Serum complement C4b, fibronectin, and prolidase are associated with the pathological changes of pulmonary tuberculosis.
Serum complement C4b, fibronectin, and prolidase are associated with the pathological changes of pulmonary tuberculosis.
复制标题
血清补体C4b、纤连蛋白、脯氨酸酶与肺结核病理改变相关
DOI：
10.1186/1471-2334-14-52
复制
发表时间：
2014-01-31
影响因子：
3.7
通讯作者：
Li JC
中科院分区：
文献类型：
--
作者：
Wang C;Li YY;Li X;Wei LL;Yang XY;Xu DD;Jiang TT;Li ZJ;Chen ZL;Zhang X;Liu JY;Ping ZP;Li JC
BackgroundMycobacterium tuberculosisinfection can activate the immune system, leading to characteristic pathological changes such as inflammatory granuloma, caseous necrosis, and cavity formation.MethodsClinical data of 187 cases of pulmonary tuberculosis (PTB) were analyzed using statistical methods, while serum levels of complement C4b (C4b), fibronectin (FN), and prolidase (PEPD) were detected using the ELISA method among the control, minimal PTB, moderate PTB, and advanced PTB groups.ResultsWe found significantly higher levels of serum C4b and PEPD (P= 0.018,P= 0.003), and significantly lower levels of serum FN (P< 0.001) in PTB patients. Furthermore, the serum levels of 3 proteins were significantly different among 3 PTB groups. FN level was significantly higher in the moderate PTB group, compared with patients in the minimal and advanced PTB groups (P< 0.05,P< 0.01). PEPD level was significantly higher in the moderate PTB group, compared with the minimal PTB group (P< 0.05). Analysis of clinical data showed that serum albumin, C-reactive protein (CRP), prealbumin, and C4 were significantly higher (P< 0.05), while serum globulin was significantly lower in patients with PTB (P< 0.001). A significant negative correlation was found between C4b and albumin, prealbumin. On the other hand, a significant positive correlation was found between C4b and globulin, CRP, PEPD, as well as between PEPD and CRP (P< 0.05).ConclusionsOur study showed that C4b, FN, and PEPD are associated with tissue damage, granuloma formation, and cavity formation, respectively, in patients with PTB. The present study provides a new experimental basis to understand the pathogenesis and pathological changes of PTB.
