title: Shigella infection induces cellular activation of T and B cells and distinct species-related changes in peripheral blood lymphocyte subsets during the course of the disease.
abstract: Immunophenotypic changes in peripheral blood lymphocytes (T, B, and NK cells) in patients during shigellosis was characterized by using triple-color flow cytometry. Eleven Shigella dysenteriae 1-infected adult patients (SDIP), 11 Shigella flexneri-infected adult patients (SFIP), 15 age- and sex-matched healthy controls from Bangladesh (C-B), and 15 healthy volunteers from Sweden (V-S) were studied. In SDIP and SFIP, a significant increase in the CD45RO+ cells in both CD4+ and CD8+ T cells were seen. We found evidence for sequential T-cell activation, as shown by increased proportions of CD25 and CD4+ cells; HLA-DR and CD38 on CD8+ cells, and CD54 on CD4+ and CD8+ cells. We found differences in the lymphocyte activation and subset patterns related to the infecting Shigella species. Thus, a decrease in CD45 expression was seen in SFIP; this decrease progressed further during the disease. The proportions of NK cells (CD56+ cells) and CD3- CD8+ cells out of the total CD8+ cells were increased in SFIP but not in SDIP. The CD3+ CD8+ CD57+ T-cell subset was significantly lower in SDIP than in C-B. The proportion of B-lymphocyte-expressing activation markers CD80 and CD23 was higher in patients than in C-B. There was a significant increase in the proportion of CD4+ T cells and a significant decrease in the percentages of total B cells, the CD3+ CD8+ CD57+ T-cell subset, and the CD56+ CD16+ NK-cell subset for V-S compared with C-B. Our results indicate that distinct subset changes and activation patterns are elicited in SDIP compared with SFIP and also that the degree of activation is related to disease severity. In addition, a common sequence of cell activation was seen during the disease course. The difference in the subset patterns seen in C-B and V-S may be related to differences in the levels or spectra of infectious agents in the environment.
authors.affiliation: Division of Clinical Bacteriology, Karolinska Institute, Huddinge University Hospital, Sweden.
authors.forename: D
authors.initials: D
authors.lastname: Islam
authors.forename: P K
authors.initials: PK
authors.lastname: Bardhan
authors.forename: A A
authors.initials: AA
authors.lastname: Lindberg
authors.forename: B
authors.initials: B
authors.lastname: Christensson
mesh_terms: D036541:ADP-ribosyl Cyclase; D051997:ADP-ribosyl Cyclase 1; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D000943:Antigens, Differentiation / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D004405:Dysentery, Bacillary / Q000276:immunology*; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D016131:Lymphocyte Subsets / Q000276:immunology*; D008297:Male; D008562:Membrane Glycoproteins; D009699:N-Glycosyl Hydrolases / Q000378:metabolism; D012762:Shigella dysenteriae / Q000276:immunology*; D012763:Shigella flexneri / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D006684:HLA-DR Antigens; D008562:Membrane Glycoproteins; D018799:Intercellular Adhesion Molecule-1; D009699:N-Glycosyl Hydrolases; D036541:ADP-ribosyl Cyclase; C498154:CD38 protein, human; D051997:ADP-ribosyl Cyclase 1