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      • KCI등재후보

        B형 만성활동성간염 환자에서 Leukoryte Adherence Inhibition ( LAI ) 반응과 그와 관련된 Prostaglandin E2 ( PGE2 ) 직 변동

        허영상(Yeong Sang Heo),안득수(Deuk Soo Ahn),김대곤(Dae Ghon Kim),안중기(Joong Ki Ahn),송석현(Suk Hyun Song),이남심(Nam Sim Lee) 대한내과학회 1989 대한내과학회지 Vol.36 No.1

        N/A A leukocyte adherence inhibition (LAI) assay was performed for the evaluation of cellular immune dysfunction in patients with chronic active hepatitis (CAH) B and the effects of prostaglandin E, (PGE,), endogenous and exogenous immune modulator, on LAI reaction were investigated. 1) In patients with CAH, the non adherence index (LAI) was 18.8±1.7 (mean±SE)%, and there was a significant (p<0.001) decrease of LAI as compared to 48.8±1.6% in the antibody positive healthy control group. In chronic HBV carriers LAI was 6.2±1.5%. There was no significant difference in contrast to 8.8±1.3% in the negative normal control group. 2) Changes of the endogenous PGE2 level in the supernatant of the mononuclear cell mixture for LAI were measured and the differences of PGE, levels by specific antigen stiumlation (HBs) and by non specific antigen stimulation (OVA) were calculated. In CAH the difference was -11.4±3.6pg/ml and this was significantly decreased as compared to 19.3±6.3 pg/ml in the positive control group. In chronic HBV carriers the difference was 6.2±1.5 pg/ml and was as low as that in the negative normal control. 3) When only exogenous PGE2 was added to the mononuclear cell mixture, significantly (p<0.01) elevated NAI was observed as compared to the untreated control. On treatment with exogenous PGE, and indomethacin (PG inhibitor), or exogenous PGE, and LiCl (adenyl cyclase inhibitor), inhibitions of increasing NAI were observed. From the above results, in patients with CAH, LAI reflected cellular immunity was declined and this might be related to decreased release of endogenous PGE2 Furthermore, it was suggested that endogenous and exogenous PGE2 should accentuate LAI reaction.

      • KCI등재후보

        소화성 위장질환에 사용하는 Cimetidine , Ranitidine , Proglumide 및 Clebopride 의 면역반응조절

        김대곤(Dae Ghon Kim),허영상(Yeong Sang Heo),안관용(Kwan Yong Ahn),이용기(Yong Gi Lee),안득수(Deuk Su Ahn) 대한내과학회 1987 대한내과학회지 Vol.33 No.1

        N/A It has been reported that among many drugs used for the treatment of peptic gastrointestinal disorder, a few drugs exerts a variety of modulating effects on immune responsiveness. This study was undertaken to investigate the effect of four of the drugs on immune response of mice to sheep red blood cells (SRBC). Four drugs used in this experiment are cimetidine, a imidazole derivative of histamine type 2 (H₂) receptor antagonist; ranitidine, a furan derivative of H₂, antagonist; proglumide, a gastrin antagonist; and clebopride, a dopamine antagonist. Mice were pretreated with daily oral administration of varying concentration of each drugs for 30 days and were immunized with 10(8) SRBC. Each mouse was challenged 4 days after the sensitization, Immune response were evaluated by measuring footpad swelling reaction at 3 hr (Arthus reaction) and 24hr (delayed type hypersensitivity, DTH) after challenge, rosette forming reaction, hemagglutinin (HA) and hemolysine (HE) titers to SRBC. The pretreatment of mice with cimetidine inhibited Arthus and rosette forming reactions, but enhanced DTH to SRBC. The pretreatment of mice with proglumide suppressed both DTH and rosette forming reaction. The pretreatment of mice with clebopride enhanced DTH, but decreased rosette forming reaction. In contrast to cellular immune response, there was not any significant difference between the drug treated and untreated control groups in HA and HE reactions. These results suggest that cimetidine, ranitidine and clebopride enhance cellular immune response, but proglumide suppress the above response and all of the drugs do not significantly change the humoral immune response.

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