Objective To explore the clinical value of adenosine deaminase (ADA),C-reactive protein (CRP)and carcinoembry-onic antigen (CEA)in the diagnosis of pulmonary tuberculosis(TB)and extrapulmonary tuberculosis (EPTB).Methods ADA was measured with the liquid dual reagent velocity method,CRP with the gold-labeled immunization test and CEA with ELISA.90 a-dults were as controls,94 cases of pulmonary TB as the pulmonary TB group and 73 cases of EPTB as the EPTB group.The ADA, CRP and CEA levels were compared among 3 groups.Results The levels of ADA,CRP and CEA in the pulmonary TB group and the EPTB group were (50.1±24.4)U/L,(53.6±21.3)mg/L and (8.7±3.4)μg/L;(49.2±23.5)U/L,(49.8±19.8)mg/L and (8.5±3.3)μg/L respectively,which were significantly higher than (17.1±5.1)U/L,(8.7±2.5)mg/L and (5.4±2.3)μg/L in the control group,the differences had statistical significance (P<0.05).The positive rates of ADA and CRP were 91.5% and 89.4% in the pulmonary TB group and 84.9% and 91.8% in the EPTB group,which were higher than 2.2% and 1.1% in the con-trol group,the difference was statistically significant (P<0.05).Conclusion The measurement of ADA,CRP and CEA is of high clinical value in the diagnosis and differential diagnosis of pulmonary TB and EPTB.

Brucella is an intracellular pathogen that invades a host and settles in its immune cells; however, the mechanism of its intracellular survival is unclear. Modification of small ubiquitin-related modifier (SUMO) occurs in many cellular activities. E2 conjugating enzyme 9 (Ubc9) is the only reported ubiquitin-conjugating enzyme that links the SUMO molecule with a target protein. Brucella's intracellular survival mechanism has not been studied with respect to SUMO-related proteins and Ubc9. Therefore, to investigate the relationship between Brucella melitensis 16M and SUMO, we constructed plasmids and cells lines suitable for overexpression and knockdown of SUMO1 and Ubc9 genes. Brucella 16M activated SUMO1/Ubc9 expression in a time-dependent manner, and Brucella 16M intracellular survival was inhibited by SUMO1/Ubc9 overexpression and promoted by SUMO1/Ubc9 depletion. In macrophages, Brucella 16M-dependent apoptosis and immune factors were induced by SUMO1/Ubc9 overexpression and restricted by SUMO1/Ubc9 depletion. We noted no effect on the expressions of SUMO1 and Ubc9 in B. melitensis 16M lipopolysaccharide-prestimulated mouse RAW264.7 macrophages. Additionally, intracellular survival of the 16M△VirB2 mutant was lower than that of Brucella 16M (p < 0.05). VirB2 can affect expression levels of Ubc9, thereby increasing intracellular survival of Brucella in macrophages at the late stage of infection. Collectively, our results demonstrate that B. melitensis 16M may use the VirB IV secretion system of Brucella to interact with SUMO-related proteins during infection of host cells, which interferes with SUMO function and promotes pathogen survival in host cells.
Animals ; Apoptosis ; Brucella melitensis ; Brucella ; Immunologic Factors ; Macrophages ; Mice ; Plasmids