Heat shock pretreatment influences the expression of PKC isoforms during sepsis.

Protein Kinase C (PKC) plays a central role in signal transduction and participates in diverse biological and biochemical functions. PKC dysfunction leads to general immunosuppression that, in turn, increases host susceptibility to infection and sepsis. In our previous study, we demonstrated that the mortality of sepsis is significantly decreased in rats treated with heat shock. It was considered that the modulation of PKC content by previous heat shock might contribute to the resistance to a severe infection. In this study, we attempted to understand the change of various PKC isoforms in the lymphocytes during sepsis and to investigate the role of previous heat shock in influencing PKC expression. Cecal ligation and puncture (CLP) was used as the experimental sepsis model for its biphasic clinical manifestation. Heat shock protein and PKC isoforms were detected by immunochemical study. Ten PKC isoforms (alpha, beta, gamma, delta, epsilon, zeta, theta, iota, lambda, and mu) were detected from peripheral lymphocytes. Results showed that all the PKC isoforms have a declination tendency along with the progression of CLP-induced sepsis, and previous heat shock treatment could prevent the declination of PKC content, particularly the isoforms beta, gamma, and epsilon, during sepsis. We suggest that heat shock response may participate in maintenance of PKC expression and contribute to decrease the severity of systemic infection.