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  1. Comparison of single-cell RNA-seq methods to enable transcriptome profiling of neutrophils in clinical samples
  2. The "Master Key" to Fighting Respiratory Viruses: Looking into Our Own Cells’ Machinery
  3. TRPA1 and TPRV1 Ion Channels Are Required for Contact Lens-Induced Corneal Parainflammation and Can Modulate Levels of Resident Corneal Immune Cells
  4. Pseudomonas aeruginosa Can Diversify after Host Cell Invasion to Establish Multiple Intracellular Niches
  5. Human tear fluid modulates the Pseudomonas aeruginosa transcriptome to alter antibiotic susceptibility
  6. Nerve‐associated transient receptor potential ion channels can contribute to intrinsic resistance to bacterial adhesion in vivo
  7. Contact lens-related corneal infection: Intrinsic resistance and its compromise
  8. DMBT1 inhibition of Pseudomonas aeruginosa twitching motility involves its N-glycosylation and cannot be conferred by the Scavenger Receptor Cysteine-Rich bacteria-binding peptide domain
  9. Type IV Pili Can Mediate Bacterial Motility within Epithelial Cells
  10. A novel murine model for contact lens wear reveals clandestine IL-1R dependent corneal parainflammation and susceptibility to microbial keratitis upon inoculation with Pseudomonas aeruginosa
  11. IL-1R and MyD88 Contribute to the Absence of a Bacterial Microbiome on the Healthy Murine Cornea
  12. Epithelial cell lysates induce ExoS expression and secretion by Pseudomonas aeruginosa
  13. Quantification of Bacterial Twitching Motility in Dense Colonies Using Transmitted Light Microscopy and Computational Image Analysis
  14. Contributions of MyD88-dependent receptors and CD11c-positive cells to corneal epithelial barrier function against Pseudomonas aeruginosa
  15. Correction: Mucosal fluid glycoprotein DMBT1 suppresses twitching motility and virulence of the opportunistic pathogen Pseudomonas aeruginosa
  16. Corneal surface glycosylation is modulated by IL-1R and Pseudomonas aeruginosa challenge but is insufficient for inhibiting bacterial binding
  17. Mucosal fluid glycoprotein DMBT1 suppresses twitching motility and virulence of the opportunistic pathogen Pseudomonas aeruginosa
  18. Pseudomonas aeruginosa Outer Membrane Vesicles Triggered by Human Mucosal Fluid and Lysozyme Can Prime Host Tissue Surfaces for Bacterial Adhesion
  19. Genomic Analysis Reveals the Molecular Basis for Capsule Loss in the Group B Streptococcus Population
  20. The Importance of the Pseudomonas aeruginosa Type III Secretion System in Epithelium Traversal Depends upon Conditions of Host Susceptibility
  21. Analysis of Two-Component Systems in Group B Streptococcus Shows That RgfAC and the Novel FspSR Modulate Virulence and Bacterial Fitness
  22. Adaptive Response of Group B Streptococcus to High Glucose Conditions: New Insights on the CovRS Regulation Network
  23. Propionibacterium acneshost cell tropism contributes to vimentin-mediated invasion and induction of inflammation
  24. A Novel Phase Variation Mechanism in the Meningococcus Driven by a Ligand-Responsive Repressor and Differential Spacing of Distal Promoter Elements
  25. The RNA Chaperone Hfq Is Involved in Stress Response and Virulence in Neisseria meningitidis and Is a Pleiotropic Regulator of Protein Expression
  26. The Hfq-Dependent Small Noncoding RNA NrrF Directly Mediates Fur-Dependent Positive Regulation of Succinate Dehydrogenase in Neisseria meningitidis
  27. OxyR tightly regulates catalase expression inNeisseria meningitidisthrough both repression and activation mechanisms