U Acetic acid

Pyrroloquinoline quinone (PQQ)-dependent dehydrogenases (quinoproteins) of acetic acid bacteria (AAB), such as the membrane-bound alcohol dehydrogenase (ADH) and the membrane-bound glucose dehydrogenase, contain PQQ as the prosthetic group. Most of them are located on the periplasmic surface of the cytoplasmic membrane, and function as primary dehydrogenases in cognate substance-oxidizing respiratory chains. Here, we have provided an overview on the function and molecular architecture of AAB quinoproteins, which can be categorized into six groups according to the primary amino acid sequences. Based on the genomic data, we discuss the types of quinoproteins found in AAB genome and how they are distributed. Our analyses indicate that a significant number of uncharacterized orphan quinoproteins are present in AAB. By reviewing recent experimental developments, we discuss how to characterize the as-yet-unknown enzymes. Moreover, our bioinformatics studies also provide insights on how quinoproteins have developed into intricate enzymes. ADH comprises at least two subunits: the quinoprotein dehydrogenase subunit encoded by adhA and the cytochrome subunit encoded by adhB, and the genes are located in a polycistronic transcriptional unit. Findings on stand-alone derivatives of adhA encourage us to speculate on a possible route for ADH development in the evolutional history of AAB. A combination of bioinformatics studies on big genome sequencing data and wet studies assisted with genetic engineering would unravel biochemical functions and physiological role of uncharacterized quinoproteins in AAB, or even in unculturable metagenome.

Acetic acid bacteria are gram-negative obligate aerobic bacteria assigned to the family Acetobacteraceae of Alphaproteobacteria. They are members of the genera Acetobacter, Gluconobacter, Gluconacetobacter, Acidomonas, Asaia, Kozakia, Swaminathania, Saccharibacter, Neoasaia, Granulibacter, Tanticharoenia, Ameyamaea, Neokomagataea, and Komagataeibacter. Many strains of Acetobacter and Komagataeibacter have been known to possess high acetic acid fermentation ability as well as the acetic acid and ethanol resistance, which are considered to be useful features for industrial production of acetic acid and vinegar, the commercial product. On the other hand, Gluconobacter strains have the ability to perform oxidative fermentation of various sugars, sugar alcohols, and sugar acids leading to the formation of several valuable products. Thermotolerant strains of acetic acid bacteria were isolated in order to serve as the new strains of choice for industrial fermentations, in which the cooling costs for maintaining optimum growth and production temperature in the fermentation vessels could be significantly reduced. Genetic modifications by adaptation and genetic engineering were also applied to improve their properties, such as productivity and heat resistance.

We established a novel mouse model of chronic kidney disease (CKD) using acetic acid and compared it with the 5/6-nephrectomized mouse model. In our novel model, significant increases were observed in blood biochemical values and urinary parameters. Moreover, a decrease in creatinine clearance (Ccr) was observed. This model also demonstrated a higher survival rate than the 5/6-nephrectomized model. Observed histological changes in our model included cell infiltration in the renal interstitium, tubular dilation, regenerated tubules, and glomerulosclerosis. Inflammation of the renal interstitium was particularly remarkable. TNF-α, IL-1β, and ICAM-1 mRNA expression were up-regulated prior to elevation of mean blood pressure and prior to changes in blood biochemical values and urinary parameters. Up-regulation of TGF-β mRNA and down-regulation of nephrin mRNA were also observed at 12 weeks after acetic acid treatment. However, no correlation between the progression of CKD and the decrease in renal blood flow was observed. Finally, repeated losartan administration attenuated the effects of acetic acid-induced renal injury. Our findings suggest that chronic kidney conditions associated with this model may be triggered by interstitial inflammation. Moreover, we suggest that this model is useful for understanding the pathophysiological mechanisms of CKD, and for evaluating the effects of therapeutic agents.