Lipopolysaccharide-cell interaction and induced cellular activation in whole 
blood of septic patients

Salomao, Reinaldo; Brunialti, Milena K. C.; Kallás, Esper G.; Martins, Paulo S.; Rigato, Otelo; Freudenberg, Marina

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Lipopolysaccharide-cell interaction and induced cellular activation in whole blood of septic patients

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Freudenberg, Marina
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Salomao, R., Brunialti, M. K. C., Kallás, E. G., Martins, P. S., Rigato, O., & Freudenberg, M. (2002). Lipopolysaccharide-cell interaction and induced cellular activation in whole blood of septic patients. Journal of Endotoxin Research, 8(5), 371-379.

Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-967F-A

Abstract

We used biotinylated LPS (LPSb) and flow cytometry to study LPS-monocyte interaction and LPS-induced cellular activation in whole blood from septic patients (SP). Expression of surface activation markers was evaluated on monocytes (HLA-DR) and T lymphocytes (CD69 and CD95), and intracellular TNF-α on monocytes. Saturating curve and kinetics of LPSb detection on monocytes were similar in SP and healthy volunteers (HV). LPSb bound to monocytes was detected after 5 min of incubation in both groups, with a more pronounced decay in SP. Monocytes from SP had a lower expression of HLA-DR as compared to HV, both constitutive and upon LPS stimulation. The proportion of monocytes producing TNF-α after LPS stimulus was higher in HV than SP (mean ± SD=25.2 ± 14.2% and 2.2 ± 2.6%, respectively, P < 0.001). LPS-induced CD69 on T CD8^₊ and CD8^₋ lymphocytes was similar for patients and controls. Expression of CD95 on T lymphocytes was higher in SP as compared to HV on T CD8^₊ cells (GMFI, mean, ± SD = 22.3 ± 14.6 and 8.6 ± 5.0, respectively, P = 0.01) and CD8^₋ cells (GMFI, mean ± SD = 28.3 ± 7.7 and 14 ± 4.3 respectively, P<0.001). Thus, monocytes and lymphocytes seem to respond differently to LPS in septic patients. Monocyte hyporesponsiveness appears not to be related to a decreased binding capacity of LPS, but rather to an impaired signal transduction.