title: Expression of Th1/Th2 cytokine mRNA in peritoneal exudative polymorphonuclear neutrophils and their effects on mononuclear cell Th1/Th2 cytokine production in MRL-lpr/lpr mice.
abstract: Peritoneal exudative polymorphonuclear neutrophils (PEC-PMN) and mononuclear cells (PEC-MNC) were obtained from normal BALB/c and from autoimmune MRL-lpr/lpr mice (lpr) with different disease severities. The spontaneous and mitogen-stimulated expression of T-helper lymphocyte type-1 (Th1) [represented by interferon-gamma (IFN-gamma) and interleukin (IL-2)] and T-helper lymphocyte type-2 (Th2) (represented by IL-4 and IL-10) cytokine mRNA in these cells was detected by reverse transcription-polymerase chain reaction (RT-PCR). The production of these cytokines was measured by enzyme-linked immunosorbent assay (ELISA). We found that the spontaneous expression of Th1/Th2 cytokine mRNA in PEC-PMN from autoimmune mice was progressively increased in parallel with disease severity but was not changed by lipopolysaccharide (LPS) stimulation. By contrast, spontaneous expression of Th1/Th2 cytokine mRNA in PEC-MNC from these mice was progressively decreased in parallel with disease severity but retained the responsiveness to phytohaemagglutinin (PHA) stimulation. To determine the effect of PEC-PMN on Th1/Th2 cytokine production by PEC-MNC, autologous PEC-PMN and PEC-MNC were co-cultured at MNC:PMN ratios of 5:0, 4:1, 3:2, 2:3, 1:4 and 0:5 with PHA stimulation for 24 hr. The production of cytokines at each ratio was compared with the expected value, by calculation. We found that PEC-PMN from autoimmune mice progressively suppressed the production of IL-4, IL-10 and IFN-gamma whereas the production of IL-2 was enhanced by autologous MNC in parallel with disease severity. These results suggest that a reciprocal relationship exists in the expression of Th1/Th2 cytokine mRNA between PEC-PMN and PEC-MNC in lpr mice in parallel with disease severity. Autoimmune PEC-PMN can exert significant modulatory effects on Th1/Th2 cytokine production by autologous MNC in stimulation.
authors.affiliation: Department of Medicine, Veterans General Hospital-Taipei, Taiwan, China.
authors.forename: C
authors.initials: C
authors.lastname: Yu
authors.forename: K
authors.initials: K
authors.lastname: Sun
authors.forename: C
authors.initials: C
authors.lastname: Tsai
authors.forename: Y
authors.initials: Y
authors.lastname: Tsai
authors.forename: S
authors.initials: S
authors.lastname: Tsai
authors.forename: D
authors.initials: D
authors.lastname: Huang
authors.forename: S
authors.initials: S
authors.lastname: Han
authors.forename: H
authors.initials: H
authors.lastname: Yu
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D001327:Autoimmune Diseases / Q000276:immunology*; D018929:Cell Culture Techniques; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D015870:Gene Expression; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D019463:Mice, Inbred MRL lpr; D009504:Neutrophils / Q000276:immunology; D010835:Phytohemagglutinins / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012720:Severity of Illness Index; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D010835:Phytohemagglutinins; D012333:RNA, Messenger