title: Inhibition of Th1- and enhancement of Th2-initiating cytokines and chemokines in trichosanthin- treated macrophages.
abstract: Trichosanthin (TCS), the major effective component from Chinese herb Trichosanthes Kirilowii Maxim, is also a potent allergen. Our previous work has shown that TCS can upregulate interleukin-4 (IL-4) and interleukin-13 (IL-13) while inhibit interferon-gamma (IFN-gamma) in mesenteric lymph node cells after TCS immunization. Thus, TCS can arouse a T helper 2 (Th2) response in the draining lymph node. However, little is known about the early effects of TCS on antigen-presenting cells, the initiator of T cell response. In the current study, the effects of TCS on macrophage cytokines and chemokine expression were investigated. Peritoneal macrophages were treated with or without TCS in the presence of lipopolysaccharide (LPS). We found that TCS increased macrophage interleukin-10 (IL-10) and monocyte chemoattractant protein-1 (MCP-1) expression, whereas it decreased interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-alpha) expression. Our study clearly demonstrated that TCS, as an allergen, has differential effects on macrophage Th1/Th2 initiative factors, effects that are likely to facilitate its inducing of Th2 and immunoglobulin E (IgE) response.
authors.affiliation: Laboratory of Molecular Immunology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
authors.forename: W
authors.initials: W
authors.lastname: Xu
authors.forename: W
authors.initials: W
authors.lastname: Hou
authors.forename: G
authors.initials: G
authors.lastname: Yao
authors.forename: Y
authors.initials: Y
authors.lastname: Ji
authors.forename: M
authors.initials: M
authors.lastname: Yeh
authors.forename: B
authors.initials: B
authors.lastname: Sun
mesh_terms: D000485:Allergens / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D002452:Cell Count; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D018925:Chemokines / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D016207:Cytokines / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D018664:Interleukin-12 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008262:Macrophage Activation / Q000187:drug effects; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D015978:Trichosanthin / Q000276:immunology / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D000485:Allergens; D018932:Chemokine CCL2; D018925:Chemokines; D016207:Cytokines; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D015978:Trichosanthin