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Aims. Hyperlipidaemia model animals have been used to elucidate the role of Chlamydia pneumoniae (Cpn) infection in atherosclerosis. The aims of this study were to investigate the proatherogenic effect of multiple Cpn infections in ApoB100only/LDLR−/− mice which based on lipid profile can be regarded as the most suitable mouse model of human hypercholesterolemia and to compare the lesion development to that in a major atherosclerosis model ApoE−/− mice. Methods and Results. Aorta samples of ApoB100only/LDLR−/− mice infected three times with Cpn were subjected to morphometric analyses. Morphometric evaluation disclosed that Cpn infections exacerbated atherosclerosis development in the aortic root and descending aorta of the mice fed with normal diet. Viable Cpn was detected in the ascending aorta by RT-PCR. Chlamydial 16SrRNA expression showed the presence of viable Cpn in the aorta of infected animals. A similar rate of acceleration of atherosclerosis was observed when the infection protocol was applied in ApoB100only/LDLR−/− and in ApoE−/− mice. Conclusion. Similar to ApoE−/− mice, ApoB100only/LDLR−/− mice with more human-relevant serum lipoprotein composition develop increased atherosclerosis after Cpn infections; thus this mouse strain can be used as a model of infection-related atherosclerosis enhancement and can provide further evidence for the proatherogenic influence of Cpn in mice. [ABSTRACT FROM AUTHOR]

Selenoesters and the selenium isostere of phthalic anhydride are bioactive selenium compounds with a reported promising activity in cancer, both due to their cytotoxicity and capacity to reverse multidrug resistance. Herein we evaluate the antiviral, the biofilm inhibitory, the antibacterial and the antifungal activities of these compounds. The selenoanhydride and 7 out of the 10 selenoesters were especially potent antiviral agents in Vero cells infected with herpes simplex virus-2 (HSV-2). In addition, the tested selenium derivatives showed interesting antibiofilm activity against Staphylococcus aureus and Salmonella enterica serovar Typhimurium, as well as a moderate antifungal activity in resistant strains of Candida spp. They were inactive against anaerobes, which may indicate that the mechanism of action of these derivatives depends on the presence of oxygen. The capacity to inhibit the bacterial biofilm can be of particular interest in the treatment of nosocomial infections and in the coating of surfaces of prostheses. Finally, the potent antiviral activity observed converts these selenium derivatives into promising antiviral agents with potential medical applications. [ABSTRACT FROM AUTHOR]

Urogenital tract infection caused by obligate intracellular bacterium Chlamydia trachomatis D (CtrD) is a leading cause of sexually transmitted diseases. Essential oil (EO) of Nigella sativa has a broad antimicrobial spectrum. The aim of this study was to evaluate the antimicrobial activity of the bioactive compounds (p-cymene, thymoquinone, carvacrol, and thymol) of N. sativa EO against CtrD. The cytotoxic effects of the compounds were determined by MTT assay. In order to quantify the anti-chlamydial activity of the compounds, HeLa cells were infected with CtrD or CtrD treated previously with the compounds. The titer of the infectious CtrD was determined by indirect immunofluorescence assay. The minimum inhibitory concentrations of the compounds were evaluated by direct quantitative PCR. None of the compounds showed a cytotoxic effect on HeLa cells in the concentrations tested. According to the immunofluorescence assay, all of the compounds significantly inhibited the growth of CtrD. The quantitative PCR revealed that the minimum concentration that exerted anti-chlamydial activity was 3.12 µM in the case of thymoquinone and p-cymene, while that of carvacrol and thymol was 6.25 µM. Therefore, it can be concluded that bioactive compounds of N. sativa EO could be used as effective antimicrobial agents against CtrD. [ABSTRACT FROM AUTHOR]

Aims: Hyperlipidaemia model animals have been used to elucidate the role of Chlamydia pneumoniae (Cpn) infection in atherosclerosis. The aims of this study were to investigate the proatherogenic effect of multiple Cpn infections in ApoB100only/LDLR -/- mice which based on lipid profile can be regarded as the most suitable mouse model of human hypercholesterolemia and to compare the lesion development to that in a major atherosclerosis model ApoE -/- mice., Methods and Results: Aorta samples of ApoB100only/LDLR -/- mice infected three times with Cpn were subjected to morphometric analyses. Morphometric evaluation disclosed that Cpn infections exacerbated atherosclerosis development in the aortic root and descending aorta of the mice fed with normal diet. Viable Cpn was detected in the ascending aorta by RT-PCR. Chlamydial 16SrRNA expression showed the presence of viable Cpn in the aorta of infected animals. A similar rate of acceleration of atherosclerosis was observed when the infection protocol was applied in ApoB100only/LDLR -/- and in ApoE -/- mice., Conclusion: Similar to ApoE -/- mice, ApoB100only/LDLR -/- mice with more human-relevant serum lipoprotein composition develop increased atherosclerosis after Cpn infections; thus this mouse strain can be used as a model of infection-related atherosclerosis enhancement and can provide further evidence for the proatherogenic influence of Cpn in mice.

Background: Pathogens can influence allergic respiratory diseases. We previously found that multiple infections with Chlamydophila pneumoniae induce the production of interleukin-17A (IL-17A) and IL-17E, which have roles in the pathogenesis of asthma. The present work was designed to investigate our hypothesis that infections with another pathogen can induce the production of IL-17A and IL-17E., Materials and Methods: At an internal of 28 days, mice were infected twice with Chlamydia muridarum; the kinetics of IL-17A and IL-17E expression was subsequently determined at the mRNA and protein levels. The amounts of IL-17 cytokines produced by the stimulated spleen cells were determined by enzyme-linked immunosorbent assay (ELISA). The presence of IL-17E in the lungs was revealed by an indirect immunofluorescence test., Results: The infection with C. muridarum induced the production of IL-17A at the early stages of infection. The quantity of IL-17E was highest on days 28 and 56 after the first infection (28 days after the second infection). In the later stages of infection, IL-17E was produced by epithelial cells. The re-stimulated peripheral spleen cells produced IL-17A., Conclusion: Multiple infection with C. muridarum induces the production of a high amount of IL-17E, which plays an important part in the pathogenesis of allergic pulmonary diseases.