The iron acquisition system is an essential virulence factor for human infection and is under tight regulatory control in a variety of pathogens. Ferric-uptake regulator (Fur) is one of Fe 2+-responsive transcription factor that maintains iron homeostasis, and the regulator of capsule synthesis (Rcs) is known to regulate exopolysaccharide biosynthesis. We speculate the Rcs may involve in iron-acquisition given the identified regulator box in the upstream of entC that participated in the biosynthesis of enterobactin. To study the coregulation by RcsAB and Fur of entC, we measured the β-galactosidase activity and relative mRNA expression of entC in WT and mutant strains. The RcsAB-and Fur-protected regions were identified by an electrophoretic mobility shift assay (EMSA) and a DNase I footprinting assay. A regulatory cascade was identified with which Fur repressed rcsA expression and reduced RcsAB and entC expression. Our study demonstrated that entC was coregulated by two different transcriptional regulators, namely, RcsAB and Fur, in response to iron availability in Klebsiella pneumoniae.
Lung infection (LI) often occurs in patients with liver transplantation (LT). This meta‐analysis was conducted to determine the risk factors associated with LI after LT. We retrieved relevant research published as of February 2020 from eight electronic databases. The studies were reviewed against the inclusion and exclusion criteria. The Z test was used to determine the combined odds ratio (OR) or the standardized mean difference (SMD) of the risk factors. We used the OR and its corresponding 95% confidence interval (CI) or the SMD and its corresponding 95% CI to identify significant differences in risk factors. A total of nine studies were included, comprising a total of 1624 recipients. Six risk factors associated with LI were identified after LT: Model for end‐stage liver disease score (MELD score) (SMD = 0.40), Child‐Pugh class C (OR = 3.00), intensive care unit (ICU) hospital stay (SMD = 1.35), mechanical ventilation (SMD = 1.03), bilirubin (SMD = 0.39), and atelectasis (OR = 7.28). Although certain risk factors have been identified as important factors for LI after LT, which may provide a basis for clinical prevention, a well‐designed prospective study should be conducted to validate the findings of this study.
Hypervirulent
Klebsiella pneumoniae
(hvKP) has been increasingly reported over the past three decades and causes severe infections. To increase our understanding of hvKP at the genome level, genome sequencing and comparative genome analysis were performed on 6 hvKPs. The whole genome DNA from 6 hvKPs with different capsular serotypes isolated in China was extracted. The genome sequencing and assembly results showed the genome size of the six hvKPs and GC content. Comparative analyses of the genomes revealed the gene homology and genome rearrangement in the 6 hvKPs compared with
Klebsiella pneumonia
NTUH-K2044. The phylogenetic tree based on full-genome SNPs of the 7 hvKPs showed that NTUH-K2044 formed a single clade, showing distant evolutionary distances with the other six strains, and the non-K1 hvKP strains had a relatively closer phylogenetic relationship. BLAST comparison analysis found that some selected virulence genes had different degrees of deletion in the non-K1 hvKPs. SNP-based virulence gene mutation analysis showed that some virulence genes had different degrees of SNP mutations. The whole-genome sequencing and comparative genome analysis of six hvKP strains with NTUH-K2044 provide us with a basic understanding of the genome composition, genetic polymorphism, evolution and virulence genes of hvKP and a basis for further research on these genes and the pathogenesis of hvKP.
Supplementary Information
The online version contains supplementary material available at 10.1007/s00203-021-02263-0.
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