Brief Reports
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2004; 10(24): 3674-3676
Published online Dec 15, 2004. doi: 10.3748/wjg.v10.i24.3674
Serum sIL-2R, TNF-α and IFN-γ in alveolar echinococcosis
Da-Zhong Shi, Fu-Rong Li, B Bartholomot, DA Vuitton, PS Craig
Da-Zhong Shi, Fu-Rong Li, Department of Parasitology, Lanzhou Medical College, Lanzhou 730000, Gansu Province, China
B Bartholomot, DA Vuitton, Department of Immunology, Besancon University, France
PS Craig, Department of Biological Sciences, Salford University, United Kingdom
Author contributions: All authors contributed equally to the work.
Supported by the STD3 Programme of the EC, No. TS3-CT94-0270
Correspondence to: Professor Da-Zhong Shi, Department of Parasitology, Lanzhou Medical College, Lanzhou 730000, Gansu Province, China. shidz@public.lz.gs.cn
Telephone: +86-931-8616962 Fax: +86-931-8616962
Received: January 12, 2004
Revised: June 14, 2004
Accepted: June 21, 2004
Published online: December 15, 2004
Abstract

AIM: To approach the relationship between alveolar echinococcosis (AE) pathology and level of sIL-2R,TNF-α and IFN-γ in sera and the significance of cytokines in development of AE.

METHODS: After 23 patients with AE were confirmed by ELISA and ultrasound, their sera were collected and the concentrations of sIL-2R,TNF-α and IFN-γ were detected by double antibody sandwich. Twelve healthy adults served as controls. According to the status of livers of AE patients by ultrasound scanning, they were divided into 4 groups: P2, P3, P4 groups and C group (control). Average of concentrations of sIL-2R,TNF-α and IFN-γ in homologous group was statistically analyzed by both ANOV and Newman-Keuls, respectively.

RESULTS: The mean of sIL-2R in P2 group was 97 ± 29, P3: 226 ± 80, P4: 194 ± 23 and control group (111 ± 30) × 103 u/L (P < 0.01). The mean of TNF-α in P2 group was 1.12 ± 0.20, P3: 3.67 ± 1.96 , P4: 1.30 ± 0.25 and control group 0.40 ± 0.19 µg/L (P < 0.01). The mean of IFN-γ in P2 group was 360 ± 20, P3: 486 ± 15, P4: 259 ± 19 and control group: 16 ± 2 ng/L (P < 0.01). Judged by ANOV and Newman-Keuls, the mean concentrations of sIL-2R, TNF-α and IFN-γ had a significant difference among groups. Except for P2 group, the mean sIL-2R between other groups of AE patients had a significant difference (P < 0.05). The mean of TNF-α concentration in P3 group was the highest (P < 0.01). The mean of IFN-γ concentration in all patients was higher than that in control group (P < 0.01), but there was no difference between AE groups (P > 0.05).

CONCLUSION: Low sIL-2R level indicates an early stage of AE or stable status, per contra, a progression stage. Higher level of TNF-α might be related to the lesion of liver. The role of single IFN-γ is limited in immunological defense against AE and it can not fully block pathological progression.

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