Einfluss von Sepsis-induzierter Immunparalyse auf die primäre B-Zellantwort

Arno Mohr
Sepsis as derangement especially of the innate immune system first leads to a phase of inflammation and secondary to immunosuppression. Suppression of immune system is responsible for high mortality and lethality of sepsis. That's why it is essential to decrypt the pathomechanism leading to paralysis of immune system. For the first time in this thesis influence of immunosuppression on primary b-cell-response was examined. Sepsis was induced by the well-established CLP-model. For CLP it has
more » ... For CLP it has already been proved that mice two days after induction of sepsis are immune suppressed. After immunization with ovalbumin at different points of time the serum antibody levels of mice were measured by ELISA. It can be shown that neither anaesthesia nor sham-op had an impact on the primary b-cell-response. CLP leads to an unspecific rise of antibody-level in serum (total IgG, total IgM) and to a rise of ovalbumin-specific IgM antibody-level. An increase of antibody-level can be detected if there is more time between CLP and immunization. Furthermore after CLP a suppression of ovalbumin-specific IgG-, IgG1- and especially IgG2a-antibody-level can be shown. The effect on production of antibodies is best to see 1-2 days between CLP and immunization. Thus it can be shown that immunosuppression induced by sepsis has an impact on the primary b-cell-response. B-cells producing IgG-, IgG1- und IgG2a-antibodies against antigen-structures that were applicated in the phase of immunosuppression were suppressed. The drop of IgG2a-specific antibodies (compared to IgG1) could show that –like typical for immunosuppression– the TH1/TH2-ratio might be switched to TH2. Inhibition of "IDO" can partially suspend the suppressed antibody response after CLP.
doi:10.5283/epub.23851 fatcat:kgeeaklv2bfejkrpzalexctipm