TNF-α, TGF-β and NO relationship in sera from tuberculosis (TB) patients of different severity

被引:45
作者
Fiorenza, G
Rateni, L
Farroni, MA
Bogué, C
Dlugovitzky, DG
机构
[1] Fac Ciencias Med, Catedra Microbiol, Secc Immunol, RA-2000 Rosario, Santa Fe, Argentina
[2] Hosp 1, Rosario, Santa Fe, Argentina
关键词
tuberculosis; immune response; TNF-alpha TGF-beta NO;
D O I
10.1016/j.imlet.2004.09.008
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tuberculosis (TB) is the main cause of death by infection diseases worldwide. Considering that NO, TNF-alpha. and TGF-beta participate a great deal in TB immunopathogenesis, we wished to analyse whether these mediators showed some relationship with the degree of pulmonary affectation. The sample comprised 29 TB (HIV-), inpatients with mild-moderate (n = 10) or advanced (n = 19) newly-diagnosed disease, together with 12 healthy controls -HCo-. Serum nitrite was assessed by reducing nitrate to nitrite, and further measured by the Griess reaction. Levels of TNF-alpha and TGF-beta were determined by ELISA (R&D Systems). Serum levels of TNF-alpha were significantly higher in the advanced TB cases if compared with HCo. (p < 0.05) and from values of Mild-Moderate TB patients (p < 0.05). Serum levels of TGF-beta from advanced TB patients have increased values if compared with Hco (p < 0.005) and Mild-Moderate patients (p < 0.05). These values were also significantly different from Mild-Moderate cases + HCo(p = 0.01) Advanced TB patients had significantly reduced nitrite levels compared with those of Mild-Moderate patients and HCo (p < 0.002). Taken as a whole NO-derived metabolites in TB patients (M-M and Advanced cases) remained lower than values in HCo (p = 0.005) A negative correlation was found when comparing the two cytokines with nitrites(r = -0.44).TGF-beta and TNF-alpha were positively correlated (r = 0.44, p < 0.01), 0.44 p < 0.01. In synthesis. the inverse correlation found between both cytokines concentrations and NO levels in TB patients may be viewed as a consequence of a more predominant TGF-beta effect. (c) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:45 / 48
页数:4
相关论文
共 15 条
[1]   INTERLEUKIN-6 ANTAGONIZES TUMOR NECROSIS FACTOR-MEDIATED MYCOBACTERIOSTATIC AND MYCOBACTERIOCIDAL ACTIVITIES IN MACROPHAGES [J].
BERMUDEZ, LE ;
WU, M ;
PETROFSKY, M ;
YOUNG, LS .
INFECTION AND IMMUNITY, 1992, 60 (10) :4245-4252
[3]   CYTOKINE MODULATION OF MYCOBACTERIUM-TUBERCULOSIS GROWTH IN HUMAN MACROPHAGES [J].
DENIS, M ;
GREGG, EO ;
GHANDIRIAN, E .
INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY, 1990, 12 (07) :721-727
[4]   Influence of disease severity on nitrite and cytokine production by peripheral blood mononuclear cells (PBMC) from patients with pulmonary tuberculosis (TB) [J].
Dlugovitzky, D ;
Bay, ML ;
Rateni, L ;
Fiorenza, G ;
Vietti, L ;
Farroni, MA ;
Bottasso, OA .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2000, 122 (03) :343-349
[5]   In vitro synthesis of interferon-γ, interleukin-4, transforming growth factor-β and interleukin-1β by peripheral blood mononuclear cells from tuberculosis patients:: Relationship with the severity of pulmonary involvement [J].
Dlugovitzky, D ;
Bay, ML ;
Rateni, L ;
Urizar, L ;
Rondelli, CFM ;
Largacha, C ;
Farroni, MA ;
Molteni, O ;
Bottasso, OA .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1999, 49 (02) :210-217
[6]  
Escalante P, 2003, AM J RESP CRIT CARE, V167, P1718, DOI 10.1164/ajrccm.167.12.912
[7]   Mechanisms of nitric oxide-related antimicrobial activity [J].
Fang, FC .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (12) :2818-2825
[8]   THE INDUCING ROLE OF TUMOR NECROSIS FACTOR IN THE DEVELOPMENT OF BACTERICIDAL GRANULOMAS DURING BCG INFECTION [J].
KINDLER, V ;
SAPPINO, AP ;
GRAU, GE ;
PIGUET, PF ;
VASSALLI, P .
CELL, 1989, 56 (05) :731-740
[9]   NICOTINAMIDE INHIBITS NITRIC-OXIDE SYNTHASE MESSENGER-RNA INDUCTION IN ACTIVATED MACROPHAGES [J].
PELLATDECEUNYNCK, C ;
WIETZERBIN, J ;
DRAPIER, JC .
BIOCHEMICAL JOURNAL, 1994, 297 :53-58
[10]   NITRIC-OXIDE SYNTHASE IS NOT A CONSTITUENT OF THE ANTIMICROBIAL ARMATURE OF HUMAN MONONUCLEAR PHAGOCYTES [J].
SCHNEEMANN, M ;
SCHOEDON, G ;
HOFER, S ;
BLAU, N ;
GUERRERO, L ;
SCHAFFNER, A .
JOURNAL OF INFECTIOUS DISEASES, 1993, 167 (06) :1358-1363