Sharma M, Vohra H, Bhasin D
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh - 160 012, India.
Parasitology. 2005 Dec;131(Pt 6):783-96. doi: 10.1017/S0031182005008541.
The virulence of Entamoeba histolytica is governed by adhesion/colonization in the gut which is mediated by a galactose specific lectin. Two morphologically identical but distinct species i.e. pathogenic E. histolytica and non-pathogenic E. dispar, can be differentiated by distinct epitopes in the lectin. Both species bind to colonic epithelial cells, but only E. histolytica infection induces an inflammatory response and subsequent pathogenesis. Thus, comparing the responses of the intestinal cells to pathogenic and non-pathogenic lectins is a point of interest. The pathogenic lectin causes cytolysis of epithelial and immune-competent cells. Our data (both qualitative and mRNA quantitation) indicate that the epithelial cells responded to E. histolytica lectin with an increased expression of pro-inflammatory IL-2, IL-6, IL-8, MIP-1alpha, MCP-1, RANTES, GROalpha and GMCSF as compared to E. dispar lectin. The pathogenic LCM induced a significant increase in intracellular calcium concentration, proliferative response and chemotaxis of lymphocytes from ALA patients as compared to non-pathogenic LCM. High RANTES and IL-6 were induced in patients' lymphocytes by pathogenic LCM, along with their receptors CCR5 and CD126 as compared to NP-LCM. The local release of such a complex network of cytokines/chemokines could explain the histopathology of E. histolytica infection. The comparative low levels of these chemokines/pro-inflammatory cytokines and high levels of anti-inflammatory IL-10 in response to non-pathogenic E. dispar could explain the absence of an acute inflammatory response and the disease process. The cytokines and chemokines may provide a mechanism for initiation, amplification or containment of inflammation during disease state.
溶组织内阿米巴的毒力由肠道中的黏附/定植所决定，这一过程由一种半乳糖特异性凝集素介导。两种形态相同但截然不同的物种，即致病性溶组织内阿米巴和非致病性迪斯帕内阿米巴，可通过凝集素中不同的表位加以区分。这两种物种均可与结肠上皮细胞结合，但只有溶组织内阿米巴感染会引发炎症反应及后续发病机制。因此，比较肠道细胞对致病性和非致病性凝集素的反应是一个有趣的点。致病性凝集素会导致上皮细胞和免疫活性细胞的细胞溶解。我们的数据（包括定性和mRNA定量）表明，与迪斯帕内阿米巴凝集素相比，上皮细胞对溶组织内阿米巴凝集素的反应是促炎细胞因子IL-2、IL-6、IL-8、MIP-1α、MCP-1、RANTES、GROα和GMCSF的表达增加。与非致病性溶组织内阿米巴滋养体凝集素（LCM）相比，致病性LCM可使来自急性肺脓肿（ALA）患者的淋巴细胞内钙浓度显著升高、增殖反应增强以及趋化性增强。与非致病性LCM相比，致病性LCM可诱导患者淋巴细胞中高表达RANTES和IL-6，以及它们的受体CCR5和CD126。如此复杂的细胞因子/趋化因子网络的局部释放可以解释溶组织内阿米巴感染的组织病理学情况。对非致病性迪斯帕内阿米巴的反应中，这些趋化因子/促炎细胞因子水平相对较低且抗炎细胞因子IL-10水平较高，这可以解释为何没有急性炎症反应和疾病进程。细胞因子和趋化因子可能为疾病状态下炎症的启动、放大或遏制提供一种机制。
