Septic syndromes are the main cause of death in the intensive care units and although the mortality rates is slowly decreasing, the occurrence of the disease has been increasing. The pathogenesis of sepsis includes countless disturbances of the host immune system starting with a harmful, infection-triggered exaggerated inflammatory cascade, followed by the development of an immunoparalysis state. The latter contributes to the failure in pathogen eradication and leads to secondary infections, which are often the cause of fatal complications. In this review, we consider different novel therapeutic strategies for restoration of immune function. The use of glucocorticoids, intravenous immunoglobulins, heparin, recombinant human activated protein C, granulocyte macrophage colony-stimulating factor, granulocyte colony-stimulating factor, interferon-γ, statins, macrolides and high-volume hemofiltration are discussed. Even though some clinical trials of these regimens are promising, the key to their successful application seems to be the precise monitoring of the status of immune system followed by implementation of the adequate therapy. Thus, in this paper we present disturbances in the immune system in the course of human sepsis, with special attention to the parameters that could be monitored and serve as markers for immunomodulatory therapies. We conclude by briefly presenting the current sepsis treatment strategy.
The leading pathophysiological changes during sepsis include systemic abnormalities in the immune response. Due to the general character of these disturbances, sepsis is usually studied as a homogenous clinical condition. We aimed to compare the immune response in intraabdominal sepsis (IAS) and pneumonia-derived sepsis (PDS). The following cell populations were examined: white blood cell count (WBC), monocytes, lymphocytes:CD3⁺, CD4⁺ and CD8⁺ T cells, B cells, and NK cells. In both studied groups (i.e. IAS and PDS), the WBC was elevated. However, it was significantly higher in the IAS group than in the PDS group. The difference was due to a lower granulocyte count, as well as a lower monocyte count in PDS. We found no significant correlation between the total lymphocyte number and CD3⁺CD8⁺ T cells in either form of sepsis. Similarly, we observed no correlation between the total lymphocyte number and the NK cells subset in IAS. However, the numbers of CD3⁺CD8⁺ and NK cells correlated similarly in both types of sepsis. Both studied types of sepsis induced profound lymphocytopenia, with marked loss of CD8⁺ T cells and the NK cells. However, the similarrelation between them, which was independent of the infection type, suggests that the NK and CD3⁺CD8⁺ cellshave shared mechanisms of regulation. The primary site of infection has an impact on the global immune reaction. These alternations include especially myeloid cells: granulocytes and monocytes which disappear from peripheral blood during PDS, but increase in IAS.
Abstract:The leading pathophysiological changes during sepsis include systemic abnormalities in the immune response. Due to the general character of these disturbances, sepsis is usually studied as a homogenous clinical condition. We aimed to compare the immune response in intraabdominal sepsis (IAS) and pneumonia-derived sepsis (PDS). The following cell populations were examined: white blood cell count (WBC), monocytes, lymphocytes: CD3 + , CD4+ and CD8 + T cells, B cells, and NK cells. In both studied groups (i.e. IAS and PDS), the WBC was elevated. However, it was significantly higher in the IAS group than in the PDS group. The difference was due to a lower granulocyte count, as well as a lower monocyte count in PDS. We found no significant correlation between the total lymphocyte number and CD3 + CD8 + T cells in either form of sepsis. Similarly, we observed no correlation between the total lymphocyte number and the NK cells subset in IAS. However, the numbers of CD3 + CD8+ and NK cells correlated similarly in both types of sepsis. Both studied types of sepsis induced profound lymphocytopenia, with marked loss of CD8 + T cells and the NK cells. However, the similar relation between them, which was independent of the infection type, suggests that the NK and CD3 + CD8+ cells have shared mechanisms of regulation. The primary site of infection has an impact on the global immune reaction. These alternations include especially myeloid cells: granulocytes and monocytes which disappear from peripheral blood during PDS, but increase in IAS.
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