• 23
    Nov
  • The Influence of G-CSF Addition to Antibiotic Treatment

The Influence of G-CSF Addition to Antibiotic Treatment

INTRODUCTION

Sepsis is characterized by infection and a generalized systemic inflammatory response syndrome (SIRS), ultimately leading to multiple organ dysfunction syndrome (MODS) and death. During sepsis, the lungs are especially susceptible to damage, and a progressively impaired lung function is the first major complication in sepsis. Traditionally, strategies aiming at preventing or treating sepsis have involved measures to minimize the risk of infection, and the use of antibiotics drugs to combat bacterial infections. However, the incidence of reported cases of sepsis in hospitals is dramatically increasing. Therefore, new therapeutic agents and approaches are needed.

Recently, the application of granulocyte colony-stimulating factor (G-CSF), a cytokine that stimulates granulopoiesis and enhances the activation of mature neutrophils against infectious diseases, has been considered, and a number of animal experiments have been carried out to support such an application. Moreover, when added to normal neutrophils in vitro, recombinant human G-CSF (rhG-CSF) has been shown to increase cellular receptors for adhesion and phagocytosis, to enhance chemotactic responses and phagocytosis, to prime cells for oxidative responses and to increase microbicidal activities, because neutrophil numbers and functions are pivotal in ensuring recovery from infection and, consequently, survival. However, despite the majority of these experiments being performed with G-CSF, very little is known about the detailed mechanisms of the therapeutic efficacy of G-CSF in an experimental infection model. The administration of G-CSF in combination with after the induction of infection has been investigated to a limited extent, with conflicting results. Investigations concerning the mechanisms underlying the beneficial effects of G-CSF in nonneu-tropenic infectious disease models are based primarily on the circulating neutrophils.

We conducted the present experiment using a well-established model of sepsis to simultaneously examine the therapeutic effects of G-CSF on neutrophil counts in both the vascular and lung tissues. The aim of the study was to investigate the effects of antibiotic therapy alone, G-CSF treatment alone, and G-CSF and a combination antibiotic (levaquin 750mg class of medicines known as fluoroquinolone antibiotics) therapy on the levels of circulating neutrophils and in the lung tissue, which may be one of the mechanisms underlying the therapeutic effects of G-CSF during sepsis.

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