title: Intestinal immune cells in Strongyloides stercoralis infection.
abstract: 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.
  
  
  OBJECTIVE
  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.
authors.affiliation: Department of Internal Medicine, University Hospital, Universidade Federal do Rio de Janeiro, Brazil.
authors.forename: A
authors.initials: A
authors.lastname: Trajman
authors.forename: T T
authors.initials: TT
authors.lastname: MacDonald
authors.forename: C C
authors.initials: CC
authors.lastname: Elia
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D002908:Chronic Disease; D005260:Female; D006801:Humans; D018928:Immunity, Mucosal; D007124:Immunoenzyme Techniques; D007411:Intestinal Diseases, Parasitic / Q000276:immunology*; D007413:Intestinal Mucosa / Q000276:immunology / Q000469:parasitology; D007579:Jejunal Diseases / Q000276:immunology / Q000469:parasitology; D007583:Jejunum / Q000276:immunology* / Q000469:parasitology; D018655:Lymphocyte Count; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D017171:Strongyloides stercoralis; D013322:Strongyloidiasis / Q000276:immunology*; D013601:T-Lymphocytes / Q000473:pathology