Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

Jiro Katahira, Kazunori Murakami, Frank C. Schmalstieg, Robert Cox, Hal Hawkins, Lillian D. Traber, Daniel L. Traber

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep (n = 18) were prepared and randomized: the LAM-(1-3) group (n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group (n = 6) was not injured or treated, and the nontreatment group (n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po2 to inspired O2 fraction decreased in the LAM-(1-3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1-3) was administered 1 h after injury. Nitrate/nitrite (NOx) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1-3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume283
Issue number5 27-5
StatePublished - Nov 1 2002

Fingerprint

Smoke Inhalation Injury
L-Selectin
Sheep
Cell Adhesion Molecules
Lung
Antibodies
Lymph
Wounds and Injuries
Smoke
Inhalation Burns
Acute Lung Injury
Capillary Permeability
Lung Injury
Nitrites
Burns
Nitrates
Endothelium
Permeability
Neutrophils
Monoclonal Antibodies

Keywords

  • Leukocyte adhesion molecule
  • Polymorphonuclear leukocyte
  • Thermal burn

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology

Cite this

Katahira, J., Murakami, K., Schmalstieg, F. C., Cox, R., Hawkins, H., Traber, L. D., & Traber, D. L. (2002). Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep. American Journal of Physiology - Lung Cellular and Molecular Physiology, 283(5 27-5).

Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep. / Katahira, Jiro; Murakami, Kazunori; Schmalstieg, Frank C.; Cox, Robert; Hawkins, Hal; Traber, Lillian D.; Traber, Daniel L.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 283, No. 5 27-5, 01.11.2002.

Research output: Contribution to journalArticle

Katahira, J, Murakami, K, Schmalstieg, FC, Cox, R, Hawkins, H, Traber, LD & Traber, DL 2002, 'Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 283, no. 5 27-5.
Katahira J, Murakami K, Schmalstieg FC, Cox R, Hawkins H, Traber LD et al. Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep. American Journal of Physiology - Lung Cellular and Molecular Physiology. 2002 Nov 1;283(5 27-5).
Katahira, Jiro ; Murakami, Kazunori ; Schmalstieg, Frank C. ; Cox, Robert ; Hawkins, Hal ; Traber, Lillian D. ; Traber, Daniel L. / Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2002 ; Vol. 283, No. 5 27-5.
@article{58fff21b980c475b8e108839eb0d3b01,
title = "Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep",
abstract = "We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep (n = 18) were prepared and randomized: the LAM-(1-3) group (n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group (n = 6) was not injured or treated, and the nontreatment group (n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po2 to inspired O2 fraction decreased in the LAM-(1-3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1-3) was administered 1 h after injury. Nitrate/nitrite (NOx) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1-3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.",
keywords = "Leukocyte adhesion molecule, Polymorphonuclear leukocyte, Thermal burn",
author = "Jiro Katahira and Kazunori Murakami and Schmalstieg, {Frank C.} and Robert Cox and Hal Hawkins and Traber, {Lillian D.} and Traber, {Daniel L.}",
year = "2002",
month = "11",
day = "1",
language = "English (US)",
volume = "283",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "5 27-5",

}

TY - JOUR

T1 - Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

AU - Katahira, Jiro

AU - Murakami, Kazunori

AU - Schmalstieg, Frank C.

AU - Cox, Robert

AU - Hawkins, Hal

AU - Traber, Lillian D.

AU - Traber, Daniel L.

PY - 2002/11/1

Y1 - 2002/11/1

N2 - We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep (n = 18) were prepared and randomized: the LAM-(1-3) group (n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group (n = 6) was not injured or treated, and the nontreatment group (n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po2 to inspired O2 fraction decreased in the LAM-(1-3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1-3) was administered 1 h after injury. Nitrate/nitrite (NOx) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1-3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

AB - We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep (n = 18) were prepared and randomized: the LAM-(1-3) group (n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group (n = 6) was not injured or treated, and the nontreatment group (n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po2 to inspired O2 fraction decreased in the LAM-(1-3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1-3) was administered 1 h after injury. Nitrate/nitrite (NOx) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1-3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

KW - Leukocyte adhesion molecule

KW - Polymorphonuclear leukocyte

KW - Thermal burn

UR - http://www.scopus.com/inward/record.url?scp=0036838289&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036838289&partnerID=8YFLogxK

M3 - Article

C2 - 12376357

AN - SCOPUS:0036838289

VL - 283

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 5 27-5

ER -