Acinetobacter baumannii (A. baumannii) causes autophagy flux disorder by degrading STX17, resulting in a serious inflammatory response. It remains unclear whether STX17 can alter the inflammatory response process by controlling autolysosome function. This study aimed to explore the role of STX17 in the regulation of pyroptosis induced by A. baumannii. Our findings indicate that overexpression of STX17 enhances autophagosome degradation, increases LAMP1 expression, reduces Cathepsin B release, and improves lysosomal function.
Conversely, knockdown of STX17 suppresses autophagosome degradation, reduces LAMP1 expression, augments Cathepsin B release, and accelerates lysosomal dysfunction. In instances of A. baumannii infection, overexpression of STX17 was found to improve lysosomal function and reduce the expression of mature of GSDMD and IL-1β, along with the release of LDH, thus inhibiting pyroptosis caused by A.
baumannii. Conversely, knockdown of STX17 led to increased lysosomal dysfunction and further enhanced the expression of mature of GSDMD and IL-1β, and increased the release of LDH, exacerbating pyroptosis induced by A. baumannii. These findings suggest that STX17 regulates pyroptosis induced by A. baumannii by modulating lysosomal function.
Co-infection of respiratory tract viruses and bacteria often result in excess mortality, especially pneumonia caused by influenza
viruses and Streptococcus pneumoniae. However, the synergistic mechanisms remain poorly understood. Therefore, it
is necessary to develop a clearer understanding of the molecular basis of the interaction between influenza virus and Streptococcus
pneumonia. Here, we developed the BALB/c mouse model and the A549 cell model to investigate inflammation
and pyroptotic cell death during co-infection. Co-infection significantly activated the NLRP3 inflammasome and induced
pyroptotic cell death, correlated with excess mortality. The E3 ubiquitin ligase NEDD4 interacted with both NLRP3 and
GSDMD, the executor of pyroptosis. NEDD4 negatively regulated NLRP3 while positively regulating GSDMD, thereby
modulating inflammation and pyroptotic cell death. Our findings suggest that NEDD4 may play a crucial role in regulating
the GSDMD-mediated pyroptosis signaling pathway. Targeting NEDD4 represents a promising approach to mitigate excess
mortality during influenza pandemics by suppressing synergistic inflammation during co-infection of influenza A virus and
Streptococcus pneumoniae.
Overexpression of DTX1 inhibits D-GalN/TNF-α-induced pyroptosis and inflammation in hepatocytes by regulating NLRP3 ubiquitination Mingshui Liu, Jing Gu, Li Chen, Wei Sun, Xiaoping Huang, Jianhe Gan Toxicology Research.2024;[Epub] CrossRef
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Mengpei Guo , Xiaolong Ma , Yan Zhou , Yinbing Bian , Gaolei Liu , Yingli Cai , Tianji Huang , Hongxia Dong , Dingjun Cai , Xueji Wan , Zhihong Wang , Yang Xiao , Heng Kang
J. Microbiol. 2023;61(1):83-93. Published online February 1, 2023
The basidiomycetous edible mushroom Stropharia rugosoannulata has excellent nutrition, medicine, bioremediation, and
biocontrol properties. S. rugosoannulata has been widely and easily cultivated using agricultural by-products showing strong
lignocellulose degradation capacity. However, the unavailable high-quality genome information has hindered the research
on gene function and molecular breeding of S. rugosoannulata. This study provided a high-quality genome assembly and
annotation from S. rugosoannulata monokaryotic strain QGU27 based on combined Illumina-Nanopore data. The genome
size was about 47.97 Mb and consisted of 20 scaffolds, with an N50 of 3.73 Mb and a GC content of 47.9%. The repetitive
sequences accounted for 17.41% of the genome, mostly long terminal repeats (LTRs). A total of 15,726 coding gene
sequences were putatively identified with the BUSCO score of 98.7%. There are 142 genes encoding plant cell wall degrading
enzymes (PCWDEs) in the genome, and 52, 39, 30, 11, 8, and 2 genes related to lignin, cellulose, hemicellulose, pectin,
chitin, and cutin degradation, respectively. Comparative genomic analysis revealed that S. rugosoannulata is superior in
utilizing aldehyde-containing lignins and is possible to utilize algae during the cultivation.
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Inflammatory responses involve the action of inflammatory
mediators that are necessary for the clearance of invading bacterial
pathogens. However, excessive production of inflammatory
mediators can damage tissues, thereby impairing bacterial
clearance. Here, we examined the effects of Weigela florida
on the expression of inflammatory cytokines induced by
Pseudomonas aeruginosa or Staphylococcus aureus infection
in macrophages. The results showed that pre-treatment with
W. florida markedly downregulated the bacterial infectionmediated
expression of cytokines. Additionally, post-treatment
also triggered anti-inflammatory effects in cells infected
with S. aureus to a greater extent than in those infected with
P. aeruginosa. Bacterial infection activated inflammation-associated
AKT (Thr308 and Ser473)/NF-κB and MAPK (p38,
JNK, and ERK) signaling pathways, whereas W. florida treatment
typically inhibited the phosphorylation of AKT/NF‐κB
and p38/JNK, supporting the anti‐inflammatory effects of
W. florida. The present results suggest that W. florida decreases
the infection-mediated expression of inflammatory
mediators by inhibiting the AKT/NF-κB and MAPK signaling
pathways, implying that it may have potential use as an
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worldwide; however, antimicrobial resistance (AMR)
is a global challenge. The β-lactam resistance in Gram-negative
bacteria is due to the production of β-lactamases, including
extended-spectrum β-lactamases, metallo-β-lactamases,
and carbapenem-hydrolyzing class D β-lactamases.
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