Alveolar macrophage activation after trauma-hemorrhage and sepsis is dependent on NF-κB and MAPK/ERK mechanisms

American Journal of Physiology - Lung Cellular and Molecular Physiology

Volumn 283, Issue 4 27-4, 2002, Pages

  Jarrar, Doraid ^a   Kuebler, Joachim F ^a   Rue III, Loring W ^a   Matalon, Sadis ^b   Wang, Ping ^a   Bland, Kirby I ^a   Chaudry, Irshad H ^a,c  

^a Center for Surgical Research   (United States)

^b UNIVERSITY OF ALABAMA AT BIRMINGHAM   (United States)

^c Kentucky   (United States)

Author keywords

Acute respiratory distress syndrome; Extracellular signal regulated kinase; Leukocytes; Macrophage inflammatory protein; Mitogen activated protein kinase; Nuclear factor B

Indexed keywords

CHEMOKINE; CYTOKINE; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; MACROPHAGE INFLAMMATORY PROTEIN 2; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE INHIBITOR; MYELOPEROXIDASE; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLEEDING; CONTROLLED STUDY; CRYSTALLOID; CYTOKINE RELEASE; ENZYME ACTIVITY; HEMORRHAGIC SHOCK; INFLAMMATION; INJURY; LEUKOCYTE ACTIVATION; LUNG ALVEOLUS MACROPHAGE; LUNG EDEMA; LUNG WEIGHT; MACROPHAGE ACTIVATION; NONHUMAN; PRIORITY JOURNAL; RAT; RESPIRATORY DISTRESS SYNDROME; RESUSCITATION; SEPSIS; SIGNAL TRANSDUCTION; SOFT TISSUE INJURY;

EID: 0036784066     PISSN: 10400605     EISSN: None     Source Type: Journal    
DOI: 10.1152/ajplung.00465.2001     Document Type: Article

References (43)

1. Neutrophils as early immunologic effectors in hemorrhage- or endotoxemia-induced acute lung injury
2. Polymicrobial sepsis selectively activates peritoneal but not alveolar macrophages to release inflammatory mediators (interleukins-1 and -6 and tumor necrosis factor)
3. Initial management of trauma. The first 5 minutes
4. Systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), multiple organ failure (MOF): Are we winning the battle?
5. The p38 MAP kinase inhibitor SB203580 enhances nuclear factor-kappa B transcriptional activity by a non-specific effect upon the ERK pathway
6. Regulation of an essential innate immune response by the p50 subunit of NF-kappaB
7. Both Erk and p38 kinases are necessary for cytokine gene transcription
8. Effect of sepsis on tissue adenine nucleotide levels
9. Pentoxifylline suppression of tumor necrosis factor gene transcription
10. The complex pattern of cytokines in sepsis. Association between prostaglandins, cachectin, and interleukins
11. Depression of cellular immunity after major injury. Its association with posttraumatic complications and its reversal with immunomodulation
12. Priming for enhanced alveolar fibrin deposition after hemorrhagic shock: Role of tumor necrosis factor
13. Transcriptional mechanisms of acute lung injury
14. Inhibitor of protein tyrosine kinase, radicicol, suppresses the expression of cyclooxygenase and pro-inflammatory cytokines in LPS-stimulated rat alveolar macrophage in part by accelerating degradation of mRNA
15. Outcome after hemorrhagic shock in trauma patients
16. Ventilation-induced chemokine and cytokine release is associated with activation of nuclear factor-kappaB and is blocked by steroids
17. Anticytokine therapies for acute inflammation and the systemic inflammatory response syndrome: IL-10 and ischemia/reperfusion injury as a new paradigm
18. Organ dysfunction following hemorrhage and sepsis: Mechanisms and therapeutic approaches
19. Hepatocellular dysfunction: "Basic considerations"
20. Genistein prevents nuclear factor-kappa B activation and acute lung injury induced by lipopolysaccharide
21. Strategies of invasive ventilatory support in ARDS
22. Hemorrhage increases cytokine expression in lung mononuclear cells in mice: Involvement of catecholamines in nuclear factor-κB regulation and cytokine expression
23. Acute hypoxia increases alveolar macrophage tumor necrosis factor activity and alters NF-kappaB expression
24. Essential role of alveolar macrophages in intrapulmonary activation of NF-kappaB
25. Alveolar macrophages exposed to hyperoxia demonstrate early enhanced cytokine productive capacity
26. Pentoxifylline attenuates oxygen-induced lung injury
27. In vivo inhibition of nuclear factor-kappa B activation prevents inducible nitric oxide synthase expression and systemic hypotension in a rat model of septic shock
28. Induction of cytokine-induced neutrophil chemoattractant (CINC) mRNA in the lungs of septic rats
29. Fibrinogen deposition at the postischemic vessel wall promotes platelet adhesion during ischemia-reperfusion in vivo
30. Activation of TNF-alpha transcription utilizes distinct MAP kinase pathways in different macrophage populations
31. H2O2 and antioxidants have opposite effects on activation of NF-kappa B and AP-1 in intact cells: AP-1 as secondary antioxidant-responsive factor
32. Early response cytokines and innate immunity: Essential roles for TNF receptor 1 and type I IL-1 receptor during Escherichia coli pneumonia in mice
33. NF-kappaB regulatory mechanisms in alveolar macrophages from patients with acute respiratory distress syndrome
34. Alterations in alveolar macrophage tumor necrosis factor (TNF) response following hemorrhagic shock
35. Acute respiratory distress syndrome: Estimated incidence and mortality rate in a 5 million-person population base
36. Roles of interleukin-6 and macrophage inflammatory protein-2 in pneumolysin-induced lung inflammation in mice
37. Prevalence, etiologies and outcome of the acute respiratory distress syndrome among hypoxemic ventilated patients
38. The p65 subunit is responsible for the strong transcription activating potential of NF-kappa B
39. Role of macrophage inflammatory protein-2 in aspiration-induced lung injury
40. Crystalloid resuscitation restores but does not maintain cardiac output following severe hemorrhage
41. A single hit model of polymicrobial sepsis: Cecal ligation and puncture
42. Essential role of nuclear factor kappaB in the induction of eosinophilia in allergic airway inflammation
43. Modulation of the nuclear factor kappa B pathway by Shp-2 tyrosine phosphatase in mediating the induction of interleukin (IL)-6 by IL-1 or tumor necrosis factor