Mitochondrial movement and distribution throughout the cytoplasm is crucial for maintaining cell homeostasis. Mitochondria are dynamic organelles but can be functionally disrupted during infection. Here, we show that the ubiquitous human pathogens HHV-1 and HHV-2 induce changes in the mitochondrial morphology and distribution in the early and late phases of productive infection in human keratinocytes (HaCaT cells). We observed a decrease in the mitochondrial potential at 2 h postinfection and a decrease in cell vitality at 24 h postinfection. Moreover, we found that mitochondria migrated to the perinuclear area, where HHV-1 and HHV-2 antigens were also observed, mainly in the early stages of infection. Positive results of real-time PCR showed a high level of HHV-1 and HHV-2 DNA in HaCaT cells and culture medium. Our data demonstrate that HHV-1 and HHV-2 cause mitochondrial dysfunction in human keratinocytes.

Iron is the crucial element for living organisms and its deficiency is described as the most common nutritional disorder all over the world. Nowadays, more effective and safe iron supplementation strategies for both humans and animals become one of the most important challenges in the therapy of nutritional deficiencies. Our previous in vivo studies confirmed safety and biodegradability of in-house manufactured zinc oxide-based nanoparticles and their rapid distribution to majority of organs and tissues in the body. In vitro examinations performed on Caco-2 cell line, a model of epithelial cells of the gastrointestinal tract, revealed a low toxicity of studied nanomaterials. In the current study, we investigated biodegradable zinc oxide nanoparticles doped with Fe(III) as a perspective supplementation strategy for iron deficiency. Biodegradable ZnO:Fe nanoparticles were intra-gastrically administered to adult mice and following 24 h, animals were sacrificed with collection of internal organs for further analyses. The iron concentration measured with atomic absorption spectrometry and histological staining (Perl’s method) showed a rapid distribution of iron-doped nanoparticles to tissues specifically related with iron homeostasis. Accumulation of iron was also visible within hepatocytes and around blood vessels within the spleen, which might indicate the transfer of Fe-doped nanoparticles from the bloodstream into the tissue. Reassuming, preliminary results obtained in the current study suggest that biodegradable ZnO nanoparticles doped with Fe might be a good carriers of exogenous iron in the living body. Therefore, subsequent investigations focus on determination an exact mechanisms related with an iron deposition in the tissue and influence of nanoparticle carriers on iron metabolism are required.

Campylobacter jejuni is a bacterial pathogen that is generally acquired as a zoonotic infection from poultry and animals. Adhesion of C. jejuni to human colorectal epithelial cells is weakened after loss of its cj0588 gene. The Cj0588 protein belongs to the type I group of TlyA (TlyA I ) enzymes, which 2 0 -O-methylate nucleotide C1920 in 23S rRNA. Slightly longer TlyA II versions of the methyltransferase are found in actinobacterial species including Mycobacterium tuberculosis, and methylate not only C1920 but also nucleotide C1409 in 16S rRNA. Loss of TlyA function attenuates virulence of both M. tuberculosis and C. jejuni. We show here that the traits impaired in C. jejuni null strains can be rescued by complementation not only with the original cj0588 (tlyA I ) but also with a mycobacterial tlyA II gene. There are, however, significant differences in the recombinant phenotypes. While cj0588 restores motility, biofilm formation, adhesion to and invasion of human epithelial cells and stimulation of IL-8 production in a C. jejuni null strain, several of these properties are further enhanced by the mycobacterial tlyA II gene, in some cases to twice the original wild-type level.These findings strongly suggest that subtle changes in rRNA modification patterns can affect protein synthesis in a manner that has serious consequences for bacterial pathogenicity. K E Y W O R D S bacterial motility, biofilms, capreomycin resistance, epithelial cell invasion, rRNA 2 0 -Omethylation

SummaryEquine herpesvirus type 1 (EHV-1) is a major viral pathogen of horses, causing respiratory disease, abortions, and equine herpes myeloencephalopathy (EHM). Like other alphaherpesviruses, EHV-1 establishes latency in neurons, but mechanisms involved in this process are still elusive. In the present study, we used antiviral drug acyclovir (ACV) to completely suppress EHV-1 replication in primary murine neuron culture. Trichostatin A (TSA), a known chemical reactivator of other herpesviruses, was used to stimulate productive EHV-1 infection. Moreover, gene expression of some cytokines was simultaneously evaluated, in order to check, whether the maintenance conditions of such a model may influence host cell response. Changes observed in IFN-α, IFN-β, and IL-10 mRNA gene expression depended on the EHV-1 strain. Although infection with either of the two EHV-1 strains investigated led to in an increase in type I IFNs gene expression, only the neuropathogenic strain caused a decrease in anti-inflammatory IL-10 gene expression. Unlike EHV-1 infection, the addition of neither ACV nor TSA caused significant changes in the expression of the above genes. We may therefore conclude that the in vitro model presented in the study is suitable for detailed investigation of the host cell-virus relationship on the molecular level.