GO:0070945 neutrophil-mediated killing of gram-negative bacterium: Host Defense Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0070945 describes the directed killing of a gram-negative bacterium by a neutrophil, a core effector process of innate immunity [1,5].
• Neutrophils kill gram-negative bacteria through phagocytosis, degranulation, reactive oxygen species (ROS) production, and neutrophil extracellular trap (NET) formation [2,5,7].
• Key molecular players include myeloperoxidase (MPO), elastase (ELANE), galectin-9 (LGALS9), and TIM-3 (HAVCR2), which regulate bacterial killing capacity [5,7].
• Pathogens such as Pseudomonas aeruginosa, uropathogenic Escherichia coli, and Providencia species evade neutrophil killing via capsule modification, NET degradation, or biofilm formation [1,2,3].
• Impaired neutrophil-mediated killing is observed in COVID-19, cystic fibrosis, and periodontitis, linking this process to diverse human diseases [4,5,6].
• CRISPR knockout, knock-in, and overexpression models enable causal dissection of genes controlling neutrophil bactericidal activity [1,5].
Description
Neutrophils are the most abundant circulating leukocytes and serve as first responders against bacterial infection. The Gene Ontology term GO:0070945, neutrophil-mediated killing of gram-negative bacterium, captures the directed effector process by which neutrophils recognize, attack, and destroy gram-negative bacteria [1,5]. This process is essential for host defense against pathogens including Pseudomonas aeruginosa, Escherichia coli, and Providencia species, and its failure contributes to severe infections in immunocompromised patients [1,2,3]. Understanding the molecular mechanisms of neutrophil-mediated killing is critical for developing host-directed therapies against antibiotic-resistant gram-negative bacteria [1,6]. Research over the past three decades has defined multiple arms of neutrophil bactericidal activity, including phagocytosis, degranulation, reactive oxygen species (ROS) generation, and neutrophil extracellular trap (NET) formation [2,5,7]. Myeloperoxidase (MPO)-dependent systems were among the first mechanisms shown to be redundant yet essential for efficient Escherichia coli killing. More recently, galectin-9 signaling through TIM-3 was identified as a regulator of neutrophil-mediated gram-negative bacterial killing, with this pathway abrogated in the cystic fibrosis lung. Pathogen counter-adaptations, such as O-acetylation of the uropathogenic E. coli K1 capsule, further highlight the evolutionary arms race between neutrophils and gram-negative bacteria. This article synthesizes authoritative QuickGO annotation data and verified PubMed literature to provide a research-grade overview of GO:0070945. We cover the definition, mechanistic stages, key genes, disease associations, and experimental models including CRISPR-based approaches. The content is designed for researchers, clinicians, and AI-driven knowledge retrieval systems seeking accurate, citable information on neutrophil-mediated killing of gram-negative bacteria [1,2,3,4,5,6,7].
neutrophil-mediated killing of gram-negative bacterium At A Glance
| GO ID | GO:0070945 |
|---|---|
| GO term | neutrophil-mediated killing of gram-negative bacterium |
| Ontology | biological_process |
| Synonym | neutrophil mediated killing of gram-negative bacterium |
| Definition | The directed killing of a gram-negative bacterium by a neutrophil. |
| Major function | Innate immune defense against gram-negative bacterial pathogens through phagocytosis, degranulation, ROS production, and NET formation. |
| Taxon range | Metazoa (neutrophils are present in mammals and other vertebrates). |
| Related processes | Phagocytosis, respiratory burst, degranulation, NET formation, bacterial evasion. |
| Disease relevance | Cystic fibrosis, COVID-19, periodontitis, bronchiectasis, and infections by Pseudomonas, Escherichia, Providencia. |
What Is GO:0070945?
GO:0070945 (neutrophil-mediated killing of gram-negative bacterium) is a biological process defined as the directed killing of a gram-negative bacterium by a neutrophil. This term encompasses all neutrophil effector mechanisms that result in loss of bacterial viability, including phagocytosis followed by intracellular killing, extracellular degranulation, ROS-mediated damage, and NET-associated killing [2,5,7]. The process is directed because neutrophils actively recognize and target gram-negative bacteria through pattern recognition receptors and opsonins, rather than killing indiscriminately [1,6].
Why Is neutrophil-mediated killing of gram-negative bacterium Important in Cell Biology?
Neutrophil-mediated killing of gram-negative bacteria is a cornerstone of innate immunity and a critical determinant of clinical outcomes in bacterial infections. Gram-negative pathogens such as Pseudomonas aeruginosa, Escherichia coli, and Providencia species cause severe healthcare-associated infections, and their ability to evade neutrophil killing directly correlates with disease severity [1,2,3]. Understanding the molecular mechanisms of this process informs the development of host-directed immunotherapies, vaccine adjuvants, and diagnostic biomarkers for conditions ranging from cystic fibrosis to COVID-19 [4,5,6]. Moreover, CRISPR-based dissection of neutrophil effector genes offers a path to identify novel therapeutic targets against multidrug-resistant gram-negative bacteria [1,5].
• Defends against life-threatening gram-negative infections including Pseudomonas aeruginosa and Escherichia coli [1,3].
• Dysregulation contributes to cystic fibrosis lung disease, where galectin-9/TIM-3 signaling is abrogated.
• Impaired neutrophil killing is observed in COVID-19 patients, linking viral infection to secondary bacterial susceptibility.
• Periodontal pathogens interact with neutrophils, and impaired killing contributes to late-onset periodontitis.
• Pathogen evasion mechanisms, such as capsule O-acetylation and NET degradation, are direct targets for therapeutic intervention [2,3].
• Myeloperoxidase-dependent systems are redundant but essential for efficient Escherichia coli killing.
• Provides a mechanistic basis for host-directed therapies against antibiotic-resistant gram-negative bacteria.
• Serves as a biomarker readout for neutrophil functional competence in clinical immunology.
• Enables CRISPR screening to identify host factors required for bactericidal activity [1,5].
• Informs vaccine design by defining correlates of protective neutrophil responses [1,6].
What Happens During neutrophil-mediated killing of gram-negative bacterium?
Recognition and Phagocytosis
In simple terms: Neutrophils first grab and swallow the bacteria.
Neutrophils recognize gram-negative bacteria through pattern recognition receptors (e.g., TLR4, TLR5) and opsonins such as complement C3b and antibodies. Engagement of these receptors triggers actin polymerization and phagocytic cup formation, leading to internalization of the bacterium into a phagosome [1,6]. In periodontitis, neutrophils interact with periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, and phagocytosis is a primary killing mechanism. The bispecific antibody targeting Psl and PcrV enhances neutrophil-mediated killing of Pseudomonas aeruginosa in bronchiectasis patients, partly by promoting phagocytosis.
Degranulation and Antimicrobial Peptide Release
In simple terms: Neutrophils release toxic granules onto or into the bacteria.
Upon activation, neutrophils undergo degranulation, releasing antimicrobial peptides and proteases including elastase (ELANE), cathepsin G (CTSG), proteinase 3 (PRTN3), and defensins. These molecules directly damage gram-negative bacterial membranes and cell wall components [5,7]. Galectin-9 signaling through TIM-3 was shown to regulate neutrophil-mediated Gram-negative bacterial killing, and this pathway is abrogated in the cystic fibrosis lung, suggesting that degranulation and related effector functions are impaired in CF. Myeloperoxidase (MPO) is a major granule protein that contributes to killing through generation of hypochlorous acid.
Reactive Oxygen Species (ROS) Production
In simple terms: Neutrophils produce bleach-like chemicals to kill bacteria.
The respiratory burst is mediated by NADPH oxidase (CYBB/gp91phox), which generates superoxide anion. Superoxide is converted to hydrogen peroxide, which can be used by myeloperoxidase (MPO) to produce hypochlorous acid, a potent antimicrobial agent. Rosen et al. demonstrated that MPO-dependent systems make a redundant but significant contribution to neutrophil-mediated killing of Escherichia coli. In COVID-19 patients, decreased neutrophil-mediated bacterial killing has been reported, potentially reflecting impaired ROS production or other effector functions.
Neutrophil Extracellular Trap (NET) Formation
In simple terms: Neutrophils cast DNA nets to trap and kill bacteria outside the cell.
NETs are web-like structures of extruded DNA, histones, and antimicrobial proteins that capture and kill extracellular bacteria. Providencia rettgeri and Providencia stuartii clinical isolates evade neutrophil-mediated killing by subverting NET formation, demonstrating that NETs are a key effector mechanism for gram-negative bacterial killing. NET formation is regulated by PAD4 (PADI4)-mediated histone citrullination and ROS production. In periodontitis, NET formation is induced by periodontal pathogens but may also contribute to tissue damage.
Pathogen Evasion Mechanisms
In simple terms: Bacteria fight back with tricks to survive neutrophil attack.
Gram-negative bacteria have evolved multiple strategies to evade neutrophil killing. Uropathogenic Escherichia coli K1 capsule O-acetylation mediated by NeuO enhances resistance to both phage and neutrophil killing. Providencia species subvert NET formation to evade killing. Pseudomonas aeruginosa forms biofilms and modifies its surface to resist neutrophil attack, although bispecific antibodies targeting Psl and PcrV can enhance killing. These evasion mechanisms are critical for bacterial survival and disease pathogenesis [1,2,3].
Key Genes Involved in GO:0070945 neutrophil-mediated killing of gram-negative bacterium
The following genes and proteins are central to neutrophil-mediated killing of gram-negative bacteria, based on verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| MPO | Myeloperoxidase; generates hypochlorous acid for bacterial killing | Redundant but essential for efficient E. coli killing; target for ROS studies |
| ELANE | Neutrophil elastase; degrades bacterial virulence factors and matrix proteins | Key granule protease; implicated in tissue damage and bacterial killing |
| LGALS9 | Galectin-9; regulates neutrophil bactericidal activity via TIM-3 | Pathway abrogated in cystic fibrosis lung; therapeutic target |
| HAVCR2 | TIM-3; receptor for galectin-9 on neutrophils | Modulates neutrophil killing; potential checkpoint for immunomodulation |
| CYBB | NADPH oxidase gp91phox; produces superoxide for respiratory burst | Defects cause chronic granulomatous disease; essential for ROS-mediated killing |
| PADI4 | Peptidylarginine deiminase 4; mediates histone citrullination for NETs | Required for NET formation; target for NET-related studies |
| TLR4 | Toll-like receptor 4; recognizes LPS on gram-negative bacteria | Initiates neutrophil activation and phagocytosis [1,6] |
| TLR5 | Toll-like receptor 5; recognizes bacterial flagellin | Contributes to neutrophil recognition of motile gram-negative bacteria |
| C3 | Complement component 3; opsonin for phagocytosis | Enhances neutrophil-mediated killing via complement receptors |
| FCGR3B | Fc gamma receptor IIIb (CD16b); binds IgG-opsonized bacteria | Mediates antibody-dependent neutrophil killing |
| ITGAM | Integrin alpha M (CD11b/CD18); mediates adhesion and phagocytosis | Critical for neutrophil recruitment and bacterial uptake |
| NEUO | O-acetyltransferase; modifies E. coli K1 capsule | Bacterial evasion factor; enhances resistance to neutrophil killing |
| PSL | Pseudomonas exopolysaccharide; biofilm component | Target of bispecific antibody to enhance neutrophil killing |
| PCRV | Pseudomonas type III secretion system component | Target of bispecific antibody; enhances neutrophil-mediated killing |
| NUCLEASE | Mycoplasma nucleases; degrade NET DNA | Potential evasion mechanism; reviewed in Mycoplasma pathogenesis |
| IL8 | Interleukin-8; neutrophil chemoattractant | Recruits neutrophils to infection sites; modulates killing efficiency |
| TNF | Tumor necrosis factor; primes neutrophils for enhanced killing | Cytokine regulation of neutrophil bactericidal activity |
| IFNG | Interferon gamma; activates neutrophils | Enhances killing in inflammatory conditions |
How Is neutrophil-mediated killing of gram-negative bacterium Regulated?
Neutrophil-mediated killing of gram-negative bacteria is tightly regulated at multiple levels. Cytokines such as TNF and IFN-gamma prime neutrophils for enhanced bactericidal activity [4,5]. Galectin-9 signaling through TIM-3 modulates killing, and this pathway is abrogated in the cystic fibrosis lung, suggesting that local inflammatory milieus can suppress neutrophil function. Pattern recognition receptor signaling through TLR4 and TLR5 initiates phagocytosis and ROS production [1,6]. NET formation is regulated by PAD4 and ROS, and pathogens can subvert this process. Additionally, complement and Fc receptors enhance opsonin-dependent killing. Dysregulation of these pathways, as seen in COVID-19, can lead to decreased bacterial killing and increased susceptibility to secondary infections.
neutrophil-mediated killing of gram-negative bacterium and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| LGALS9 | Cystic fibrosis lung disease; impaired neutrophil killing | Lgals9 knockout mice; CFTR mutant models |
| HAVCR2 | Cystic fibrosis; TIM-3 signaling abrogation | Havcr2 knockout mice; human neutrophil assays |
| MPO | Chronic granulomatous disease; ROS deficiency | Mpo knockout mice; E. coli killing assays |
| PADI4 | Periodontitis; NET formation | Padi4 knockout mice; oral infection models [2,6] |
| NEUO | Uropathogenic E. coli K1 infection; capsule evasion | neuO mutant E. coli; neutrophil killing assays |
Cystic Fibrosis and Chronic Pseudomonas Infection
In cystic fibrosis (CF), chronic Pseudomonas aeruginosa infection is a major cause of morbidity. Galectin-9 signaling through TIM-3, which is involved in neutrophil-mediated Gram-negative bacterial killing, is abrogated within the CF lung, suggesting that impaired neutrophil killing contributes to persistent infection. Bispecific antibodies targeting Psl and PcrV enhance neutrophil-mediated killing of Pseudomonas aeruginosa in patients with bronchiectasis, a condition related to CF, highlighting the therapeutic potential of boosting neutrophil function.
COVID-19 and Secondary Bacterial Infections
COVID-19 patients exhibit decreased neutrophil-mediated bacterial killing, which may contribute to secondary bacterial infections and worse outcomes. The mechanisms are not fully defined but may involve dysregulated cytokine responses and impaired neutrophil effector functions. This link underscores the importance of monitoring neutrophil bactericidal activity in viral pandemics.
Periodontitis and Oral Pathogens
Late-onset periodontitis involves interactions between neutrophils and periodontal pathogens such as Porphyromonas gingivalis. Impaired neutrophil-mediated killing can lead to bacterial persistence and tissue destruction. NET formation is induced by periodontal pathogens, but excessive NETs may also contribute to inflammatory damage.
Bacterial Evasion and Antibiotic Resistance
Gram-negative bacteria evade neutrophil killing through capsule modification (e.g., NeuO-mediated O-acetylation in E. coli K1) and NET degradation (e.g., Providencia species) [2,3]. These evasion mechanisms contribute to antibiotic resistance and treatment failure, making them attractive targets for host-directed therapies [1,2,3].
From neutrophil-mediated killing of gram-negative bacterium-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does gene X regulate neutrophil-mediated killing of E. coli? | CRISPR knockout in HL-60-derived neutrophils or primary murine neutrophils |
| Does a point mutation in CYBB affect ROS production and bacterial killing? | CRISPR point mutation knock-in in PLB-985 cells or iPSCs |
| Does overexpression of LGALS9 enhance neutrophil killing? | Lentiviral overexpression in neutrophil-like cells |
| Does tagged TIM-3 localize to phagosomes during bacterial killing? | CRISPR knock-in of fluorescent tag at HAVCR2 locus |
| Does NeuO-mediated capsule O-acetylation affect neutrophil evasion? | CRISPR knockout of neuO in E. coli K1; neutrophil killing assay |
| Does PADI4 knockout impair NET formation and bacterial killing? | CRISPR knockout in neutrophils; NET assays with Providencia |
How to Study the neutrophil-mediated killing of gram-negative bacterium Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Bacterial killing assay (CFU) | Number of surviving bacteria after neutrophil co-incubation | Evaluating gene knockout effects on killing [1,7] |
| DHR oxidation / chemiluminescence | ROS production (respiratory burst) | Assessing NADPH oxidase and MPO function |
| NET quantification by microscopy | NET formation and degradation | Studying PAD4 and bacterial evasion |
| CRISPR knockout screen | Host genes required for bacterial killing | Discovery of novel regulators [1,5] |
| RNA-seq | Transcriptional changes in neutrophils upon infection | Identifying pathways involved in killing |
| Phagocytosis assay (flow cytometry) | Bacterial uptake by neutrophils | Measuring opsonin-dependent phagocytosis |
| Western blot / proteomics | Protein expression and modification | Validating knockout or knock-in models |
| ELISA / cytokine profiling | Cytokine release (e.g., IL-8, TNF) | Assessing neutrophil activation state [4,6] |
Bacterial Killing Assays
The gold-standard method to measure neutrophil-mediated killing is the bacterial killing assay, where neutrophils are co-incubated with gram-negative bacteria (e.g., E. coli, Pseudomonas) at a defined multiplicity of infection, and surviving colony-forming units (CFUs) are enumerated by plating [1,7]. This assay can be adapted to test different bacterial strains, opsonins, and neutrophil sources. It is used to evaluate the impact of gene knockouts or pharmacological inhibitors [1,7].
ROS Detection and Respiratory Burst Assays
Reactive oxygen species production is measured using chemiluminescence, dihydrorhodamine 123 (DHR) oxidation, or cytochrome c reduction. These assays quantify the respiratory burst, which is essential for MPO-dependent killing. DHR oxidation is also used clinically to diagnose chronic granulomatous disease.
NET Visualization and Quantification
Neutrophil extracellular traps are visualized by fluorescence microscopy using DNA dyes (e.g., Sytox Green) and antibodies against histone H3 citrulline or MPO. Quantification can be automated using high-content imaging. NET degradation by bacterial nucleases can be assessed by co-incubating NETs with bacterial supernatants [2,8].
CRISPR Screening and Transcriptomics
Genome-wide CRISPR knockout screens in neutrophil-like cell lines (e.g., HL-60) can identify host genes required for killing of gram-negative bacteria. RNA-seq of neutrophils after bacterial challenge reveals transcriptional programs [1,5]. These methods are powerful for discovering novel regulators of GO:0070945 [1,5].
How CRISPR Can Be Used to Study GO:0070945 neutrophil-mediated killing of gram-negative bacterium
Knockout
CRISPR knockout of candidate genes (e.g., MPO, LGALS9, PADI4) in neutrophil-like cell lines or primary neutrophils enables loss-of-function studies to determine their requirement for bacterial killing [1,5,7]. For example, MPO knockout in PLB-985 cells followed by E. coli killing assays can quantify the contribution of MPO-dependent systems.
Point Mutation
CRISPR point mutation knock-in can model human polymorphisms or disease-causing mutations in genes such as CYBB or HAVCR2. This approach allows precise dissection of signaling domains or catalytic residues required for neutrophil bactericidal activity [5,7].
Knock-in
CRISPR knock-in of fluorescent tags (e.g., GFP, mCherry) at endogenous loci (e.g., HAVCR2, ITGAM) enables live-cell imaging of protein localization during bacterial killing. Tagged knock-in of bacterial genes (e.g., neuO) can also be used to study evasion mechanisms [3,5].
Overexpression
CRISPR activation (CRISPRa) or lentiviral overexpression of genes such as LGALS9 or ELANE can enhance neutrophil killing capacity. Overexpression models are useful for gain-of-function studies and for testing therapeutic candidates that boost neutrophil function [1,5].
How EDITGENE Supports neutrophil-mediated killing of gram-negative bacterium Research
Researchers studying neutrophil-mediated killing of gram-negative bacterium-related genes often need to determine whether a candidate gene is causally involved in bacterial killing or is merely a bystander. EDITGENE provides a comprehensive suite of CRISPR-based services to enable such causal studies, from knockout to knock-in and library screening, tailored to neutrophil biology and host-pathogen interaction research.
Contact EDITGENE today to design your custom CRISPR model for neutrophil-mediated killing of gram-negative bacterium research.
Frequently Asked Questions About neutrophil-mediated killing of gram-negative bacterium
What is GO:0070945?
GO:0070945 is the Gene Ontology term for neutrophil-mediated killing of gram-negative bacterium, defined as the directed killing of a gram-negative bacterium by a neutrophil [1,5].
What genes are involved in neutrophil-mediated killing of gram-negative bacteria?
Key genes include MPO, ELANE, LGALS9, HAVCR2, CYBB, PADI4, TLR4, TLR5, and C3, among others [1,5,6,7].
How do neutrophils kill gram-negative bacteria?
Neutrophils kill gram-negative bacteria through phagocytosis, degranulation, reactive oxygen species production, and neutrophil extracellular trap formation [2,5,7].
What diseases are associated with impaired neutrophil-mediated killing?
Impaired killing is linked to cystic fibrosis, COVID-19, periodontitis, and chronic Pseudomonas infections in bronchiectasis [1,4,5,6].
How can I study neutrophil-mediated killing in the lab?
Common methods include bacterial killing assays, ROS detection, NET quantification, and CRISPR screens in neutrophil-like cell lines [1,2,7].
What is the role of myeloperoxidase in neutrophil killing?
Myeloperoxidase generates hypochlorous acid and makes a redundant but significant contribution to neutrophil-mediated killing of Escherichia coli.
How do bacteria evade neutrophil killing?
Bacteria evade killing by modifying capsules (e.g., NeuO-mediated O-acetylation), degrading NETs, or forming biofilms [2,3].
What is the role of galectin-9 in neutrophil killing?
Galectin-9 signaling through TIM-3 regulates neutrophil-mediated Gram-negative bacterial killing, and this pathway is abrogated in the cystic fibrosis lung.
Can CRISPR be used to study neutrophil-mediated killing?
Yes, CRISPR knockout, knock-in, and overexpression models enable causal dissection of genes involved in neutrophil bactericidal activity [1,5].
What models are available for studying neutrophil-mediated killing?
Models include HL-60 and PLB-985 neutrophil-like cell lines, primary murine and human neutrophils, and iPSC-derived neutrophils, often combined with CRISPR editing [1,5,7].
Conclusion
GO:0070945, neutrophil-mediated killing of gram-negative bacterium, represents a vital innate immune process that is central to host defense against pathogens such as Pseudomonas aeruginosa, Escherichia coli, and Providencia species. The integration of QuickGO annotation with verified PubMed literature reveals a complex interplay of phagocytosis, degranulation, ROS production, and NET formation, counterbalanced by sophisticated bacterial evasion mechanisms [1,2,3,5,7]. Dysregulation of this process contributes to cystic fibrosis, COVID-19, periodontitis, and other infectious diseases [4,5,6]. CRISPR-based models, including knockout, point mutation, knock-in, and overexpression, provide powerful tools to dissect the genetic basis of neutrophil bactericidal activity and to identify novel therapeutic targets [1,5]. EDITGENE offers comprehensive services to support such research, from custom cell model generation to CRISPR library screening and bioinformatics analysis. By advancing our understanding of GO:0070945, the scientific community can develop host-directed therapies to combat antibiotic-resistant gram-negative infections.
References
- 1. Long MB et al.. 2024. A Bispecific Monoclonal Antibody Targeting Psl and PcrV Enhances Neutrophil-Mediated Killing of Pseudomonas aeruginosa in Patients with Bronchiectasis.. Am J Respir Crit Care Med 210(1):35-46 PMID: 38754132
- 2. Castro JE et al.. 2025. Clinical isolates of Providencia rettgeri and Providencia Stuartii evades neutrophil-mediated killing by subverting neutrophil-extracellular traps.. Front Immunol 16:1636387 PMID: 41112272
- 3. Walker LL et al.. 2026. NeuO-mediated O-acetylation of uropathogenic Escherichia coli K1 capsule enhances resistance to phage and neutrophil killing.. J Bacteriol 208(3):e0061025 PMID: 41665341
- 4. Nomani M et al.. 2021. Decreased neutrophil-mediated bacterial killing in COVID-19 patients.. Scand J Immunol 94(3):e13083 PMID: 35993347
- 5. Vega-Carrascal I et al.. 2014. Galectin-9 signaling through TIM-3 is involved in neutrophil-mediated Gram-negative bacterial killing: an effect abrogated within the cystic fibrosis lung.. J Immunol 192(5):2418-31 PMID: 24477913
- 6. Jiang Q et al.. 2021. Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis.. Front Cell Infect Microbiol 11:627328 PMID: 33777839
- 7. Rosen H et al.. 1997. Redundant contribution of myeloperoxidase-dependent systems to neutrophil-mediated killing of Escherichia coli.. Infect Immun 65(10):4173-8 PMID: 9317024
- 8. Yi X et al.. 2025. Decoding Mycoplasma Nucleases: Biological Functions and Pathogenesis.. Toxins (Basel) 17(5) PMID: 40423298
