Abstract
Systemic inflammation plays a crucial role in formation of various pathological conditions, including sepsis, burns, and traumas. The main effector cells participating in progression of systemic inflammation response and sepsis are monocytes, which regulate both innate and acquired immunity via phagocytosis, synthesis of cytokines and chemokines, antigen presentation, and lymphocyte activation. Thus, the monocytes are considered as a link between innate and acquired immunity. The monocyte subpopulations taken into consideration in the study essentially determine the progression of systemic inflammation and could serve as targets for therapeutic intervention. The complexity of the analysis of pathophysiology of systemic inflammation lies in its high variability conditioned by individual peculiarities of the patients and inflammation progression specifications. To overcome these limitation, model of experimental endotoxemia (EE) is used. The results of EE, in turn, cannot be directly extrapolated on patients with the systemic inflammatory response. This review is dedicated to discussing the role of monocyte subpopulations in progression of systemic inflammation/sepsis and EE.
Highlights
Systemic inflammatory response syndrome (SIRS) is excessive protective reaction of the body on a damaging stress factor for localization and further elimination of endogenous or exogenous damaging agent
Rodriguez-Rosales showed that the quantity of all the subpopulations of monocytes in circulation is noticeably decreased during sepsis
Subpopulations of monocytes play an essential role in formation of antibacterial defense of the organism
Summary
Systemic inflammatory response syndrome (SIRS) is excessive protective reaction of the body on a damaging stress factor (infection, trauma, surgery, or acute inflammation) for localization and further elimination of endogenous or exogenous damaging agent. Excessive inflammatory reactions lead to cell and tissue damage leading to dysfunction of organs and even multiple organ failure Another threat of such inflammation is the subsequent formation of immunosuppressive condition that facilitates the development of secondary infections [2]. We regard SI as an important part of generalized nonregulated inflammatory response progression of infectious origin leading to development of sepsis. A large group of patients is needed for clinical trials to determine the effects of the undertaken interventions. The goal of the current review is comparison of the behaviour of monocyte subpopulations during EE and sepsis focusing on the possibilities and limitations of extrapolation of the results obtained on the model onto the real clinical conditions
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