@article {817,
	title = {Metatranscriptomic analysis reveals gut microbiome bacterial genes in pyruvate and amino acid metabolism associated with hyperuricemia and gout in humans.},
	journal = {Sci Rep},
	volume = {15},
	year = {2025},
	month = {2025 Mar 22},
	pages = {9981},
	abstract = {<p>Several pathologies with metabolic origin, such as hyperuricemia and gout, have been associated with the gut microbiota taxonomic profile. However, there is no evidence of which bacterial genes are being expressed in the gut microbiome, and of their potential effects on hyperuricemia and gout. We sequenced the RNA of 26 fecal samples from 10 healthy normouricemic controls, 10 with asymptomatic hyperuricemia (AH), and six gout patients. The coding sequences were mapped to KEGG orthologues (KO). We compared the expression levels using generalized linear models and validated the expression of four KO in a larger sample by qRT-PCR. A distinct genetic expression pattern was identified among groups. AH individuals and gout patients showed an over-expression of KOs mainly related to pyruvate metabolism (Log2foldchange > 23, p-adj <= 3.56 {\texttimes} 10), the pentose pathway (Log2foldchange > 24, p-adj < 1.10 {\texttimes} 10) and purine metabolism (Log2foldchange > 22, p-adj < 1.25 {\texttimes} 10). AH subjects had lower expression of KO related to glycine metabolism (Log2foldchange=-18, p-adj < 1.72 {\texttimes} 10) than controls. Gout patients had lower expression (Log2foldchange=-22.42, p-adj < 3.31 {\texttimes} 10) of a KO involved in phenylalanine biosynthesis, in comparison to controls and AH subjects. The over-expression seen for the KO related to pyruvate metabolism and the pentose pathway in gout patients{\textasciiacute} microbiome was validated. There is a differential gene expression pattern in the gut microbiome of normouricemic individuals, AH subjects and gout patients. These differences are mainly located in metabolic pathways involved in acetate precursors and bioavailability of amino acids.</p>},
	keywords = {Adult, Aged, Amino Acids, Bacteria, Case-Control Studies, Feces, Female, Gastrointestinal Microbiome, Gene Expression Profiling, Genes, Bacterial, Gout, Humans, Hyperuricemia, Male, Middle Aged, Pyruvic Acid, Transcriptome},
	issn = {2045-2322},
	doi = {10.1038/s41598-025-93899-1},
	author = {Mart{\'\i}nez-Nava, Gabriela Ang{\'e}lica and Altamirano-Molina, Efren and V{\'a}zquez-Mellado, Janitzia and Casimiro-Soriguer, Carlos S and Dopazo, Joaquin and Lozada-P{\'e}rez, Carlos and Herrera-L{\'o}pez, Br{\'\i}gida and Mart{\'\i}nez-G{\'o}mez, Laura Edith and Mart{\'\i}nez-Armenta, Carlos and Guido-G{\'o}mora, Dafne Lissete and Valle-Guti{\'e}rrez, Sarah{\'\i} and Suarez-Ahedo, Carlos and Camacho-Rea, Mar{\'\i}a Del Carmen and Mart{\'\i}nez-Garc{\'\i}a, Mireya and Guti{\'e}rrez-Esparza, Guadalupe and Amezcua-Guerra, Luis M and Zamudio-Cuevas, Yessica and Mart{\'\i}nez-Flores, Karina and Fern{\'a}ndez-Torres, Javier and Burguete-Garc{\'\i}a, Ana I and Orbe-Orihuela, Yaneth Citlalli and Lagunas-Mart{\'\i}nez, Alfredo and M{\'e}ndez-Salazar, Eder Orlando and Francisco-Balderas, Adriana and Palacios-Gonz{\'a}lez, Berenice and Pineda, Carlos and L{\'o}pez-Reyes, Alberto}
}
@article {578,
	title = {Exploring the antimicrobial action of a carbon monoxide-releasing compound through whole-genome transcription profiling of Escherichia coli.},
	journal = {Microbiology (Reading)},
	volume = {155},
	year = {2009},
	month = {2009 Mar},
	pages = {813-824},
	abstract = {<p>We recently reported that carbon monoxide (CO) has bactericidal activity. To understand its mode of action we analysed the gene expression changes occurring when Escherichia coli, grown aerobically and anaerobically, is treated with the CO-releasing molecule CORM-2 (tricarbonyldichlororuthenium(II) dimer). Microarray analysis shows that the E. coli CORM-2 response is multifaceted, with a high number of differentially regulated genes spread through several functional categories, namely genes involved in inorganic ion transport and metabolism, regulators, and genes implicated in post-translational modification, such as chaperones. CORM-2 has a higher impact in E. coli cells grown anaerobically, as judged by the repression of genes belonging to eight functional classes which are not seen in the response of aerobically CORM-2-treated cells. The biological relevance of the variations caused by CORM-2 was substantiated by studying the CORM-2 sensitivity of selected E. coli mutants. The results show that the deletion of redox-sensing regulators SoxS and OxyR increased the sensitivity to CORM-2 and suggest that while SoxS plays an important role in protection against CORM-2 under both growth conditions, OxyR seems to participate only in the aerobic CORM-2 response. Under anaerobic conditions, we found that the heat-shock proteins IbpA and IbpB contribute to CORM-2 defence since the deletion of these genes increases the sensitivity of the strain. The induction of several met genes and the hypersensitivity to CORM-2 of the DeltametR, DeltametI and DeltametN mutant strains suggest that CO has effects on the methionine metabolism of E. coli. CORM-2 also affects the transcription of several E. coli biofilm-related genes and increases biofilm formation in E. coli. In particular, the absence of tqsA or bhsA increases the resistance of E. coli to CORM-2, and deletion of tsqA leads to a strain that has lost its capacity to form biofilm upon treatment with CORM-2. In spite of the relatively stable nature of the CO molecule, our results show that CO is able to trigger a significant alteration in the transcriptome of E. coli which necessarily has effects in several key metabolic pathways.</p>},
	keywords = {Biofilms, Carbon Monoxide, Escherichia coli, Escherichia coli Proteins, Gene Expression Profiling, Gene Expression Regulation, Bacterial, Genes, Bacterial, Genes, Regulator, Genetic Complementation Test, Methionine, Microbial Viability, mutation, Oligonucleotide Array Sequence Analysis, Organometallic Compounds, Phenotype, RNA, Bacterial},
	issn = {1350-0872},
	doi = {10.1099/mic.0.023911-0},
	author = {Nobre, L{\'\i}gia S and Al-Shahrour, F{\'a}tima and Dopazo, Joaquin and Saraiva, L{\'\i}gia M}
}
