Impaired inducibility of heat shock protein 70 in peripheral blood lymphocytes of patients with severe sepsis

Citation
S. Schroeder et al., Impaired inducibility of heat shock protein 70 in peripheral blood lymphocytes of patients with severe sepsis, CRIT CARE M, 27(6), 1999, pp. 1080-1084
Citations number
38
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
27
Issue
6
Year of publication
1999
Pages
1080 - 1084
Database
ISI
SICI code
0090-3493(199906)27:6<1080:IIOHSP>2.0.ZU;2-1
Abstract
Objective: To determine the extent of the potentially protective heat shock protein 70 response in peripheral blood lymphocytes of patients with sever e sepsis after ex vivo lipopolysaccharide stimulation. Design: Entry study of consecutive patients with severe sepsis, those who w ere critically ill or nonseptic after major surgery, and healthy blood dono rs, Setting: Surgical intensive care unit in a university hospital, Patients: Ten patients with diagnoses of severe sepsis; ten critically ill, nonseptic patients after major surgery; and ten healthy blood donors, Interventions: None. Measurements and Main Results: We investigated the ex vivo endotoxin-induci ble expression of heat shock protein 70 in peripheral blood lymphocytes of patients with severe sepsis by means of flow cytometry, Only negligible amo unts of inducible intracellular heat shock protein 70 accumulation (<4.2% o f lymphocytes) could be detected in peripheral blood lymphocytes without li popolysaccharide stimulation. The proportion of cells accumulating heat sho ck protein 70 after treatment with lipopolysaccharide was distinctly lower in patients with severe sepsis (p < .05) than in critically ill, nonseptic patients after major surgery and healthy blood donors (38.3 +/- 3.3%, 82.2 +/- 4.5%, and 70.9 +/- 3.9%, respectively; mean +/- SEM; n = 10), Patients with clinical signs of recovery from severe sepsis showed an increase in he at shock protein 70 expression. Conclusions: Inducibility of ex vivo heat shock protein 70 was impaired in peripheral blood lymphocytes of patients with severe sepsis, The impaired e xpression of the potentially protective heat shock protein 70 may contribut e in vivo to immune dysfunction, because intact functioning of T and B lymp hocyte responses is of central importance in resisting infection in severe sepsis, Monitoring of inducible heat shock protein 70 in peripheral blood l ymphocytes may contribute to the evaluation of the immune consequences of s evere sepsis.