Sunset Yellow dye effects on gut microbiota, intestinal integrity, and the induction of inflammasomopathy with pyroptotic signaling in male Wistar rats.

Although concern persists regarding possible adverse effects of consumption of synthetic azo food dyes, the mechanisms of any such effects remain unclear. We have tested the hypothesis that chronic consumption of the food dye Sunset Yellow (SY) perturbs the composition of the gut microbiota and alters gut integrity. Male rats were administered SY orally for 12 weeks. Analysis of fecal samples before and after dye administration demonstrated SY-induced microbiome dysbiosis. SY treatment reduced the abundance of beneficial taxa such as Treponema 2, Anaerobiospirillum, Helicobacter, Rikenellaceae RC9 gut group, and Prevotellaceae UCG-003, while increasing the abundance of the potentially pathogenic microorganisms Prevotella 2 and Oribacterium. Dysbiosis disrupted gut integrity, altering the jejunal adherens junction complex E-cadherin/ß-catenin and decreasing Trefoil Factor (TFF)-3. SY administration elevated LPS serum levels, activated the inflammatory inflammasome cascade TLR4/NLRP3/ASC/cleaved-activated caspase-1 to mature IL-1ß and IL-18, and activated caspase-11 and gasdermin-N, indicating pyroptosis and increased intestinal permeability. The possibility that consumption of SY by humans could have effects similar to those that we have observed in rats should be examined.

The membrane-cytoplasmic linker defines activity of FtsH proteases in Pseudomonas aeruginosa clone C.

Pandemic Pseudomonas aeruginosa clone C strains encode two inner-membrane associated ATP-dependent FtsH proteases. PaftsH1 is located on the core genome and supports cell growth and intrinsic antibiotic resistance, whereas PaftsH2, a xenolog acquired through horizontal gene transfer from a distantly related species, is unable to functionally replace PaftsH1. We show that purified PaFtsH2 degrades fewer substrates than PaFtsH1. Replacing the 31-amino acid-extended linker region of PaFtsH2 spanning from the C-terminal end of the transmembrane helix-2 to the first seven highly divergent residues of the cytosolic AAA+ ATPase module with the corresponding region of PaFtsH1 improves hybrid-enzyme substrate processing in vitro and enables PaFtsH2 to substitute for PaFtsH1 in vivo. Electron microscopy indicates that the identity of this linker sequence influences FtsH flexibility. We find membrane-cytoplasmic (MC) linker regions of PaFtsH1 characteristically glycine-rich compared to those from FtsH2. Consequently, introducing three glycines into the membrane-proximal end of PaFtsH2's MC linker is sufficient to elevate its activity in vitro and in vivo. Our findings establish that the efficiency of substrate processing by the two PaFtsH isoforms depends on MC linker identity and suggest that greater linker flexibility and/or length allows FtsH to degrade a wider spectrum of substrates. As PaFtsH2 homologs occur across bacterial phyla, we hypothesize that FtsH2 is a latent enzyme but may recognize specific substrates or is activated in specific contexts or biological niches. The identity of such linkers might thus play a more determinative role in the functionality of and physiological impact by FtsH proteases than previously thought.

First clinical isolation report of Shewanella algae from the stools of a patient with acute enteritis in Spain / Primer aislamiento clínico en España de Shewanella algae en heces de un paciente con enteritis aguda

We report a case of acute enteritis caused by Shewanella algae in a cirrhotic patient. Biochemical identification systems revealed to be insufficient to identify the Shewanella isolate at the species level, thus requiring 16S rRNA and gyrB partial gene sequencing. Even if co-infection by Clostridium difficile could not be ruled out, this is, to our knowledge, the first report of acute enteritis caused by Shewanella algae in Europe

Presentamos un caso de enteritis aguda causada por Shewanella algae en un paciente cirrótico. Los sistemas de identificación mediante pruebas bioquímicas no fueron adecuados para la identificación de S. algae a nivel especie, por lo que se requirió la secuenciación parcial de los genes 16S rRNA y gyrB. Aunque la enfermedad debida a la co-infección por Clostridium difficile no podría ser descartado, este es, a nuestro entender, el primer caso de enteritis aguda causada por Shewanella algae en Europa