“…For example, up to 31% of mcr -resistant strains were isolated directly from the feces of patients [ 49 ]. mcr-1 [ 50 ], mcr-1.1 [ 51 ], mcr-1.4 [ 51 ], mcr-5 [ 52 ], mcr-10 [ 53 ] were isolated from hospital wastewater. Additionally, mcr-1 [ 54 ], mcr-5.3 [ 55 ], and mcr-8 [ 56 ] were isolated from animal waste.…”
Colistin is regarded as an antibiotic of last resort against multidrug-resistant Gram-negative bacteria, including Klebsiella pneumoniae and Escherichia coli. Colistin resistance is acquired by microorganisms via chromosome-mediated mutations or plasmid-mediated mobile colistin resistance (mcr) gene, in which the transfer of mcr is the predominant factor underlying the spread of colistin resistance. However, the factors that are responsible for the spread of the mcr gene are still unclear. In this study, we observed that mcr-1 inhibited the transfer of the pHNSHP45 backbone in liquid mating. Similar inhibitory effect of mcr-1.6 and chromosomal mutant ΔmgrB suggested that colistin resistance, acquired from either plasmid or chromosomal mutation, hindered the transfer of colistin resistance-related plasmid in vitro. Dual plasmid system further proved that co-existing plasmid transfer was reduced too. However, this inhibitory effect was reversed in vivo. Some factors in the gut, including bile salt and anaerobic conditions, could increase the transfer frequency of the mcr-1-containing plasmid. Our results demonstrated the potential risk for the spread of colistin resistance in the intestine, provide a scientific basis against the transmission of colistin resistance threat.
“…For example, up to 31% of mcr -resistant strains were isolated directly from the feces of patients [ 49 ]. mcr-1 [ 50 ], mcr-1.1 [ 51 ], mcr-1.4 [ 51 ], mcr-5 [ 52 ], mcr-10 [ 53 ] were isolated from hospital wastewater. Additionally, mcr-1 [ 54 ], mcr-5.3 [ 55 ], and mcr-8 [ 56 ] were isolated from animal waste.…”
Colistin is regarded as an antibiotic of last resort against multidrug-resistant Gram-negative bacteria, including Klebsiella pneumoniae and Escherichia coli. Colistin resistance is acquired by microorganisms via chromosome-mediated mutations or plasmid-mediated mobile colistin resistance (mcr) gene, in which the transfer of mcr is the predominant factor underlying the spread of colistin resistance. However, the factors that are responsible for the spread of the mcr gene are still unclear. In this study, we observed that mcr-1 inhibited the transfer of the pHNSHP45 backbone in liquid mating. Similar inhibitory effect of mcr-1.6 and chromosomal mutant ΔmgrB suggested that colistin resistance, acquired from either plasmid or chromosomal mutation, hindered the transfer of colistin resistance-related plasmid in vitro. Dual plasmid system further proved that co-existing plasmid transfer was reduced too. However, this inhibitory effect was reversed in vivo. Some factors in the gut, including bile salt and anaerobic conditions, could increase the transfer frequency of the mcr-1-containing plasmid. Our results demonstrated the potential risk for the spread of colistin resistance in the intestine, provide a scientific basis against the transmission of colistin resistance threat.
“…In addition, the mcr-5 gene has been detected in an Enterobacter sp. isolated from hospital sewage in China ( 13 ), and an MCR-5.3-producing Stenotrophomonas sp. has been isolated from animal waste in China ( 14 ).…”
Colistin resistance mediated by
mcr
genes in Gram-negative bacteria has gained significant attention worldwide. This is due to the ability of these genes to be horizontally transferred between different bacterial genera and species.
“…Molecular mechanisms of colistin resistance can be attributed to chromosomal mutations and plasmid-mediated mobile colistin resistance genes ( mcr ). The first mcr gene, mcr-1 was identified from Escherichia coli in 2016 in China [5] , which variants have also been found in Enterobacter spp., including mcr-1 [6] , mcr-3 [7] , mcr-4 [8] , mcr-5 [9] , mcr-9 [10] , and mcr-10 [11] . The modification of LPS via two-component system (TCS) was a common strategy to reduce colistin susceptibility in Gram-negative bacteria [4] .…”
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.