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Intestinal immune cells in Strongyloides stercoralis infection
A Trajman1, T T MacDonald, C C Elia
1Department of Internal Medicine, University Hospital, Universidade Federal do Rio de Janeiro, Brazil.
Background:
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.
Aims:
To investigate intestinal histopathology and mucosal immunity in immunocompetent patients with chronic S stercoralis infection.
Methods:
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.
Results:
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.
Conclusions:
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.
Insights
Chronic Strongyloides stercoralis infection in immunocompetent individuals does not alter intestinal mucosal structure or increase inflammatory cells. However, mature macrophages and dividing enterocytes are significantly reduced in the jejunum.
Area of Science:
- Gastroenterology
- Infectious Diseases
- Immunology
Background:
- Strongyloides stercoralis causes a spectrum of human disease, from asymptomatic to fatal hyperinfection.
- Rodent models show spontaneous expulsion of Strongyloides spp.
- Mast cells, goblet cells, and eosinophils are implicated in expulsion mechanisms.
Purpose of the Study:
- To investigate intestinal histopathology and mucosal immunity in immunocompetent patients with chronic Strongyloides stercoralis infection.
Main Methods:
- Jejunal biopsies from 19 immunocompetent patients with mild S stercoralis infection and 7 healthy controls.
- Histopathological analysis using immunoperoxidase and alkaline phosphatase staining.
- Monoclonal antibodies assessed T cell subsets, macrophages, proliferating cells, HLA-DR, collagen IV, CD25, mast cells, IgE, calprotectin, and neutrophil elastase.
Main Results:
- Jejunal morphology, T cells, mast cells, IgE cells, eosinophils, and goblet cells were unaffected by S stercoralis infection.
- Significant reduction in mature macrophages and dividing crypt enterocytes observed in infected patients.
- No significant differences in HLA-DR expression on enterocytes or presence of activated CD25+ cells between groups.
Conclusions:
- Clinically mild strongyloidiasis in immunocompetent Brazilians showed no mucosal structural abnormalities or increased non-specific inflammatory cells.
- No increase in mucosal T cells or macrophages was detected in infected individuals.
- Reduced mature macrophages and crypt enterocyte proliferation are key findings in mild chronic S stercoralis infection.