The effect of cetirizine on IFN-gamma and IL-10 production in children with allergic rhinitis.

Cetirizine, one of the most commonly used antihistamines for the treatment of allergic diseases, possesses some anti-inflammatory properties. Despite its common use, the effect of cetirizine on the production of cytokines from peripheral blood mononuclear cells (PBMCs) needs further clarification. The aim of this study was to investigate whether cetirizine changes interleukin (IL)-10, (IF)-gamma and IL-4 production from PBMCs in children with allergic rhinitis. Thirteen children with allergic rhinitis sensitized to house dust mite (HDM) were treated with cetirizine for four weeks. Blood samples were drawn just prior to the treatment, on the last day of the treatment and two weeks following the cessation of treatment The cytokine production from PBMCs was tested in the presence or absence of HDM allergen and measured by ELISA assay. An augmentation in IL-10 production was observed in PBMCs at the 4th week of cetirizine treatment (p<0.05). Furthermore, a significant increase in IFN-gamma production was observed following the therapy. IL-4 release did not change at all time points tested. In addition, IFN-gamma/IL-4 ratio increased following cetirizine treatment. Cetirizine induced a shift in the human Th1/Th2 cytokine balance toward a Th1 type response by increasing IFN-gamma production and augmenting suppressor cytokine release (IL-10). We concluded that apart from its known antihistaminic properties, cetirizine may modulate allergic inflammation while the patients are on regular treatment schedules.

Rapid decline of anti-pneumococcal antibody levels in nephrotic children.

Nephrotic children are at increased risk for pneumococcal infections. Antibody responses to the currently recommended pneumococcal polysaccharide vaccine have been variable and maintenance of adequate antibody levels over time has not been well documented. In this study, we determined total IgG antibody levels against pneumococcal polysaccharides before and 1, 6, 12 and 36 months after 23-valent pneumococcal polysaccharide vaccine (PPV) administration in nine children with steroid-responsive nephrotic syndrome during remission while off corticosteroids. The baseline antibody levels were between 4 and 86 mg/l. Four weeks after vaccination, the titer increased at least twofold in all patients with a mean arithmetic value of 165.4 mg/l. At the 6th month, the levels decreased in six out of nine subjects to a mean of 94.6 mg/l. At the 36th month, the control antibody levels were below the baseline or below the early postvaccination values in four out of nine subjects. Only two patients had stable high concentrations through the study period. Our data show that nephrotic patients may not retain their antibody levels despite reasonably good initial responses to the pneumococcal vaccine and that susceptibility to infections may continue in vaccinated children.

Apoptosis of cord blood neutrophils and their response to colony-stimulating factors.

Neutrophil production and functions are immature in newborns. Although neutrophil kinetics during neonatal period have been widely studied, little is known about the effect of apoptosis on these defects. In this study, we examine the apoptosis of neonatal neutrophils and the effects of colony-stimulating factors (CSF) on this process. The study was performed using three different methodologies (morphological analysis, surface Fas expression, and mitochondrial 7A6 antigen expression) and the results were compared with adult controls. Neonatal neutrophils more rapidly underwent apoptosis in comparison to adult neutrophils. The above-mentioned three different methods gave similar results. Granulocyte-CSF (G-CSF) and granulocyte-macrophage CSF (GM-CSF) decreased the apoptosis of neutrophils in newborns and adults. This effect was significantly more pronounced in adults than newborns in morphological analysis. Increased apoptosis may contribute to qualitative and quantitative defects of neutrophils during neonatal period and may be an explanation for the proneness of newborn to develop neutropenia during systemic infections.