Mechanisms of bacterial resistance and response to bile

Gunn, John S.

doi:10.1016/s1286-4579(00)00392-0

Cited by 288 publications

(301 citation statements)

References 67 publications

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“…In addition to its widely known role as a detergent that disrupts the bacterial envelope (Gunn 2000), bile causes DNA-damaging activity on S. enterica and induces DNA rearrangements and point mutations (Prieto et al 2004). This study provides evidence that, like its detergent activity, the DNA-damaging capacity of bile resides in bile salts.…”

Section: Discussionmentioning

confidence: 71%

“…Because bile is not a strong mutagen, it seems, a priori, unlikely that bile-induced DNA damage can be a significant source of genetic polymorphism during intestinal infection (Prieto et al 2004). However, Salmonella serovars that cause systemic and chronic infections colonize the gall bladder, where bile can reach a steady concentration of 15% or higher (Gunn 2000). Furthermore, the formation of biofilms on gallstones exposes Salmonella to even higher Either process generates single-stranded DNA that can induce the SOS response.…”

Section: Discussionmentioning

confidence: 99%

“…The composition of bile is complex and includes bile salts, cholesterol, bilirubin, phospholipids, and a variety of proteins (Hofmann 1998). Bile salts act as detergents and have strong antibacterial activity (Gunn 2000). A decrease in bile production, which can be caused either by malnourishment or by biliary pathological conditions, increases the susceptibility of the individual to a variety of bacterial pathogens (Gunn 2000).…”

mentioning

confidence: 99%

“…Bile salts act as detergents and have strong antibacterial activity (Gunn 2000). A decrease in bile production, which can be caused either by malnourishment or by biliary pathological conditions, increases the susceptibility of the individual to a variety of bacterial pathogens (Gunn 2000). However, enteric bacteria are resistant to bile.…”

mentioning

confidence: 99%

“…An especially interesting case of bile/pathogen interaction is found in S. enterica, which encounters bile in two different situations: (i) in the lumen of the mammalian intestine, where concentrations of bile salts range from 0.2 to 2% (Gunn 2000), and (ii) in the gall bladder, where much higher concentrations of bile are found (Hofmann 1998). The presence of S. enterica serovar Typhi in the gall bladder is characteristic of the asymptomatic ''carrier state'' of typhoid.…”

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confidence: 99%

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Repair of DNA Damage Induced by Bile Salts in Salmonella enterica

2006

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Exposure of Salmonella enterica to sodium cholate, sodium deoxycholate, sodium chenodeoxycholate, sodium glychocholate, sodium taurocholate, or sodium glycochenodeoxycholate induces the SOS response, indicating that the DNA-damaging activity of bile resides in bile salts. Bile increases the frequency of GC / AT transitions and induces the expression of genes belonging to the OxyR and SoxRS regulons, suggesting that bile salts may cause oxidative DNA damage. S. enterica mutants lacking both exonuclease III (XthA) and endonuclease IV (Nfo) are bile sensitive, indicating that S. enterica requires base excision repair (BER) to overcome DNA damage caused by bile salts. Bile resistance also requires DinB polymerase, suggesting the need of SOS-associated translesion DNA synthesis. Certain recombination functions are also required for bile resistance, and a key factor is the RecBCD enzyme. The extreme bile sensitivity of RecB À , RecC À , and RecA À RecD À mutants provides evidence that bile-induced damage may impair DNA replication.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Repair of DNA Damage Induced by Bile Salts in Salmonella enterica

2006

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A dysregulated bile acids pool is associated with metabolic syndrome and gut microbial dysbiosis in early adolescence

Mancera‐Hurtado,

Lopez‐Contreras,

Flores‐Lopez

et al. 2023

Obesity

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Objective: The increased prevalence of childhood metabolic syndrome (MetS) is a public health issue. It has been shown that a dysregulated bile acid (BA) profile could be involved in the development of MetS, in which the gut microbiota could have a significant role in BA levels. This study aimed to evaluate differences in serum BA levels in children with and without MetS and whether these levels were associated with gut microbial composition.Methods: A total of 100 children aged 10 to 12 years were enrolled in this study, 42 children with MetS (cases) and 58 control participants. Serum BAs were measured by liquid chromatography-tandem mass spectrometry and gut microbiota was determined by 16S ribosomal RNA gene sequencing.Results: Children with MetS showed higher levels of total, secondary, and 12αhydroxylated BAs, as well as deoxycholic acid, and these were associated with dyslipidemia and insulin resistance markers. Interestingly, total BAs were negatively correlated with gut bacterial diversity (Shannon index: rho = À0.218, p = 0.035), whereas total, 12α-hydroxylated, and secondary BAs, as well as deoxycholic acid, showed negative correlations with genera known for their potential health effects, including Bifidobacterium, Akkermansia, and Faecalibacterium.Conclusions: This study suggests that childhood MetS is associated with a dysregulated BA pool and that these alterations could influence the abundance of potentially beneficial bacteria, thus contributing to gut microbial dysbiosis.

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The crystal structures of the Salmonella type III secretion system tip protein SipD in complex with deoxycholate and chenodeoxycholate

et al. 2010

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The type III secretion system (T3SS) is a protein injection nanomachinery required for virulence by many human pathogenic bacteria including Salmonella and Shigella. An essential component of the T3SS is the tip protein and the Salmonella SipD and the Shigella IpaD tip proteins interact with bile salts, which serve as environmental sensors for these enteric pathogens. SipD and IpaD have long central coiled coils and their N-terminal regions form a-helical hairpins and a short helix a3 that pack against the coiled coil. Using AutoDock, others have predicted that the bile salt deoxycholate binds IpaD in a cleft formed by the a-helical hairpin and its long central coiled coil. NMR chemical shift mapping, however, indicated that the SipD residues most affected by bile salts are located in a disordered region near helix a3. Thus, how bile salts interact with SipD and IpaD is unclear. Here, we report the crystal structures of SipD in complex with the bile salts deoxycholate and chenodeoxycholate. Bile salts bind SipD in a region different from what was predicted for IpaD. In SipD, bile salts bind part of helix a3 and the C-terminus of the long central coiled coil, towards the C-terminus of the protein. We discuss the biological implication of the differences in how bile salts interact with SipD and IpaD.

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Mechanisms of bacterial resistance and response to bile

Cited by 288 publications

References 67 publications

Repair of DNA Damage Induced by Bile Salts in Salmonella enterica

Repair of DNA Damage Induced by Bile Salts in Salmonella enterica

A dysregulated bile acids pool is associated with metabolic syndrome and gut microbial dysbiosis in early adolescence

The crystal structures of the Salmonella type III secretion system tip protein SipD in complex with deoxycholate and chenodeoxycholate

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