The pathophysiology of Q fever endocarditis is characterized by the suppression of antigen-specific cell-mediated immune responses. We investigated the production of interleukin-10 (IL-10) and transforming growth factor beta (TGF-beta), known to interfere with the development of protective cell immunity. IL-10 was markedly released by unstimulated peripheral blood mononuclear cells (PBMC) from patients with Q fever endocarditis. This release resulted from the upregulation of IL-10 gene transcription. Similarly, the release of TGF-beta1 and TGF-beta2 was significantly higher in patient PBMC than in control cells, but the expression of their respective mRNA was not enhanced in patient cells. In contrast, lipopolysaccharide-stimulated transcription and release of IL-10 and TGF-beta were similar in patients and controls. The release of IL-10 by PBMC but not that of TGF-beta was correlated with the clinical status of the patients. First, IL-10 production was correlated with specific antibody levels. Second, IL-10 release remained elevated in patients prone to relapse. Taken together, our results suggest that the release of IL-10 and TGF-beta is upregulated in Q fever endocarditis. IL-10 might be considered as a marker of disease relapses and might be instrumental in monitoring the efficiency of the treatment.

The occurrence of Q fever endocarditis likely involves some alterations in the responses of monocytes, the in vivo targets of Coxiella burnetii. To test this hypothesis, the production of the inflammatory cytokines tumor necrosis factor alpha, interleukin-1␤, and interleukin-6 was assessed in monocytes from patients with Q fever endocarditis. Spontaneous transcription and secretion of tumor necrosis factor and interleukin-1 were significantly higher in patient monocytes than in healthy controls. The interleukin-6 transcripts were also upregulated in patient cells. Moreover, in patients with recent endocarditis exhibiting high titers of immunoglobulin G directed to C. burnetii in phase I, monocytes released significantly higher levels of tumor necrosis factor and interleukin-1 than in patients with stabilized endocarditis. Immunoglobulin G titers and the overproduction of tumor necrosis factor and interleukin-1 were significantly correlated. Hence, the overproduction of inflammatory cytokines might be a marker of disease activity.

A well designed targeted chemotherapy is considered one of the goals of anticancer treatment, significantly improving the survival rate, but there is evidence suggesting it may presents significant drawbacks. Oxidative stress is frequently associated with chemotherapeutic agents, generating increased reactive oxygen species which may alter the female genital system. There are numerous opinions suggesting supplemental antioxidants in chemotherapy represent a positive therapeutic strategy. This study aim was to assess if antioxidants as zinc are able to preserve female rat�s genital system in cyclophosphamide (CP) - induced oxidative stress. In experiment there was used 21 female Wistar rats which were randomly divided in three groups: control, cyclophosphamide - administered group and cyclophosphamide-ZnCl2 administered group. After four weeks, blood was collected to determine malondialdehyde (MDA) level and glutathione peroxidase (GPx) activity. Our results suggests that zinc reduces the deleterious effect of oxidative stress on female rats genital system, the decrease of MDA level together with GPx increase being considered as a result of Zn administration.

AbstractApelin (AP) and leptin (LEP) are adipokines with vasomotor actions. Taking into account the published data on the role of obesity in the development of pulmonary hypertension, we studied the implications of apelin on leptin relaxing effects on isolated rat pulmonary arteries. LEP had vasodilatatory effects on phenylephrine-precontracted rat pulmonary arteries from normal and ovalbumin-sensitized rats, but not on rats with monocrotaline-induced pulmonary hypertension. AP13 pretreatment increased LEP effects by one-half. Our studies revealed the existence of synergistic favorable effects of these adipokines on pulmonary vessels.