Journal of Bacteriology最新文献

{"title":"\"Pupdates\" on proteasomal degradation in bacteria.","authors":"Shoshanna C Kahne, K Heran Darwin","doi":"10.1128/jb.00111-25","DOIUrl":"https://doi.org/10.1128/jb.00111-25","url":null,"abstract":"<p><p>Proteasomes are multi-subunit proteases found in all domains of life. The central components of proteasomal degradation are conserved, but how proteins are targeted to proteasomes diverges significantly. Despite the vast amount of information learned about how proteasomal degradation is regulated in eukaryotes, much less is known about the regulation of proteasome activity in bacteria. In this minireview, we highlight recent findings revealing how and when specific proteins are targeted to bacterial proteasomes, with a focus on ATP-dependent proteolysis.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0011125"},"PeriodicalIF":2.7,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic analysis of flagellar-mediated surface sensing by <i>Pseudomonas aeruginosa</i> PA14.","authors":"Sherry L Kuchma, C J Geiger, Shanice S Webster, Yu Fu, Robert Montoya, George A O'Toole","doi":"10.1128/jb.00520-24","DOIUrl":"10.1128/jb.00520-24","url":null,"abstract":"<p><p>Surface sensing is a key aspect of the early stage of biofilm formation. For <i>Pseudomonas aeruginosa</i> PA14, the type IV pili (T4P), the T4P alignment complex, and PilY1 were shown to play a key role in c-di-GMP signaling upon surface contact. The role of the flagellar machinery in surface sensing is less well understood for <i>P. aeruginosa</i>. Here, we show, consistent with findings from other groups, that a mutation in the gene encoding the flagellar hook protein (Δ<i>flgK</i>) or flagellin (Δ<i>fliC</i>) results in a strain that overproduces the Pel exopolysaccharide (EPS) with a concomitant increase in c-di-GMP levels. We use a candidate gene approach and genetic screens, combined with phenotypic assays, to identify key roles for the MotAB and MotCD stators and the FliG protein, a component of the flagellar switch complex, in stimulating the surface-dependent, increased c-di-GMP level noted for these flagellar mutants. These findings are consistent with previous studies showing a role for the stators in surface sensing. We also show that mutations in the genes coding for the DGCs SadC and RoeA, as well as SadB, a protein involved in early surface colonization, abrogate the increased c-d-GMP-related phenotypes of the Δ<i>flgK</i> mutant. Together, these data indicate that bacteria monitor the status of flagellar synthesis and function during surface sensing as a mechanism to trigger the biofilm program.</p><p><strong>Importance: </strong>Understanding how the flagellum contributes to surface sensing for <i>P. aeruginosa</i> is key to elucidating the mechanisms of biofilm initiation by this important opportunistic pathogen. Here, we take advantage of the observation that mutations in the flagellar hook protein or flagellin enhance surface sensing. We exploit this phenotype to identify key players in this signaling pathway, a critical first step in understanding the mechanistic basis of flagellar-mediated surface sensing. Our findings establish a framework for the future study of flagellar-based surface sensing.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0052024"},"PeriodicalIF":2.7,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resisting the resistance: the antimicrobial peptide DGL13K selects for small colony variants of <i>Staphylococcus aureus</i> that show increased resistance to its stereoisomer LGL13K, but not to DGL13K.","authors":"Sven-Ulrik Gorr","doi":"10.1128/jb.00505-24","DOIUrl":"https://doi.org/10.1128/jb.00505-24","url":null,"abstract":"<p><p>About 30% of the population are nasal carriers of <i>Staphylococcus aureus</i>, a leading cause of bacteremia, endocarditis, osteomyelitis, and skin and soft tissue infections. Antibiotic-resistant bacteria, in particular, are an increasing problem in both hospital and community settings. In this study, we sought to determine the cellular consequences of long-term exposure of <i>S. aureus</i> to the antimicrobial peptide stereoisomers, DGL13K and LGL13K. Both peptides selected for mutations in the chorismate/menaquinone biosynthetic pathway, which resulted in increased resistance to LGL13K but not DGL13K. DGL13K-selected isolates showed a mutation in <i>aroF</i>, while <i>menA</i> and <i>menH</i> were mutated in LGL13K-selected isolates. The latter also contained a mutation of <i>frsA</i>. The peptide-selected isolates exhibited golden coloration, suggesting increased production of the carotenoid staphyloxanthin, which could enhance resistance to cationic antimicrobial peptides (AMPs). The peptide-selected isolates grew as small colony variants, which have also been associated with resistance to AMPs. Addition of menaquinone to the growth medium reduced the generation time of DGL13K-selected mutants, but not LGL13K-selected mutants. Instead, the latter showed an increased MIC to LGL13K and greatly reduced ATP levels. The peptide-selected isolates showed increased biofilm formation and decreased autolysis, which was further reduced by alkaline shock, consistent with increased Asp23 expression. The mechanisms behind the differential effect of DGL13K and LGL13K on <i>S. aureus</i> resistance remain to be elucidated. The finding that DGL13K induced resistance to the stereoisomer LGL13K but not to DGL13K itself suggests that peptide primary structure is responsible for inducing bacterial defense mechanisms, but the peptide secondary structure determines if the defense mechanisms are effective against each peptide.</p><p><strong>Importance: </strong>This work examines resistance to stereoisomers of the antimicrobial peptide GL13K in <i>Staphylococcus aureus</i>. Both DGL13K and LGL13K isomers cause mutations in the menaquinone pathway. While LGL13K causes resistance to LGL13K, the bacteria remain susceptible to DGL13K. Conversely, DGL13K also raises resistance to LGL13K, but the cells remain susceptible to DGL13K. The resistant isolates exhibit a small colony variant phenotype and overproduce the pigment staphyloxanthin. Menaquinone supplementation decreases the long generation time of DGL13K-selected isolates and increases the MIC of LGL13K-selected isolates.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0050524"},"PeriodicalIF":2.7,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacterial ribosome heterogeneity facilitates rapid response to stress.","authors":"Yi-Lin Shen, Lei Xu, Ying Zhou, Bang-Ce Ye","doi":"10.1128/jb.00058-25","DOIUrl":"https://doi.org/10.1128/jb.00058-25","url":null,"abstract":"<p><p>Bacteria live under constant pressure from external signals, necessitating a rapid capacity to reprogram their metabolism. The ribosome, once considered a uniform and static entity, is now recognized for its compositional heterogeneity. Despite its prevalence, the role of this heterogeneity in regulating bacterial translation remains incompletely understood. This review explores how ribosomal heterogeneity may serve as a conserved mechanism for fine-tuning gene expression, enabling swift adjustments to environmental stress. We present recent findings on the regulatory potential of ribosome heterogeneity and its broader implications for bacterial adaptation, pathogenesis, and the development of novel antimicrobial strategies.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0005825"},"PeriodicalIF":2.7,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144208564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A deoxynucleoside triphosphate triphosphohydrolase promotes cell cycle progression in <i>Caulobacter crescentus</i>.","authors":"Chandler N Hellenbrand, David M Stevenson, Katarzyna A Gromek, Daniel Amador-Noguez, David M Hershey","doi":"10.1128/jb.00145-25","DOIUrl":"10.1128/jb.00145-25","url":null,"abstract":"<p><p>Intracellular pools of deoxynucleoside triphosphates (dNTPs) are strictly maintained throughout the cell cycle to ensure accurate and efficient DNA replication. DNA synthesis requires an abundance of dNTPs, but elevated dNTP concentrations in nonreplicating cells delay entry into S phase. Enzymes known as deoxyguanosine triphosphate triphosphohydrolases (Dgts) hydrolyze dNTPs into deoxynucleosides and triphosphates, and we propose that Dgts restrict dNTP concentrations to promote the G1 to S phase transition. We characterized a Dgt from the bacterium <i>Caulobacter crescentus</i> termed <i>flagellar signaling suppressor C</i> (<i>fssC</i>) to clarify the role of Dgts in cell cycle regulation. Deleting <i>fssC</i> increases dNTP levels and extends the G1 phase of the cell cycle through a mechanism independent of the response regulator CtrA. Segregation and duplication of the chromosomal origin of replication (<i>oriC</i>) are delayed in ∆<i>fssC</i>, but the rate of replication elongation is unchanged. We conclude that dNTP hydrolysis by FssC promotes the initiation of DNA replication. This work further establishes Dgts as important regulators of the G1 to S phase transition, and the high conservation of Dgts across all domains of life implies that Dgt-dependent cell cycle control may be widespread in many organisms.IMPORTANCECells must faithfully replicate their genetic material in order to proliferate. Studying the regulatory pathways that determine when a cell initiates DNA replication is important for understanding fundamental biological processes, and it can also improve the strategies used to treat diseases that affect the cell cycle. Here, we identify a nucleotide signaling pathway that influences when cells begin DNA replication. We show that this pathway promotes the transition from the G1 to the S phase of the cell cycle in the bacterium <i>Caulobacter crescentus</i> and propose that this pathway is prevalent in all domains of life.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0014525"},"PeriodicalIF":2.7,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental pH controls antimicrobial production by human probiotic <i>Streptococcus salivarius</i>.","authors":"Dieu Linh Nguyen, Subhasree Saha, Aswin Thacharodi, Bharat Bhushan Singh, Sonali Mitra, Hackwon Do, Muthiah Kumaraswami","doi":"10.1128/jb.00059-25","DOIUrl":"https://doi.org/10.1128/jb.00059-25","url":null,"abstract":"<p><p><i>Streptococcus salivarius</i> K12 (SAL) is an oral probiotic used to treat or prevent oral infections caused by human pathogens. SAL produces at least three antimicrobials to exert its antimicrobial activity, namely, salivaricin A and salivaricin B, and the newly identified salivabactin. Salivabactin production is catalyzed by a polyketide/non-ribosomal peptide synthase hybrid biosynthetic gene cluster (BGC), termed as <i>sar-BGC</i>. The <i>sar-BGC</i> expression and salivabactin production are transient during SAL growth <i>in vitro</i> and <i>in vivo</i>, which may negatively impact SAL probiotic efficacy. To understand the molecular basis for transient <i>sar-BGC</i> expression, we assessed the impact of environmental pH on <i>sar-BGC</i> expression. We found that environmental acidification is a critical factor in promoting salivabactin antimicrobial activity and production by inducing <i>sar-BGC</i> expression. We further showed that acidic pH directly influences the quorum-sensing system that controls <i>sar-BGC</i> expression. During environmental acidification, SAL cytosol is acidified, which is sensed by a pH-sensitive histidine switch in the cytosolic transcription regulator, NrpR. The protonation of histidine during cytosolic acidification promotes high-affinity interactions between NrpR and its cognate intercellular signaling peptide, NIP, which leads to upregulation of <i>sar-BGC</i> expression. Collectively, our results indicate that SAL uses a sophisticated regulatory mechanism to orchestrate salivabactin production in an environment that is conducive to its antimicrobial activity.</p><p><strong>Importance: </strong>Probiotic bacteria are important tools in combating bacterial infections. Probiotics exert their antimicrobial activity via several mechanisms, including antimicrobial production. However, discrepancies exist between the <i>in vitro</i> and <i>in vivo</i> efficacies of probiotics in inhibiting pathogen growth. Understanding the host and environmental factors that influence antimicrobial production and activity is critical for improving probiotic efficacy. In this study, we showed that the antimicrobial salivabactin produced by human oral probiotic <i>Streptococcus salivarius</i> K12 is active at acidic pH. We further elucidated the molecular mechanism by which <i>S. salivarius</i> coordinates salivabactin production in concert with environmental acidification, thereby maximizing salivabactin antimicrobial activity.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0005925"},"PeriodicalIF":2.7,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Controlled burn: interconnections between energy-spilling pathways and metabolic signaling in bacteria.","authors":"Nicolaus Jakowec, Steven E Finkel","doi":"10.1128/jb.00542-24","DOIUrl":"10.1128/jb.00542-24","url":null,"abstract":"<p><p>Bacterial energy-spilling pathways-such as overflow metabolism and futile cycles-have been considered inefficient forms of metabolism that result from poor regulatory control or function as mechanisms to cope with excess energy. However, mounting evidence places these seemingly wasteful reactions at the fulcrum between metabolic signaling and stress adaptation in bacteria. Specifically, energy-spilling pathways may mediate the metabolic reprogramming observed when cells encounter growth-limiting constraints (i.e., nutrient limitation). Recent insights spotlight microbial metabolism as an intricate signaling network that coordinates physiological programming with energy and nutrient conditions. Such intracellular metabolic cross stalk is pivotal to survival in competitive, fluctuating environments that bacteria frequently encounter in nature. In light of this paradigm of metabolic signaling, energy-spilling pathways are increasingly recognized as regulatory strategies that enable metabolic rewiring in response to stress. Overflow metabolism or futile cycles may generate secondary metabolites with signaling properties, alter the flux of metabolic pathways and the rate of nutrient acquisition, or stimulate regulatory nodes to trigger specific metabolic programs in response to environmental challenges. Furthermore, the observation of such expensive pathways under laboratory conditions purported to be \"energy limiting\" may in fact suggest energy sufficiency, compelling us to rethink how we model energy limitation and starvation for bacteria.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0054224"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the gut microbiota's role in obesity: key metabolites, microbial species, and therapeutic insights.","authors":"Majid Iqbal, Qian Yu, Jingqun Tang, Juanjuan Xiang","doi":"10.1128/jb.00479-24","DOIUrl":"10.1128/jb.00479-24","url":null,"abstract":"<p><p>Obesity, characterized by excessive fat accumulation, stems from an imbalance between energy intake and expenditure, with the gut microbiota playing a crucial role. This review highlights how gut microbiota influences metabolic pathways, inflammation, and adipose tissue regulation in obesity. Specific bacteria and metabolites, such as lipopolysaccharides (LPS) and short-chain fatty acids (SCFAs), modulate gut permeability, inflammation, and energy harvest, impacting obesity development. Certain gut bacteria, including <i>Clostridium XIVb</i>, <i>Dorea</i> spp., <i>Enterobacter cloacae</i>, and <i>Collinsella aerofaciens</i>, promote obesity by increasing energy harvest, gut permeability, and inflammatory response through LPS translocation into the bloodstream. Conversely, beneficial bacteria like <i>Akkermansia muciniphila</i>, <i>Lactobacillus</i> spp., and <i>Bifidobacterium</i> spp. enhance gut barrier integrity, regulate SCFA production, and modulate fasting-induced adipose factor, which collectively support metabolic health by reducing fat storage and inflammation. Metabolites such as SCFAs (acetate, propionate, and butyrate) interact with G-protein coupled receptors to regulate lipid metabolism and promote the browning of white adipose tissue (WAT), thus enhancing thermogenesis and energy expenditure. However, LPS contributes to insulin resistance and fat accumulation, highlighting the dual roles of these microbial metabolites in both supporting and disrupting metabolic function. Therapeutic interventions targeting gut microbiota, such as promoting WAT browning and activating brown adipose tissue (BAT), hold promise for obesity management. However, personalized approaches are necessary due to individual microbiome variability. Further research is essential to translate these insights into microbiota-based clinical therapies.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0047924"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mobile genetic elements in <i>Klebsiella pneumoniae</i>.","authors":"Ting Pan, Qingrong Li","doi":"10.1128/jb.00012-25","DOIUrl":"10.1128/jb.00012-25","url":null,"abstract":"<p><p><i>Klebsiella pneumoniae</i> is a clinically important pathogenic bacteria that poses a serious threat to human health. In particular, the emergence of hypervirulent and multidrug-resistant <i>K. pneumoniae</i> has posed great challenges in clinical anti-infective therapy. In the <i>K. pneumoniae</i> genome, mobile genetic elements (MGEs), such as plasmids, prophages, transposons, and insertion sequences, enhance bacterial viability and adaptation by mediating the horizontal transfer of virulence genes, antibiotic resistance genes, and other adaptive genes. This paper reviews the types and characteristics of the main MGEs in <i>K. pneumoniae</i>, focusing on their effects on bacterial virulence and antibiotic resistance, with the aim of providing clues for developing infection control measures and new antibacterial drugs.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0001225"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond anaerobic respiration-new physiological roles for DmsABC and other S-/N-oxide reductases in <i>Escherichia coli</i>.","authors":"Qifeng Zhong, Marufa Nasreen, Ruizhe Yang, Michel Struwe, Bostjan Kobe, Ulrike Kappler","doi":"10.1128/jb.00463-24","DOIUrl":"10.1128/jb.00463-24","url":null,"abstract":"<p><p>Sulfoxide reductases in pathogenic bacteria have recently received increasing attention for their association with virulence and survival within the host. Here, we have re-investigated the physiological role of the molybdenum-containing DmsABC dimethyl sulfoxide (DMSO) reductase from <i>Escherichia coli</i>, which has a proposed role in anaerobic respiration with DMSO. Our investigation into potential physiological substrates revealed that DmsABC efficiently reduces pyrimidine N-oxide, nicotinamide N-oxide, and methionine sulfoxide, and exposure to host cell-produced stressors such as hypochlorite or hydrogen peroxide specifically increased expression of the <i>E. coli dmsA</i> gene. <i>E. coli</i> strains lacking <i>dmsA</i> showed increased lag times in the presence of hypochlorite, and these strains also showed up to a 90% reduction in adherence to human bladder cells. Interestingly, in the presence of hypochlorite, expression of multiple alternative S-/N-oxide reductases present in <i>E. coli</i> was elevated by 2- to 4-fold in a ∆<i>dmsA</i> strain compared to the wild-type strain, suggesting functional redundancy. The phenotypes of the <i>E. coli</i> ∆<i>dmsA</i> strains were strikingly similar to ∆<i>dmsA</i> strains of the respiratory pathogen <i>Haemophilus influenzae</i>, which confirms the role of both enzymes in supporting host-pathogen interactions. We propose that this function is conserved in enzymes closely related to <i>E. coli</i> DmsABC. Our study also uncovered that the expression of many <i>E. coli</i> Mo enzymes was induced by oxidative stressors, including metals such as copper, and further work should be directed at determining the connection of these enzymes to host-pathogen interactions.IMPORTANCEBacterial urinary tract infections are debilitating and frequently recurring in human populations worldwide, and <i>Escherichia coli</i> strains are a major cause of these infections. In this study, we have uncovered a new mechanism by which <i>E. coli</i> can avoid being killed by the human immune system. The bacteria use a set of seven related enzymes that can reverse damage to essential cell components such as amino acids, vitamins, and DNA building blocks. Antibacterial compounds produced by the human immune system specifically induced the production of these enzymes, confirming that they play a role in helping <i>E. coli</i> survive during infection and making these enzymes potential future drug targets.</p>","PeriodicalId":15107,"journal":{"name":"Journal of Bacteriology","volume":" ","pages":"e0046324"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}