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Rough-Form-Lipopolysaccharide Increase Apoptosis in Human CD4+ and CD8+ T-Lymphocytes



Rough-Form-Lipopolysaccharide Increase Apoptosis in Human CD4+ and CD8+ T-Lymphocytes







Immunosuppression induced by lymphocyte apoptosis is considered an important factor in the pathogenesis of sepsis and has been demonstrated in both animal models of LPS-induced endotoxemia and septic patients. Since rough-form lipopolysaccharide (R-LPS) recently have been shown to elicit a stronger immunological response than regular smooth-form LPS (S-LPS), we aimed to assess the apoptosis-inducing capabilities of R-LPS in different subsets of lymphocytes (CD4+ T-cells, CD8+ T-cell, B-cells, and NK-cells).Using multicolor flow cytometry on human peripheral blood mononuclear cells, we found that R-LPS increased apoptosis in CD4+ and CD8+ T-cells assessed by annexin V and propidium iodide (AV+PI-), compared to both S-LPS and unstimulated cells. 7-amino-actinomycin D (7-AAD) and staining for intracellular active caspase-3, which are considered later signs of apoptosis, did not reveal the same results. Both forms appeared to inhibit apoptosis in B-cells, but no LPS-form-specific effect was seen on B- or NK cells. Our results indicate that R-LPS induce a stronger AV+PI- assessed apoptotic response in T-cells than S-LPS. Our findings emphasize the importance of T-cell apoptosis in endotoxemia and advocates for control of LPS-form in both endotoxemia research and clinical trials with Gram-negative infections.

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Accession: 036182611

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DOI: 10.1111/j.1365-3083.2011.02613.x


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