Regulation of macrophage iron homeostasis is associated with the localization of bacteria

Metallomics ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 454-461 ◽  
Author(s):  
Zhenshun Gan ◽  
Xueyou Tang ◽  
Zhenjie Wang ◽  
Jiahui Li ◽  
Zhen Wang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Salmonella Typhimurium ◽  
Iron Homeostasis ◽  
Intracellular Bacteria ◽  
First Time

We describe, for the first time, the changes of iron homeostasis in response to the infection of macrophages with extracellular bacteriaEscherichia coliK88 and intracellular bacteriaSalmonella typhimurium.

Iso-octenidine: Promising Octenidine Analogue with Improved Solubility

2020 ◽  
Vol 17 ◽  
Author(s):  
Igor K. Yakuschenko ◽  
Nataliya N. Pozdeeva ◽  
Viktoriya A. Mumyatova ◽  
Alexey A. Terentiev ◽  
Svyatoslav Ya. Gadomsky
Keyword(s):  
Escherichia Coli ◽  
Antibacterial Activity ◽  
Micrococcus Luteus ◽  
Octenidine Dihydrochloride ◽  
First Time

: Iso-octenidine, an isomer of octenidine dihydrochloride, was synthesized and studied for the first time. Isooctenidine was demonstrated to be 3-fold more soluble in water in comparison to original octenidine, and both substances had remarkably similar antibacterial activity (tested on Escherichia Coli and Micrococcus luteus).

scholarly journals An infection-induced RhoB-Beclin 1-Hsp90 complex enhances clearance of uropathogenic Escherichia coli

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chunhui Miao ◽  
Mingyu Yu ◽  
Geng Pei ◽  
Zhenyi Ma ◽  
Lisong Zhang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Treatment Strategies ◽  
Uropathogenic Escherichia Coli ◽  
Beclin 1 ◽  
Host Cells ◽  
Infection Model ◽  
Intracellular Bacteria ◽  
Bladder Epithelium ◽  
Binding Residue

AbstractHost cells use several anti-bacterial pathways to defend against pathogens. Here, using a uropathogenic Escherichia coli (UPEC) infection model, we demonstrate that bacterial infection upregulates RhoB, which subsequently promotes intracellular bacteria clearance by inducing LC3 lipidation and autophagosome formation. RhoB binds with Beclin 1 through its residues at 118 to 140 and the Beclin 1 CCD domain, with RhoB Arg133 being the key binding residue. Binding of RhoB to Beclin 1 enhances the Hsp90-Beclin 1 interaction, preventing Beclin 1 degradation. RhoB also directly interacts with Hsp90, maintaining RhoB levels. UPEC infections increase RhoB, Beclin 1 and LC3 levels in bladder epithelium in vivo, whereas Beclin 1 and LC3 levels as well as UPEC clearance are substantially reduced in RhoB+/− and RhoB−/− mice upon infection. We conclude that when stimulated by UPEC infections, host cells promote UPEC clearance through the RhoB-Beclin 1-HSP90 complex, indicating RhoB may be a useful target when developing UPEC treatment strategies.

scholarly journals Structure of the master regulator Rns reveals an inhibitor of enterotoxigenic Escherichia coli virulence regulons

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Charles R. Midgett ◽  
Kacey Marie Talbot ◽  
Jessica L. Day ◽  
George P. Munson ◽  
F. Jon Kull
Keyword(s):  
Escherichia Coli ◽  
Small Molecules ◽  
Family Member ◽  
Shigella Flexneri ◽  
Decanoic Acid ◽  
Enterotoxigenic Escherichia Coli ◽  
Gram Negative Bacteria ◽  
Enteric Infections ◽  
First Time ◽  
Arac Family

AbstractEnteric infections caused by the gram-negative bacteria enterotoxigenic Escherichia coli (ETEC), Vibrio cholerae, Shigella flexneri, and Salmonella enterica are among the most common and affect billions of people each year. These bacteria control expression of virulence factors using a network of transcriptional regulators, some of which are modulated by small molecules as has been shown for ToxT, an AraC family member from V. cholerae. In ETEC the expression of many types of adhesive pili is dependent upon the AraC family member Rns. We present here the 3 Å crystal structure of Rns and show it closely resembles ToxT. Rns crystallized as a dimer via an interface similar to that observed in other dimeric AraC’s. Furthermore, the structure of Rns revealed the presence of a ligand, decanoic acid, that inhibits its activity in a manner similar to the fatty acid mediated inhibition observed for ToxT and the S. enterica homologue HilD. Together, these results support our hypothesis that fatty acids regulate virulence controlling AraC family members in a common manner across a number of enteric pathogens. Furthermore, for the first time this work identifies a small molecule capable of inhibiting the ETEC Rns regulon, providing a basis for development of therapeutics against this deadly human pathogen.

scholarly journals Deletion Formation Between the Two Salmonella typhimurium Flagellin Genes Encoded on the Mini F Plasmid: Escherichia coli ssb Alleles Enhance Deletion Rates and Change Hot-Spot Preference for Deletion Endpoints

Genetics ◽  
1997 ◽  
Vol 145 (3) ◽  
pp. 563-572 ◽  
Author(s):  
Takafumi Mukaihara ◽  
Masatoshi Enomoto
Keyword(s):  
Escherichia Coli ◽  
Salmonella Typhimurium ◽  
Hot Spots ◽  
Hot Spot ◽  
Direct Repeats ◽  
Replication Slippage ◽  
Detection Systems ◽  
Deletion Formation ◽  
Homologous Sequences ◽  
Deletion Detection

Deletion formation between the 5′-mostly homologous sequences and between the 3′-homeologous sequences of the two Salmonella typhimurium flagellin genes was examined using plasmid-based deletion-detection systems in various Escherichia coli genetic backgrounds. Deletions in plasmid pLC103 occur between the 5′ sequences, but not between the 3′ sequences, in both RecA-independent and RecA-dependent ways. Because the former is predominant, deletion formation in a recA background depends on the length of homologous sequences between the two genes. Deletion rates were enhanced 30- to 50-fold by the mismatch repair defects, mutS, mutL and uvrD, and 250-fold by the ssb-3 allele, but the effect of the mismatch defects was canceled by the ΔrecA allele. Rates of the deletion between the 3′ sequences in plasmid pLC107 were enhanced 17- to 130-fold by ssb alleles, but not by other alleles. For deletions in pLC107, 96% of the endpoints in the recA+ background and 88% in ΔrecA were in the two hot spots of the 60- and 33-nucleotide (nt) homologous sequences, whereas in the ssb-3 background >50% of the endpoints were in four- to 14-nt direct repeats dispersed in the entire 3′ sequences. The deletion formation between the homeologous sequences is RecA-independent but depends on the length of consecutive homologies. The mutant ssb allele lowers this dependency and results in the increase in deletion rates. Roles of mutant SSB are discussed with relation to misalignment in replication slippage.

scholarly journals Autophagy—A Story of Bacteria Interfering with the Host Cell Degradation Machinery

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 110
Author(s):  
Anna K. Riebisch ◽  
Sabrina Mühlen ◽  
Yan Yan Beer ◽  
Ingo Schmitz
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Listeria Monocytogenes ◽  
Salmonella Typhimurium ◽  
Innate Immune ◽  
Intracellular Pathogens ◽  
Response Mechanism ◽  
Pathogenic Escherichia Coli

Autophagy is a highly conserved and fundamental cellular process to maintain cellular homeostasis through recycling of defective organelles or proteins. In a response to intracellular pathogens, autophagy further acts as an innate immune response mechanism to eliminate pathogens. This review will discuss recent findings on autophagy as a reaction to intracellular pathogens, such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium tuberculosis, Staphylococcus aureus, and pathogenic Escherichia coli. Interestingly, while some of these bacteria have developed methods to use autophagy for their own benefit within the cell, others have developed fascinating mechanisms to evade recognition, to subvert the autophagic pathway, or to escape from autophagy.

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