Accessing occupational exposure to fungi in a cork industry

In this study we aimed to access fungal exposure in workers from one cork industry through the mycological analysis of their nasal exudate and the environmental fungal contamination of their surroundings as well. Nasal mucous samples from 127 workers were taken with sterilized cotton swabs.The fungal species identified in the collected nose swabs were shown to be correlated with the results obtained in the environment. Eighty workers (63.0%) presented contamination of their nose nostril with Chrysonilia sitophila, which number of colonies was countless. Within the Aspergillus genus, the complexes Fumigati, Circumdati, Versicolores and Candidi were isolated. No azole-resistant Aspergillus isolates grew in the selective media used (screened itraconazole and voriconazole resistance).This approach allowed us to estimate the risk associated with these tasks performance. Moreover, the cork industry is related to high dust contamination and this can promote exposure to fungi since dust particles can act as carriers of fungi to the worker’s nose. Assessment by molecular tools will ensure the specific targeting of DNA from P. glabrum complex in workers nose

γδ-T cells promote IFN-γ–dependent Plasmodium pathogenesis upon liver-stage infection

Cerebral malaria (CM) is a major cause of death due to Plasmodium infection. Both parasite and host factors contribute to the onset of CM, but the precise cellular and molecular mechanisms that contribute to its pathogenesis remain poorly characterized. Unlike conventional αβ-T cells, previous studies on murine γδ-T cells failed to identify a nonredundant role for this T cell subset in experimental cerebral malaria (ECM). Here we show that mice lacking γδ-T cells are resistant to ECM when infected with Plasmodium berghei ANKA sporozoites, the liver-infective form of the parasite and the natural route of infection, in contrast with their susceptible phenotype if challenged with P. berghei ANKA-infected red blood cells that bypass the liver stage of infection. Strikingly, the presence of γδ-T cells enhanced the expression of Plasmodium immunogenic factors and exacerbated subsequent systemic and brain-infiltrating inflammatory αβ-T cell responses. These phenomena were dependent on the proinflammatory cytokine IFN-γ, which was required during liver stage for modulation of the parasite transcriptome, as well as for downstream immune-mediated pathology. Our work reveals an unanticipated critical role of γδ-T cells in the development of ECM upon Plasmodium liver-stage infection.info:eu-repo/semantics/publishedVersio

RNA Interference Knockdown of hU2AF(35) Impairs Cell Cycle Progression and Modulates Alternative Splicing of Cdc25 Transcripts

U2AF is a heterodimeric splicing factor composed of a large (U2AF(65)) and a small (U2AF(35)) subunit. In humans, alternative splicing generates two U2AF(35) variants, U2AF(35)a and U2AF(35)b. Here, we used RNA interference to specifically ablate the expression of each isoform in HeLa cells. Our results show that knockdown of the major U2AF(35)a isoform reduced cell viability and impaired mitotic progression, leading to accumulation of cells in prometaphase. Microarray analysis revealed that knockdown of U2AF(35)a affected the expression level of ∼500 mRNAs, from which >90% were underrepresented relative to the control. Among mRNAs underrepresented in U2AF(35)a-depleted cells we identified an essential cell cycle gene, Cdc27, for which there was an increase in the ratio between unspliced and spliced RNA and a significant reduction in protein level. Furthermore, we show that depletion of either U2AF(35)a or U2AF(35)b altered the ratios of alternatively spliced isoforms of Cdc25B and Cdc25C transcripts. Taken together our results demonstrate that U2AF(35)a is essential for HeLa cell division and suggest a novel role for both U2AF(35) protein isoforms as regulators of alternative splicing of a specific subset of genes