Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion

N M Bless, R L Warner, V A Padgaonkar, A B Lentsch, B J Czermak, H Schmal, H P Friedl, P A Ward

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

We evaluated the roles of the C-X-C chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) as well as the complement activation product C5a in development of lung injury after hindlimb ischemia-reperfusion in rats. During reperfusion, CD11b and CD18, but not CD11a, were upregulated on neutrophils [bronchoalveolar lavage (BAL) and blood] and lung macrophages. BAL levels of CINC and MIP-2 were increased during the ischemic and reperfusion periods. Treatment with either anti-CINC or anti-MIP-2 IgG significantly reduced lung vascular permeability and decreased lung myeloperoxidase content by 93 and 68%, respectively (P < 0.05). During the same period, there were significant increases in serum C5a-related neutrophil chemotactic activity. Treatment with anti-C5a decreased lung vascular permeability, lung myeloperoxidase, and BAL CINC by 51, 58, and 23%, respectively (P < 0.05). The data suggest that the C-X-C chemokines CINC and MIP-2 as well as the complement activation product C5a are required for lung neutrophil recruitment and full induction of lung injury after hindlimb ischemia-reperfusion in rats.

OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology (Consolidated)
Vol/bind276
Udgave nummer1 Pt 1
Sider (fra-til)L57-63
ISSN0002-9513
StatusUdgivet - jan. 1999

Fingeraftryk

Neutrophils
Lung
Peroxidase
Neutrophil Infiltration
Macrophages
Serum

Citer dette

Bless, N. M., Warner, R. L., Padgaonkar, V. A., Lentsch, A. B., Czermak, B. J., Schmal, H., ... Ward, P. A. (1999). Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion. American Journal of Physiology (Consolidated), 276(1 Pt 1), L57-63.
Bless, N M ; Warner, R L ; Padgaonkar, V A ; Lentsch, A B ; Czermak, B J ; Schmal, H ; Friedl, H P ; Ward, P A. / Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion. I: American Journal of Physiology (Consolidated). 1999 ; Bind 276, Nr. 1 Pt 1. s. L57-63.
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abstract = "We evaluated the roles of the C-X-C chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) as well as the complement activation product C5a in development of lung injury after hindlimb ischemia-reperfusion in rats. During reperfusion, CD11b and CD18, but not CD11a, were upregulated on neutrophils [bronchoalveolar lavage (BAL) and blood] and lung macrophages. BAL levels of CINC and MIP-2 were increased during the ischemic and reperfusion periods. Treatment with either anti-CINC or anti-MIP-2 IgG significantly reduced lung vascular permeability and decreased lung myeloperoxidase content by 93 and 68{\%}, respectively (P < 0.05). During the same period, there were significant increases in serum C5a-related neutrophil chemotactic activity. Treatment with anti-C5a decreased lung vascular permeability, lung myeloperoxidase, and BAL CINC by 51, 58, and 23{\%}, respectively (P < 0.05). The data suggest that the C-X-C chemokines CINC and MIP-2 as well as the complement activation product C5a are required for lung neutrophil recruitment and full induction of lung injury after hindlimb ischemia-reperfusion in rats.",
keywords = "Animals, Antibodies, Bronchoalveolar Lavage Fluid, Cell Adhesion Molecules, Chemokine CXCL2, Chemokines, Chemokines, CXC, Chemotactic Factors, Complement C5a, Growth Substances, Hindlimb, Intercellular Signaling Peptides and Proteins, Ischemia, Lung, Macrophages, Male, Monokines, Rats, Rats, Long-Evans, Reperfusion Injury, Journal Article",
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Bless, NM, Warner, RL, Padgaonkar, VA, Lentsch, AB, Czermak, BJ, Schmal, H, Friedl, HP & Ward, PA 1999, 'Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion', American Journal of Physiology (Consolidated), bind 276, nr. 1 Pt 1, s. L57-63.

Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion. / Bless, N M; Warner, R L; Padgaonkar, V A; Lentsch, A B; Czermak, B J; Schmal, H; Friedl, H P; Ward, P A.

I: American Journal of Physiology (Consolidated), Bind 276, Nr. 1 Pt 1, 01.1999, s. L57-63.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion

AU - Bless, N M

AU - Warner, R L

AU - Padgaonkar, V A

AU - Lentsch, A B

AU - Czermak, B J

AU - Schmal, H

AU - Friedl, H P

AU - Ward, P A

PY - 1999/1

Y1 - 1999/1

N2 - We evaluated the roles of the C-X-C chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) as well as the complement activation product C5a in development of lung injury after hindlimb ischemia-reperfusion in rats. During reperfusion, CD11b and CD18, but not CD11a, were upregulated on neutrophils [bronchoalveolar lavage (BAL) and blood] and lung macrophages. BAL levels of CINC and MIP-2 were increased during the ischemic and reperfusion periods. Treatment with either anti-CINC or anti-MIP-2 IgG significantly reduced lung vascular permeability and decreased lung myeloperoxidase content by 93 and 68%, respectively (P < 0.05). During the same period, there were significant increases in serum C5a-related neutrophil chemotactic activity. Treatment with anti-C5a decreased lung vascular permeability, lung myeloperoxidase, and BAL CINC by 51, 58, and 23%, respectively (P < 0.05). The data suggest that the C-X-C chemokines CINC and MIP-2 as well as the complement activation product C5a are required for lung neutrophil recruitment and full induction of lung injury after hindlimb ischemia-reperfusion in rats.

AB - We evaluated the roles of the C-X-C chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) as well as the complement activation product C5a in development of lung injury after hindlimb ischemia-reperfusion in rats. During reperfusion, CD11b and CD18, but not CD11a, were upregulated on neutrophils [bronchoalveolar lavage (BAL) and blood] and lung macrophages. BAL levels of CINC and MIP-2 were increased during the ischemic and reperfusion periods. Treatment with either anti-CINC or anti-MIP-2 IgG significantly reduced lung vascular permeability and decreased lung myeloperoxidase content by 93 and 68%, respectively (P < 0.05). During the same period, there were significant increases in serum C5a-related neutrophil chemotactic activity. Treatment with anti-C5a decreased lung vascular permeability, lung myeloperoxidase, and BAL CINC by 51, 58, and 23%, respectively (P < 0.05). The data suggest that the C-X-C chemokines CINC and MIP-2 as well as the complement activation product C5a are required for lung neutrophil recruitment and full induction of lung injury after hindlimb ischemia-reperfusion in rats.

KW - Animals

KW - Antibodies

KW - Bronchoalveolar Lavage Fluid

KW - Cell Adhesion Molecules

KW - Chemokine CXCL2

KW - Chemokines

KW - Chemokines, CXC

KW - Chemotactic Factors

KW - Complement C5a

KW - Growth Substances

KW - Hindlimb

KW - Intercellular Signaling Peptides and Proteins

KW - Ischemia

KW - Lung

KW - Macrophages

KW - Male

KW - Monokines

KW - Rats

KW - Rats, Long-Evans

KW - Reperfusion Injury

KW - Journal Article

M3 - Journal article

VL - 276

SP - L57-63

JO - American Journal of Physiology (Consolidated)

JF - American Journal of Physiology (Consolidated)

SN - 0002-9513

IS - 1 Pt 1

ER -

Bless NM, Warner RL, Padgaonkar VA, Lentsch AB, Czermak BJ, Schmal H et al. Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion. American Journal of Physiology (Consolidated). 1999 jan;276(1 Pt 1):L57-63.