Background and Purpose:MicroRNAs are small non-coding RNAs with 19-24 nucleotides in length. Up- or down-regulation of many miRNAs has been shown by stimulation of Toll-like receptors (TLRs) in the innate immune system. Up-regulation of miR-146a has been reported by both TLR and heat-killed Candida albicans. In this study, we aimed to evaluate the expression of miR-146a in cultured monocyte-derived macrophages (MDMs) infected by Candida glabrata at 12, 24, and 48 hours. Materials and Methods:miR-146a expression was evaluated by qRT-real time polymerase chain reaction (PCR) at three time points in C. glabrata-infected MDMs. The data was analyzed using repeated measures ANOVA.Results:miR-146a expression was down-regulated in infected MDMs compared to the control group (P<0.018). The expression of miR-146a was at its highest level at 48 h, as compared to 12 and 24 h (P<0.018) .The differences between the experimental group compared to the control group were statistically significant (P<0.018). Conclusion:These results suggest that miR-146a can be involved in regulating macrophage function following TLR stimulation in C. glabrata-infected MDMs.

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Background: Aspergillus fumigatus is the most common species causing invasive aspergillosis (IA), a lifethreatening infection with more than 80% mortality. Interactions between A. fumigatus and human blood platelets lead to intravascular thrombosis and localized infarcts. To better understand A. fumigatus pathogenesis, we aimed to analyze the genetic basis of interactions between the pathogen and blood platelets. Methods: A bioinformatic pipeline on microarray gene expression dataset, including analysis of differentially expressed genes (DEGs) using Limma R package and their molecular function, as well as biological pathways identification, was conducted to find the effective genes involved in IA. In the wet phase, the gene expression patterns following fungal exposure to blood platelets at 15, 30, 60, and 180 min were evaluated by quantitative reverse transcriptase-PCR analysis. Results: Three genes encoding aspartic endopeptidases including (Pep1), (Asp f 13), and (β-glucanase) were the standing candidates. The invasion-promoting fungal proteinase-encoding genes were downregulated after 30 min of hyphal incubation with blood platelets, and then up-regulated at 60 and 180 min, although only Pep1 was greater than the control at the 60and 180 min time points. Also, the same genes were downregulated in more the clinical isolates relative to the standard strain CBS 144.89. Conclusions: Our findings delineate the possible induction of fungal-encoded proteinases by blood platelets. This provides a new research line into A. fumigatus' molecular pathogenesis. Such insight into IA pathogenesis might also guide researchers toward novel platelet-based therapies that involve molecular interventions, especially in IA patients.