Interleukin 10 production in patients undergoing cardiopulmonary bypass: Evidence of inhibition of Th-1-type responses

Citation
A. Naldini et al., Interleukin 10 production in patients undergoing cardiopulmonary bypass: Evidence of inhibition of Th-1-type responses, CYTOKINE, 11(1), 1999, pp. 74-79
Citations number
31
Categorie Soggetti
Cell & Developmental Biology
Journal title
CYTOKINE
ISSN journal
10434666 → ACNP
Volume
11
Issue
1
Year of publication
1999
Pages
74 - 79
Database
ISI
SICI code
1043-4666(199901)11:1<74:I1PIPU>2.0.ZU;2-#
Abstract
The cardiopulmonary bypass (CPB) procedure has long been associated with a generalized immunosuppression. To understand further the cytokine-mediated regulation of the complex physiological and immunological changes induced b y CPB, the authors decided to investigate whether CPB affects the release o f interleukin (IL)-10, as well as other cytokines, in correlation to the in hibition of T cell responses. Using phytohaemagglutinin (PHA) as mitogen an d peripheral blood mononuclear cells (PBMC) isolated from patients undergoi ng CPB, we investigated whether this procedure has an effect on the secreti on of different patterns of cytokines (Th1- and Th2-type) and PBMC prolifer ation. In all patients, CPB significantly enhances IL-10 and IL-6 productio n in resting and PHA-stimulated PBMC, On the other hand, IL-2 production, i n response to PH;I, was significantly diminished. Reduced IL-2 and enhanced IL-10 production were associated with a significant decrease in PBMC proli feration. Immunosuppression was also associated to lymphopenia, while neutr ophil counts were significantly enhanced. These results show that after CPB there is a transient but clear unbalanced immune response demonstrated by a differentiated production of Th1- and Th2-type cytokines, The release of different patterns of cytokines observed after CPB may be helpful in unders tanding and preventing the development of infectious and immune complicatio ns in surgical procedure employing CPB, (C) 1999 Academic Press.