Trajman A, MacDonald T T, Elia C C
Department of Internal Medicine, University Hospital, Universidade Federal do Rio de Janeiro, Brazil.
J Clin Pathol. 1997 Dec;50(12):991-5. doi: 10.1136/jcp.50.12.991.
Strongyloides stercoralis can cause a wide spectrum of disease in man, ranging from a chronic asymptomatic infection to a hyperinfective, often fatal syndrome. In rodents, spontaneous expulsion of Strongyloides spp occurs after experimental infection. Mast cells, goblet cells, and eosinophils have been identified as possible effectors of this expulsion.
To investigate intestinal histopathology and mucosal immunity in immunocompetent patients with chronic S stercoralis infection.
Jejunal biopsies were performed in 19 immunocompetent patients with a positive stool examination for S stercoralis and few or no symptoms, and in seven healthy controls. Specimens were processed for histopathological analysis and stained by the immunoperoxidase technique, using the following monoclonal antibodies: CD2, CD3, CD4, CD8, anti-T cell receptor (TcR) gamma/delta, RFD1 and RFD7 (two different macrophage markers), Ki67+ (proliferating) cells, antihuman leucocyte antigen (HLA)-DR, and anticollagen IV. In addition, CD25+ cells, mast cells, IgE expressing cells, calprotectin containing cells, and neutrophil elastase positive cells were stained by the alkaline phosphatase method.
Jejunal morphology and the numbers of different T cell subsets, mast cells, IgE expressing cells, eosinophils, and goblet cells were unaffected by S stercoralis infection. Conversely, the numbers of mature macrophages and dividing enterocytes in the crypts were reduced significantly. Crypt enterocytes did not express HLA-DR in both groups. The expression of HLA-DR by villus enterocytes was also comparable in patients and controls. There were no activated (CD25+) cells in the mucosa of either patients or controls.
Compared with seven healthy uninfected volunteers, a group of 19 Brazilians with clinically mild strongyloides infection showed no abnormality of mucosal structure and no increase in non-specific inflammatory cells. Likewise, there was no increase in mucosal T cells or macrophages.
粪类圆线虫可在人类中引发广泛的疾病，从慢性无症状感染到高感染性、常为致命性的综合征。在啮齿动物中，实验感染后会出现粪类圆线虫属的自发排出。肥大细胞、杯状细胞和嗜酸性粒细胞已被确定为这种排出的可能效应细胞。
研究免疫功能正常的慢性粪类圆线虫感染患者的肠道组织病理学和黏膜免疫。
对19例粪便检查粪类圆线虫阳性且症状轻微或无症状的免疫功能正常患者以及7名健康对照者进行空肠活检。标本进行组织病理学分析，并采用免疫过氧化物酶技术，使用以下单克隆抗体进行染色：CD2、CD3、CD4、CD8、抗T细胞受体（TcR）γ/δ、RFD1和RFD7（两种不同的巨噬细胞标志物）、Ki67 +（增殖）细胞、抗人白细胞抗原（HLA）-DR和抗胶原蛋白IV。此外，采用碱性磷酸酶法对CD25 +细胞、肥大细胞、表达IgE的细胞、含钙卫蛋白的细胞和中性粒细胞弹性蛋白酶阳性细胞进行染色。
空肠形态以及不同T细胞亚群、肥大细胞、表达IgE的细胞、嗜酸性粒细胞和杯状细胞的数量不受粪类圆线虫感染的影响。相反，隐窝中成熟巨噬细胞和分裂期肠上皮细胞的数量显著减少。两组患者隐窝肠上皮细胞均不表达HLA-DR。绒毛肠上皮细胞HLA-DR的表达在患者和对照中也相当。患者和对照的黏膜中均无活化（CD25 +）细胞。
与7名未感染的健康志愿者相比，一组19例临床症状轻微的巴西粪类圆线虫感染患者未出现黏膜结构异常，非特异性炎症细胞也未增加。同样，黏膜T细胞或巨噬细胞也未增加。
