Involvement of CD40-CD40L signaling in postischemic lung injury

Department of Physiology, University of Alabama College of Medicine, Mobile, Alabama 36688-0002 Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative meas...

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Published inAmerican journal of physiology. Lung cellular and molecular physiology Vol. 283; no. 6; pp. 1255 - L1262
Main Authors Moore, Timothy M, Shirah, W. Bradley, Khimenko, Pavel L, Paisley, Peyton, Lausch, Robert N, Taylor, Aubrey E
Format Journal Article
LanguageEnglish
Published United States 01.12.2002
Subjects
Animals
CD40 Antigens - physiology
CD40 Ligand - physiology
In Vitro Techniques
Interleukin-10 - pharmacology
Interleukin-10 - physiology
Ischemia - complications
Ischemia - pathology
Ischemia - physiopathology
Lung - pathology
Lung - physiopathology
Male
Pneumonia - etiology
Pneumonia - pathology
Pneumonia - physiopathology
Pulmonary Circulation
Rats
Rats, Inbred Strains
Recombinant Proteins - pharmacology
Reperfusion Injury - complications
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Signal Transduction - physiology
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Abstract Department of Physiology, University of Alabama College of Medicine, Mobile, Alabama 36688-0002 Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient ( K f,c ). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events, results in significantly lower postischemic K f,c values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 production. Rat lymphocytes activated ex vivo with phorbol 12-myristate, 13-acetate increased K f,c in isolated lungs independently of I/R, and this increase was prevented by pretreating lungs with anti-CD40. In addition to lymphocyte involvement via CD40-CD40L interactions, our studies also show that I/R injury is potentiated by antagonism of IL-10 produced locally within the postischemic lung, whereas exogenous, rat recombinant IL-10 provided protection against I/R-induced microvascular damage. Thus acute lymphocyte involvement in lung I/R injury involves CD40-CD40L signaling mechanisms, and these events may be influenced by local IL-10 generation. inflammation; filtration coefficient; lymphocytes; macrophage inflammatory protein-2
AbstractList Department of Physiology, University of Alabama College of Medicine, Mobile, Alabama 36688-0002 Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient ( K f,c ). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events, results in significantly lower postischemic K f,c values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 production. Rat lymphocytes activated ex vivo with phorbol 12-myristate, 13-acetate increased K f,c in isolated lungs independently of I/R, and this increase was prevented by pretreating lungs with anti-CD40. In addition to lymphocyte involvement via CD40-CD40L interactions, our studies also show that I/R injury is potentiated by antagonism of IL-10 produced locally within the postischemic lung, whereas exogenous, rat recombinant IL-10 provided protection against I/R-induced microvascular damage. Thus acute lymphocyte involvement in lung I/R injury involves CD40-CD40L signaling mechanisms, and these events may be influenced by local IL-10 generation. inflammation; filtration coefficient; lymphocytes; macrophage inflammatory protein-2
Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient ( K f,c ). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events, results in significantly lower postischemic K f,c values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 production. Rat lymphocytes activated ex vivo with phorbol 12-myristate, 13-acetate increased K f,c in isolated lungs independently of I/R, and this increase was prevented by pretreating lungs with anti-CD40. In addition to lymphocyte involvement via CD40-CD40L interactions, our studies also show that I/R injury is potentiated by antagonism of IL-10 produced locally within the postischemic lung, whereas exogenous, rat recombinant IL-10 provided protection against I/R-induced microvascular damage. Thus acute lymphocyte involvement in lung I/R injury involves CD40-CD40L signaling mechanisms, and these events may be influenced by local IL-10 generation.
Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient (K(f,c)). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events, results in significantly lower postischemic K(f,c) values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 production. Rat lymphocytes activated ex vivo with phorbol 12-myristate, 13-acetate increased K(f,c) in isolated lungs independently of I/R, and this increase was prevented by pretreating lungs with anti-CD40. In addition to lymphocyte involvement via CD40-CD40L interactions, our studies also show that I/R injury is potentiated by antagonism of IL-10 produced locally within the postischemic lung, whereas exogenous, rat recombinant IL-10 provided protection against I/R-induced microvascular damage. Thus acute lymphocyte involvement in lung I/R injury involves CD40-CD40L signaling mechanisms, and these events may be influenced by local IL-10 generation.
Author Paisley, Peyton
Taylor, Aubrey E
Moore, Timothy M
Lausch, Robert N
Shirah, W. Bradley
Khimenko, Pavel L
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Snippet Department of Physiology, University of Alabama College of Medicine, Mobile, Alabama 36688-0002 Our studies show that ischemia-reperfusion (I/R) in the...
Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular...
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SubjectTerms Animals
CD40 Antigens - physiology
CD40 Ligand - physiology
In Vitro Techniques
Interleukin-10 - pharmacology
Interleukin-10 - physiology
Ischemia - complications
Ischemia - pathology
Ischemia - physiopathology
Lung - pathology
Lung - physiopathology
Male
Pneumonia - etiology
Pneumonia - pathology
Pneumonia - physiopathology
Pulmonary Circulation
Rats
Rats, Inbred Strains
Recombinant Proteins - pharmacology
Reperfusion Injury - complications
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Signal Transduction - physiology
Title Involvement of CD40-CD40L signaling in postischemic lung injury
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