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  1. The emerging oral pathogen, Filifactor alocis , extends the functional lifespan of human neutrophils
  2. Filifactor alocis manipulates human neutrophils affecting their ability to release neutrophil extracellular traps induced by PMA
  3. Filifactor alocis modulates human neutrophil antimicrobial functional responses
  4. Peptoanaerobacter stomatis Primes Human Neutrophils and Induces Granule Exocytosis
  5. Filifactor alocis Promotes Neutrophil Degranulation and Chemotactic Activity
  6. Contrasting Inflammatory Responses in Severe and Non-severe Community-acquired Pneumonia
  7. Filifactor alocis Infection and Inflammatory Responses in the Mouse Subcutaneous Chamber Model
  8. Oral Community Interactions of Filifactor alocis In Vitro
  9. Inhibition of Neutrophil Exocytosis Ameliorates Acute Lung Injury in Rats
  10. Understanding the roles of cytokines and neutrophil activity and neutrophil apoptosis in the protective versus deleterious inflammatory response in pneumonia
  11. Exocytosis of Neutrophil Granule Subsets and Activation of Prolyl Isomerase 1 Are Required for Respiratory Burst Priming
  12. Application of proteomics to neutrophil biology
  13. Granule exocytosis contributes to TNF-α and PAF-induced priming in human neutrophils
  14. Alcohol-induced S-adenosylhomocysteine accumulation in the liver sensitizes to TNF hepatotoxicity: Possible involvement of mitochondrial S-adenosylmethionine transport
  15. S-adenosylmethionine (SAMe) modulates interleukin-10 and interleukin-6, but not TNF, production via the adenosine (A2) receptor
  16. Modulation of endotoxin stimulated interleukin-6 production in monocytes and Kupffer cells by S-adenosylmethionine (SAMe)
  17. S-adenosylhomocysteine sensitizes to TNF-α hepatotoxicity in mice and liver cells: A possible etiological factor in alcoholic liver disease
  18. MAPK-activated protein kinase-2 participates in p38 MAPK-dependent and ERK-dependent functions in human neutrophils
  19. Effect of Macrolide Antibiotics on Human Endothelial Cells Activated by Chlamydia pneumoniae Infection and Tumor Necrosis Factor–α