactic response to N‐formyl‐L‐methionyl‐leucyl‐phenylalanine. Thus, it is speculated that the PMNs of the patients might have already been activated in vivo by G‐CSF and thus could not respond further to this agent in vitro . We examined G‐CSF and GM‐CSF mRNA expressions in peripheral mononuclear cells stimulated with LPS, PMA, and Con A by Northern hybridization. G‐CSF mRNA expression levels in BD patients were higher than in the controls, while GM‐CSF mRNA expression levels were lower than in the controls. We also examined the serum levels of the two CSFs by ELISA and EIA. However, all levels of the two CSFs in both patients and controls were not detectable, except in the case of one BD patient in the active stage of the disease, who showed high levels of G‐CSF, but not of GM‐CSF. Based on the present findings, it is suggested that G‐CSF may be more intensively involved in BD than GM‐CSF.