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Characterization of metal(loid)s and antibiotic resistance in bacteria of human gut microbiota from chronic kidney disease subjects. | LitMetric

Characterization of metal(loid)s and antibiotic resistance in bacteria of human gut microbiota from chronic kidney disease subjects.

Biol Res

Molecular microbiology and food research laboratory, Facultad de ciencias para el cuidado de la salud, Escuela de nutrición y dietética, Universidad San Sebastián, Carmen Sylva 2444, Providencia Santiago, Santiago, Chile.

Published: June 2022

Background: Human Gut Microbiota (HGM) is composed of more than one thousand species, playing an important role in the health status of individuals. Dysbiosis (an HGM imbalance) is augmented as chronic kidney disease (CKD) progresses, as loss of kidney function accelerates. Increased antibiotic use in CKD subjects and consumption of nephrotoxic heavy metals and metalloids such as lead, cadmium, arsenic, and mercury in tap water increases the dysbiosis state. Studies in people with stage 3 CKD are complex to carry out, mainly because patients are self-reliant who rarely consult a specialist. The current work focused on this type of patient.

Results: Lead and arsenic-resistant bacteria were obtained from self-reliant (that stands on its own) stage 3 CKD subjects. Pathogen-related Firmicutes and Proteobacteria genus bacteria were observed. Resistance and potentiation of antibiotic effects in the presence of metal(loid)s in vitro were found. Furthermore, the presence of the following genes markers for antibiotic and metal(loid) resistance were identified by qPCR: oxa10, qnrB1, mphB, ermB, mefE1, arr2, sulll, tetA, floR, strB, dhfr1, acrB, cadA2k, cadA3k, arsC, pbrA. We observed a decrease in the number of metal resistance markers.

Conclusions: The presence of cadA and arsC genetic markers of antibiotics and metal(loid)s resistance were detected in samples from stage 3 CKD subjects. Lower gene amplification in advanced stages of CKD were also observed, possibly associated with a decrease in resident HGM during kidney disease progression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9205139PMC
http://dx.doi.org/10.1186/s40659-022-00389-zDOI Listing

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