Abstract
Sepsis is an immunologic disorder with a high rate of mortality which is caused by the exacerbation of the inflammatory response. The purpose of this study was to characterise the etiologic spectrum and the profile of the most significant pro-inflammatory and anti-inflammatory citokines in patients with sistemic infections, by analysing the relationship between the type of etiologic agents and the intensity of the inflammatory response. The study was carried out on a number of 33 patients with systemic infections who were hospitalized in the �Saint Parascheva �Infectious Diseases Clinic Hospital in Galati, Romania. The intensity of the inflammatory response was higher in the sepsis with Gram-negative Bacilli (BGN) as compared to the systemic infections produced by Gram-positive Cocci (CGP). In the case of the patients with bacterial etiology (CGP and BGN) there was evidence of an increase levels of analysed cytokines (TNF-a, IL-1, IL-4, IL-6, IL-10), while the fungal etiology was correlated with high serum concentrations of TNF-a. The levels of IL-4 and IL-6 were similar in all patients with systemic infections, regardless of their etiology. The Klebsiella pneumoniae sepsis has led to the occurrennce of high serum levels both in the case of pro-inflammatory and anti-inflammatory citokines. The obtained results outline the necessity of monitoring pro-inflammatory and anti- inflammatory cytokines in sepsis, which might provide clues about the intensity of the generalized inflammatory reaction, representing not only an important diagnosis criteria but also a useful guide in the therapeutic methods chosen and the monitoring of these severe infections.
Highlights
Sepsis has an ever-growing incidence constituting the main cause of mortality in the Intensive Care wards and the third cause of mortality in the developed countries, being to some extent equal with the number of deaths caused by acute myocardial infarction [1,2]
More than one in four deaths are caused by sepsis every year in the world [3]
Systemic infections are triggered by etiologic agents, most often a bacterial type and their virulence factors but are maintained and modulated by a multitude of endogenous immunological mediators activated in a flow of complex cellular and humoral actions
Summary
Sepsis has an ever-growing incidence constituting the main cause of mortality in the Intensive Care wards and the third cause of mortality in the developed countries, being to some extent equal with the number of deaths caused by acute myocardial infarction [1,2]. Systemic infections are triggered by etiologic agents, most often a bacterial type and their virulence factors (infectivity, aggression, toxigenity) but are maintained and modulated by a multitude of endogenous immunological mediators activated in a flow of complex cellular and humoral actions. The cells of innate activated immunity induce an acute inflammatory response which is triggered by the means of pro-inflammatory cytokines and of anti-inflammatory ones which regulate the inflammatory answer [4]. The synthesis and excessive release of these circular mediators can lead to side effects harmful to the body, i.e.: the uncontrolled activation of different leukocyte subpopulations, of the complement system, of the coagulation activation pathways and of the fibrinolytic system which can generate microvascular lesions, tissue ischemia, organ dysfunctions and to the patient’s death [7,8]
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