Alterations of innate and adaptive immune responses of patients with septic syndrome due to ventilator-associated pneumonia
Abstract number: P1067
Pelekanou A., Kotsaki A., Vaki I., Karagianni V., Kranidioti H., Spyridaki E., Giamarellos-Bourboulis E.J.
Objectives: Sepsis is the clinical expression of deregulated immune response. This study aims at investigating the expression of immune system components in septic patients with ventilator-associated pneumonia (VAP), the leading cause of morbidity and mortality among nosocomial infections in intensive care units.
Methods: Peripheral venous blood was sampled from 52 patients with sepsis, severe sepsis or septic shock (according to ACCP/SCCM 1992 criteria) within 24 hours of diagnosis. Twenty six suffered from VAP; 26 from other infections, namely pyelonephritis, bacteraemia and intraabdominal infection, all well-matched for severity, age and sex and they were used as controls. After lysis of red blood cells with ammonium chloride, white blood cells (WBCs) were stained by FITC-conjugated monoclonal antibodies for CD3, CD19, CD14, Annexin-V, and PE-conjugated antibodies for CD4, CD8, CD(16+56) and HLA-DR. Flow cytometry was used to determine subpopulations of mononuclear cells, apoptosis and HLA-DR expression.
Results: In patients with VAP, median expression of CD3/CD4, CD3/CD8, CD3/CD(16+56), CD(16+56) and CD19 was found in 35.01%, 21.29%, 4.02%, 8.91% and 8.89% of WBCs respectively. Moreover, expression of Annexin-V (marker of apoptosis) on monocytes, T-helper and T-cytotoxic lymphocytes was 15.39%, 4.90% and 2.98% respectively. CD(16+56) expression was positively correlated to both CD3/CD8 and CD14/HLA-DR (p 0.026 and 0.019 respectively). Median CD14/HLA-DR in patients with VAP was 56.88% and in controls 73.17% (p 0.046). Respective expression of CD3/CD(16+56) was 4.02% and 6.62% (p 0.025) and of CD(16+56) 8.92% and 18.07% (p 0.011).
Conclusions: In patients with VAP increased immunoparalysis is found as evidenced by lower CD14/HLA-DR expression. This is accompanied by decrease of T-LGL and NK cells and may explain increased mortality observed among patients with VAP. It may also constitute a future therapeutic target.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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