232 results on '"Zetoune, Firas S."'
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2. The Impact of Extracellular Histones and Absence of Toll-like Receptors on Cardiac Functional and Electrical Disturbances in Mouse Hearts.
3. Complement as a Major Inducer of Harmful Events in Infectious Sepsis
4. THE IMMUNOPATHOGENESIS OF POLYMICROBIAL SEPSIS
5. Role of Complement in Multi-Organ Dysfunction Syndrome
6. Organ distribution of histones after intravenous infusion of FITC histones or after sepsis
7. Phagocyte-derived catecholamines enhance acute inflammatory injury
8. Generation of C5a in the absence of C3: a new complement activation pathway
9. Role of Complement and Histones in Sepsis
10. Requirement of Complement C6 for Intact Innate Immune Responses in Mice
11. Inflammatory Disorders
12. Murine Complement Interactions with Pseudomonas aeruginosa and Their Consequences During Pneumonia
13. Regulation by C5a of Neutrophil Activation during Sepsis
14. Anti-complement Strategies in Experimental Sepsis
15. Increased C5a receptor expression in sepsis
16. A20 INHIBITS NF-κB ACTIVATION DOWNSTREAM OF MULTIPLE MAP3 KINASES AND INTERACTS WITH THE IκB SIGNALOSOME
17. Harmful Roles of TLR3 and TLR9 in Cardiac Dysfunction Developing during Polymicrobial Sepsis
18. Complement Destabilizes Cardiomyocyte Function in Vivo after Polymicrobial Sepsis and In Vitro 2
19. Complement‐induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction
20. Selective Biological Responses of Phagocytes and Lungs to Purified Histones
21. Regulation of IL-17 Family Members by Adrenal Hormones During Experimental Sepsis in Mice
22. Complement Destabilizes Cardiomyocyte Function In Vivo after Polymicrobial Sepsis and In Vitro
23. Complement‐induced activation of the cardiac NLRP3 inflammasome in sepsis
24. Bidirectional Crosstalk between C5a Receptors and the NLRP3 Inflammasome in Macrophages and Monocytes
25. C5a interaction with both C5aR and C5L2 receptors is required for production of G-CSF during the acute inflammatory response
26. Role of extracellular histones in the cardiomyopathy of sepsis
27. Cutting Edge: Critical Role for C5aRs in the Development of Septic Lymphopenia in Mice
28. Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3
29. Complement-induced activation of the cardiac NLRP3 inflammasome in sepsis.
30. Role of Complement in Multi-Organ Dysfunction Syndrome
31. Critical Role for the NLRP3 Inflammasome during Acute Lung Injury
32. Persistent Neutrophil Dysfunction and Suppression of Acute Lung Injury in Mice following Cecal Ligation and Puncture Sepsis
33. Induction of M2 Regulatory Macrophages through the β2-Adrenergic Receptor with Protection during Endotoxemia and Acute Lung Injury
34. Extracellular histones are essential effectors of C5aR‐ and C5L2‐mediated tissue damage and inflammation in acute lung injury
35. Zonulin as prehaptoglobin2 regulates lung permeability and activates the complement system
36. The interaction between C5a and both C5aR and C5L2 receptors is required for production of G‐CSF during acute inflammation
37. CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury
38. Inflammatory Disorders
39. Complement Activation Product C5a Is a Selective Suppressor of TLR4-Induced, but Not TLR3-Induced, Production of IL-27(p28) from Macrophages
40. Anti‐inflammatory effects of β 2 adrenergic receptor agonists in experimental acute lung injury
41. Evidence for anti‐inflammatory effects of C5a on the innate IL‐17A/IL‐23 axis
42. The Outcome of Polymicrobial Sepsis Is Independent of T and B CellS
43. MyD88‐dependent production of IL‐17F is modulated by the anaphylatoxin C5aviathe Akt signaling pathway
44. Complement dependency of cardiomyocyte release of mediators during sepsis
45. C5aR negatively regulates in vivo and in vitro production of IL-17A
46. Cross-Talk between TLR4 and FcγReceptorIII (CD16) Pathways
47. Immunopathogenesis of lipopolysaccharide- and IgG immune complex-induced acute lung injury in rodents
48. Functions of the complement components C3 and C5 during sepsis
49. Acute Lung Injury Induced by Lipopolysaccharide Is Independent of Complement Activation
50. Functional roles for C5a receptors in sepsis
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