Background: Cryptococcus neoformans is the most common cause of fungal meningitis among individuals with HIV/AIDS, which is uniformly fatal without proper treatment. The underlying mechanism of disease development in the brain that leads to cryptococcal meningoencephalitis remains incompletely understood. We have previously demonstrated that inositol transporters (ITR) are required for Cryptococcus virulence. The itr1aΔ itr3cΔ double mutant of C. neoformans was attenuated for virulence in a murine model of intra-cerebral infection; demonstrating that Itr1a and Itr3c are required for full virulence during brain infection, despite a similar growth rate between the mutant and wild type strains in the infected brain.
Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis disease (TB), is a typical intracellular pathogen. Mtb has evolved sophisticated strategies to adapt to a variety of stresses. MarR-family transcription factors are involved in resistance towards external survival stresses and can regulate the transcription of multidrug efflux pumps and antioxidant enzymes in other organisms. However, whether and how Mtb MarR-family transcription factors are involved in stress responses remains elusive. In this study, we have characterized the role and mechanism of action of the MarR-type transcriptional factor Rv3095 in the response to oxidative stress by using hxlR deletion mutant and MSMEG_6581 deletion strain. The qRT-PCR results showed that HxlR repressed transcription of MSMEG_6581, and the transcription levels of hxlR and MSMEG_6581 were increased with increased concentration of H2O2. The EMSA results showed that HxlR could bind to the promoters of target genes. HxlR dimers could further form tetramer via the disulfide bonds under oxidative stress, resulting in derepression of target genes transcription. The point-mutation results identified that HxlRC11A mutant protein was impaired in oligomerization, and ultimately impacted the DNA-binding activity, which indicating a specific role of Cys11 in redox sensing. Phenotype results indicated that hxlR or MSMEG_6581 could alter the sensitivity of bacteria towards H2O2 disinfectants. In conclusion, HxlR was identified as a novel redox-sensitive transcription factor involved in mycobacteria resistance to H2O2 via unique mode.
Background Perforated duodenal ulcer is a common condition. The associated microbiome and relationship with treatment success remain to be explored in addition to the well recognized role of Helicobacter pylori.Methods Metagenomic sequencing were used to profile the microbes underlying duodenal ulcer. The metagenome results of 6 duodenal ulcer samples (3 ulcer foci and 3 sites around the ulcer foci) were obtained and compared.Findings Ulcer patients and healthy control have different gut-type. Streptococcus mitis was highly enriched in duodenal ulcer patients.Interpretation The dysbiosis of microbiomes might underlie the duodenal ulcer, while the increased abundance of Streptococcus mitis is a novel finding. Whether there is causal link between S.mitis and duodenal ulcer remains to be determined.
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