WEDNESDAY, Dec. 21 (HealthDay News) -- Patients who die with active severe sepsis have reduced cytokine secretion and other changes indicative of immunosuppression, according to a study published in the Dec. 21 issue of the Journal of the American Medical Association.
Jonathan S. Boomer, Ph.D., from the Washington University School of Medicine in St. Louis, and colleagues examined the association of sepsis with changes in host innate and adaptive immunity. Immune status at the time of death was characterized using rapid post-mortem spleen and lung tissue harvested from 40 patients who died in intensive care units with active severe sepsis. Control spleens and lungs were obtained from 29 and 20 patients, respectively. Potential mechanisms of immune dysfunction were identified.
The investigators found that, compared with control patients, in sepsis patients, there were significant reductions in cytokine secretion among anti-CD3/anti-CD28-stimulated splenocytes. Five-hour lipopolysaccharide-stimulated cytokine secretion was similarly reduced. In sepsis patients, cytokine secretion was generally less than 10 percent of that seen in controls, independent of age, sepsis duration, corticosteroid use, and nutritional status. Flow cytometric analysis showed elevated expression of certain inhibitory receptors and ligands, and expansion of suppressor cell populations in both spleens and lungs, although there were differences between the two. Immune cells isolated from the lungs of septic patients, versus control lungs, displayed unique differences in cellular inhibitory molecular expression. Extensive depletion of splenic CD4, CD8, and HLA-DR and expression of inhibitory receptor ligands on lung epithelial cells were seen using immunohistochemical staining.
"These data provide a unique insight into the status of the immune system during sepsis, not only in a lymphoid organ but in peripheral tissue," the authors write.
One of the study authors disclosed financial ties to the pharmaceutical industry.
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