JOURNAL OF BACTERIOLOGY细菌学杂志
JOURNAL OF BACTERIOLOGY(英文缩写 J BACTERIOL),ISSN 0021-9193,eISSN 1098-5530,中文译名:细菌学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.476 | Q3 |
| 2022 | 3.200 | Q3 |
| 2023 | 2.700 | Q3 |
| 2024 | 3.000 | Q3 |
| 2025 | 3.800 | Q2 |
JOURNAL OF BACTERIOLOGY 最新收录文献
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1. {"_":"A minimalist opportunist: the emergence of .","i":["Acinetobacter baumannii"]}
1. 极简的机会主义者：鲍曼不动杆菌的出现PMID:日期:2026-09-29has evolved from a relatively overlooked nosocomial pathogen into one of the most concerning multidrug-resistant threats worldwide. Its global dissemination, accelerated by healthcare-associated transmission and the emergence of carbapenem-resistant strains, has established as a critical priority pathogen. While initially studied primarily through the lens of antimicrobial resistance, growing evidence indicates that the remarkable success of cannot be attributed to resistance alone. Unlike many classical bacterial pathogens, lacks an extensive arsenal of virulence factors and major secretion systems. Instead, its success relies on a highly effective "persist and resist" strategy, combining intrinsic tolerance, extensive genomic plasticity, metabolic adaptability, and multilayered regulatory networks that enable survival under severe environmental and host-imposed stresses. This apparent simplicity, coupled with exceptional resilience, makes a particularly informative system for understanding how limited pathogenic determinants can generate profound clinical success. In this review, we highlight the key biological features that have established as a model system. We discuss milestone discoveries that have reshaped our understanding of its pathogenesis, emphasizing how this pathogen leverages adaptability rather than an extensive virulence arsenal to succeed as an opportunistic pathogen, expanding the field beyond antibiotic resistance toward broader questions of host-pathogen interaction and environmental adaptation. Finally, we outline major open questions in the field, including the contribution of intracellular reservoirs to chronic infection and treatment failure. Together, these perspectives position as a unique system for investigating how a seemingly minimalist pathogen achieves extraordinary adaptability and clinical success.
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2. {"_":"Impaired acid stress resistance in Typhi Ty2.","i":["Salmonella"]}
2. 伤寒Ty2菌株酸应激耐受性受损PMID:日期:2026-09-23encounters acid stress during gastrointestinal transit and within the phagosomal environment of macrophages. Acid stress resistance has been well characterized in serovar Typhimurium, but comparative studies in the human-adapted serovar Typhi are limited. We compared the growth of . Typhimurium 14028s and . Typhi Ty2 at pH values ranging from 3 to 8 and observed that serovar Typhimurium exhibits enhanced growth at pH 4.5 compared to . Typhi. Comparative transcriptomic profiling of . Typhimurium and . Typhi at pH 4.5 and 7.5 identified numerous differentially expressed acid-induced genes (DEGs), including genes encoding membrane proteins (OmpC, PhoE, HydB), a transcriptional regulator (RpoS), and stress response proteins (YciG, STM14_1829, YmdF). Targeted deletion of selected genes in . Typhimurium significantly suppressed growth at acidic pH, confirming their role in acid stress resistance. These resistance mechanisms are compromised in . Typhi due to pseudogenization. Heterologous expression of pseudogenized genes in . Typhi restored acid tolerance. Collectively, these findings suggest that . Typhi has lost the ability to withstand acid stress due to genomic decay and the loss of multiple genes essential for acid survival in . Typhimurium, reflecting divergent evolutionary paths in these two serovars. Typhimurium must adapt to acidic pH conditions in the intestinal tract and the intracellular environment to cause infection. In this study, we show that the enteric fever serovar Typhi exhibits impaired growth at pH 4.5 in comparison to Typhimurium. We further show that the loss of specific membrane proteins, a transcriptional regulator, and a family of stress response proteins in Typhi are responsible for this difference. Collectively, these observations suggest that Typhi has evolutionarily lost the ability to withstand acid stress due to differences in its interaction with the human host. This has important implications for the pathogenesis of typhoid fever.
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3. {"_":"Strain-specific outcomes of cytosine-base editing in .","i":["Streptomyces"]}
PMID:日期:2026-09-18The clustered regularly interspaced short palindromic repeats (CRISPR)-Cas system has facilitated gene editing of different organisms. Specifically, programmable base editing enables stable conversion of a single nucleotide to another nucleotide without causing DNA double-strand breaks. Cas9-derived base editors, including adenine and cytidine base editors, catalyze the formation of transition mutations with high efficiency. The third-generation cytidine base editors comprise a nickase-Cas9 fused to a cytidine deaminase and uracil DNA glycosylase inhibitor to enable the transition from C:G to T:A. We observed that in certain spp., this cytidine base editor produced C:G to G:C transversions at a surprisingly high rate of 44, while in other strains, it yielded the expected C:G to T:A transition mutations. There was also a notable timing difference for base editing between distinct strains. Bioinformatics analysis revealed differences in DNA mismatch repair and nucleotide excision repair pathways, including the presence of helicase gene only in the C:G to G:C transversion strain. Expression of in the C:G to T:A transition strain led to higher rates of C:G to G:C transversions. These discoveries will aid in the development of efficient C:G to G:C base editors. Base editors are useful tools that allow genetic engineers to precisely change single bases in an organism's genome. Most base editors catalyze transition mutations (e.g., A-to-G or C to-T). Transversion mutations, which convert a purine base to a pyrimidine base, have been described but operate at much lower efficiency. Here, we describe a surprising discovery that a transition base editor produced high-efficiency transversion mutations in a species of . This information was used to engineer a high-efficiency transversion base editor.
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4. {"_":"The status of RpoS impacts the 2-aminoacrylate stress paradigm in mutants of serovar Typhimurium.","i":["ridA","Salmonella enterica"]}
PMID:日期:2026-09-18Bacterial metabolism is composed of a complex system of anabolic and catabolic processes, and productive growth results from the regulated interplay of these processes. Genetic and biochemical studies on the LT2 type strain of serovar Typhimurium determined the need for RidA to prevent metabolic stress caused by 2-aminoacrylate (2AA). RidA is an enamine deaminase, and in its absence, 2AA accumulates and can irreversibly damage critical pyridoxal 5'-phosphate-dependent enzymes. Unexpectedly, the disruption of in a virulent type strain ( serovar Typhimurium strain 14028s) did not replicate the serine sensitivity observed in LT2. Consistent with reported differences between these strains, the status of impacted the phenotypes caused by a mutation. Specifically, serine sensitivity in the 14028s strain background occurred only when an insertion in was combined with a mutation in . Further data suggest the 14028s growth deficiency is due to poor expression of , which encodes an Fe-S cluster serine deaminase. Additional combinatorial effects of lesions in and indicate that the functional status of RpoS modulates the metabolic network in multiple ways that impact the cellular response to 2AA.IMPORTANCERidA is an enamine/imine deaminase known for mediating 2-aminoacrylate (2AA)-induced stress in several bacterial models. Best characterized in , manipulations to RidA have been used to probe metabolic flux in various bacteria. Here, we find that a key factor in the manifestation of 2AA stress is the status of transcriptional regulator RpoS. Our results indicate that a functional RpoS mediates some of the stress induced by exogenous serine in a mutant strain and further implicates this regulator in modulating the metabolic network. These results bolster our understanding of the flux and robustness integral to bacterial metabolism and emphasize a need to better understand the involvement of the RpoS regulon.
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5. {"_":"Chloramphenicol-mobilized transiently expresses resistance to multiple antibiotics, including the glycopeptides phleomycin and bleomycin.","i":["Bacillus subtilis"]}
PMID:日期:2026-09-18Antibiotic resistance presents an urgent global crisis, exacerbated by antibiotic overuse. Understanding the regulation of resistance genes within bacterial populations can inform strategies to prevent the spread of antibiotic resistance, and reveal how antibiotics shape microbial communities. We identified upregulation of five antibiotic resistance loci in colonies on solid growth media, following exposure to subinhibitory chloramphenicol concentrations. Notably, four resistance loci, and are regulated by transcription attenuation. Full expression depends upon antibiotic-induced ribosome stalling on upstream leader peptides, promoting transcription of the downstream gene. Here, we use luciferase reporter constructs fused to the 5' regulatory region of each resistance gene to show differential spatiotemporal patterns of antibiotic resistance gene expression, revealing an intrinsic activation in addition to chloramphenicol induction in mobilized colonies. Because expression is under translational regulation, the data suggest natural translation pausing, in addition to antibiotic exposure, is an endogenous function that regulates these antibiotic resistance genes. While VmlR and TlrB have been previously characterized as conferring resistance to LSPs (lincosamides, streptogramin A, and pleuromutilin) and tylosin, respectively, antibiotics for BmrCD and YtbDE resistance complexes have not yet been identified. We demonstrate that although these resistance genes do not provide resistance to chloramphenicol, pre-exposure to chloramphenicol improved growth when cells were subsequently exposed to subinhibitory concentrations of respective antibiotics. We discovered that BmrCD confers resistance to the DNA-damaging glycopeptides, phleomycin and bleomycin, revealing that resistance arising from stalled ribosomes extends beyond drugs that target translation. Antibiotics are a natural component of bacterial communities that are vital to modern medicine and combating antibiotic-resistant pathogens. Understanding the roles antibiotics play in microbial populations provides insights into the origins of antibiotic resistance. Many studies show that subinhibitory concentrations of antibiotics stimulate bacterial gene expression, including antibiotic resistance, and influence community dynamics. This study shows that bacteria on an agar surface transiently elevate expression of intrinsic resistance genes for multiple antibiotics. Subinhibitory chloramphenicol exposure stimulates the bacterial population both to expand across the surface and to enhance expression of the resistance genes in a heterogeneous pattern. The results illustrate how exposure to some antibiotics substantially changes bacterial population dynamics that include the spatiotemporally controlled expression of endogenous antibiotic resistance.
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6. Rock-making bacteria: manganese oxidation and biomineralization in pseudomonads.
PMID:日期:2026-09-18The oxidation of manganese from Mn(II) to Mn(III) or Mn(IV) is a common trait in the genus. Many pseudomonads oxidize Mn enzymatically using one or more multicopper oxidases (MnxG and McoA) and in some cases a heme peroxidase (MopA). The oxidation of Mn leads to the extracellular precipitation of reactive Mn oxides in association with extracellular polymeric substances (EPS). Here, we review the current state of knowledge on Mn oxidation and biomineralization in pseudomonads. While most of the genetic, biochemical, and physiological insights we present derive from studies on GB-1, we also examine the mechanisms of Mn oxidation in other Mn-oxidizing pseudomonads and survey the potential for Mn oxidation across the genus through phylogenetic analysis. Although the physiological and microbial community function(s) for Mn oxidation and biomineralization have yet to be elucidated, we discuss possible roles for Mn oxidation and identify key knowledge gaps regarding the mechanism and function of this trait in the genus.
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7. {"_":"How became a model for invasive bacterial predation.","i":["Bdellovibrio bacteriovorus"]}
PMID:日期:2026-09-18is a gram-negative Proteobacterium that has evolved to use a novel, predatory, intrabacterial lifestyle. Once encountered under a microscope, in a lecture, or a textbook, it is seldom forgotten. speedily collides with, enters, modifies, and kills other gram-negative bacteria. Residing inside the periplasm of the dead prey for several hours, it uses prey molecules for growth and replication, only bursting out from that temporary home when its progeny are fully formed predators themselves. Rapid motility whilst hunting contrasts with sessility during prey consumption-these key behaviors, studied by early researchers, have been followed by molecular studies in recent times. Genomic analysis has enabled the linkage and discovery of proteins involved in key regulatory circuits, allied to enzymology describing prey cell manipulation and deconstruction. Indeed, the prey bacterium of a is the natural "petri dish" of suitable components for predator growth. A fascinating conundrum continues to be: "how does a predator consume materials very similar to those from which it is built, without self-damage?". More has been discovered and is yet to be learned about these bacterial damaging enzymes: how predators use them in nature and whether they can be applied to assist human conflicts with pathogens. However, the elegance and molecular complexity, with which accomplishes its intrabacterial lifestyle, will continue to challenge researchers and present new biology in the 21st century. New discoveries, tools, and approaches position research for many more breakthroughs.
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9. {"_":"Polyunsaturated fatty acids: host-derived antimicrobials against glycolytic .","i":["Staphylococcus aureus"]}
9. 多不饱和脂肪酸：宿主来源的抗糖酵解金黄色葡萄球菌抗菌剂PMID:日期:2026-09-17Metabolic flexibility allows to survive killing by antibiotics and antimicrobial immune molecules while infecting every niche of the mammalian host. Whether is using glycolysis, aerobic respiration, or anaerobic respiration to generate energy, these cellular processes must be accurately attuned to the infected host tissue. Shifting from respiration to glycolysis lowers metabolic throughput, allowing the transition to a persistent infection and avoiding killing by most antimicrobial molecules, which typically target rapidly dividing cells. Previously, we reported that arachidonic acid (AA), an abundant host polyunsaturated fatty acid (PUFA), kills through a lipid peroxidation mechanism. Here, we report that the extent of PUFA killing of can be predicted by the autoxidation rate constant, extending our previous AA findings to include all PUFAs. Contrasting many other antimicrobial molecules, AA kills glycolytic more effectively than respiring . Elevating cellular ATP levels protects from PUFA killing, indicating that glycolytic strains cannot sufficiently energize the ATP-dependent processes that allow to survive PUFA toxicity. This report defines cellular metabolism as a key determinant in PUFA resistance and demonstrates that PUFAs are effective antimicrobials against glycolytic , including persister cells and small colony variants. Furthermore, identifying and validating the ATP-dependent processes that protect from PUFA killing will define pathways that can be targeted to accentuate killing by the host immune system, leading to the clearance of persistent infections.IMPORTANCE causes significant human morbidity and mortality. The metabolic diversity of this pathogen makes eradication challenging, leading to persistent infections in many patient populations. Polyunsaturated fatty acids (PUFAs) are host-derived antimicrobial molecules that are abundant at the host-pathogen interface. Here, we define the mechanism of killing by PUFAs in metabolically limited strains. These strains are difficult to eradicate because most therapies target rapidly dividing cells. We demonstrate that PUFAs kill slow-growing through a lipid peroxidation mechanism better than their normal growth counterparts. Restoring ATP levels in these strains protects against PUFA killing, demonstrating that the PUFA survival response is not fully energized in the low metabolic state.
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10. {"_":"An integrated view of metabolic and physiological regulation of toxin production in .","i":["Clostridioides difficile"]}
PMID:日期:2026-09-14is a leading cause of antibiotic-associated diarrhea, with pathogenesis driven primarily by the glucosylating toxins TcdA and TcdB. Traditionally, toxin gene expression has been explained through regulation of the pathogenicity locus by global transcriptional regulators that integrate nutrient availability, growth phase, and environmental signals. While this framework provides a foundation for understanding toxin regulation, recent advances have broadened this perspective to include diverse metabolic and physiological inputs, including carbon and amino acid metabolism, metal ion homeostasis, redox balance, and cellular energy status. Collectively, these factors suggest that toxin gene expression is a dynamic emergent property that reflects a high level of integration of metabolic and physiological networks. In this minireview, we discuss canonical mechanisms of toxin regulation alongside new insights that highlight population heterogeneity, energy demand conflicts, metabolic constraints, purine metabolism, and cross-regulatory networks linking sporulation and virulence. We further examine discoveries from small-molecule chemical genetics demonstrating that perturbation of metabolic pathways can suppress toxin biosynthesis without substantially affecting bacterial viability. Together, these findings redefine toxin regulation as a systems-level process in which metabolic and physiological states mediate toxin production and contribute to phenotypic heterogeneity. Elucidating these networks may reveal promising targets for the development of anti-virulence strategies for infection.