Perflubron attenuates neutrophil adhesion to activated endothelial cells in vitro

American Journal of Physiology - Lung Cellular and Molecular Physiology - Tập 278 Số 5 - Trang L1008-L1017 - 2000
Conor Woods1, Gerald G. Neslund1, Elisabeth S. Kornbrust1, Stephen F. Flaim1
11 Department of Biological Research, Alliance Pharmaceutical Corporation, San Diego, California 92121

Tóm tắt

Infiltration of activated neutrophils into the lung appears to be a key element in the severe lung injury that develops in animal models of acute lung injury. Partial liquid ventilation with perflubron has been shown to ameliorate tissue damage compared with conventional mechanical ventilation in acute lung injury models. Pilot experiments indicated that indirect exposure to perflubron could modulate the degree to which subsequent neutrophil binding to endothelial cell monolayers was upregulated after lipopolysaccharide activation. Endothelial cell monolayers preexposed to perflubron showed >40% reductions in the surface steady-state levels of E-selectin and intercellular adhesion molecule-1 achieved after proinflammatory activation ( P < 0.05), which correlated with a reduction in the real-time association constants measured by biosensor techniques. These results indicate that direct contact with the perflubron liquid phase is not necessary to attenuate inflammatory responses. Rather, diffusion of perflubron from the alveolar space into the adjacent pulmonary vascular endothelial layer may modulate neutrophil adhesion and thereby reduce the rate of infiltration of activated neutrophils into the injured lung.

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Tài liệu tham khảo

10.1021/bi00019a035

10.1164/ajrccm.154.1.8680703

10.1073/pnas.84.24.9238

Carlos TM, 1994, Blood, 84, 2068, 10.1182/blood.V84.7.2068.2068

Colton D, 1994, Surg Forum, 1055, 668

10.1165/ajrcmb.19.4.f145

Doerschuk CM, 1996, J Immunol, 157, 4609, 10.4049/jimmunol.157.10.4609

Doerschuk CM, 1990, J Immunol, 144, 2327, 10.4049/jimmunol.144.6.2327

10.1172/JCI119189

10.1006/abio.1996.9922

10.1152/jappl.1997.82.6.1743

10.1164/ajrccm/136.5.1225

10.1165/ajrcmb.10.4.7510985

10.1378/chest.108.2.500

10.1097/00003246-199606000-00021

10.1152/jappl.1994.77.4.1795

10.1146/annurev.ph.57.030195.000525

10.1016/0092-8674(91)90393-D

Lawrence MB, 1993, J Immunol, 151, 6338, 10.4049/jimmunol.151.11.6338

10.1016/0022-1139(96)03415-X

10.1152/jappl.1987.62.3.1236

Masinovsky B, 1990, J Immunol, 145, 2886, 10.4049/jimmunol.145.9.2886

Mulligan MS, 1996, Proc Assoc Am Physicians, 108, 198

10.1172/JCI116029

Mulligan MS, 1995, J Immunol, 154, 1350, 10.4049/jimmunol.154.3.1350

10.1097/00003246-199409000-00015

10.1172/JCI119129

10.1016/S0006-3495(97)78821-0

Obraztsov VV, 1993, Biokhimiya, 58, 879

Pober JS, 1996, J Immunol, 136, 1680, 10.4049/jimmunol.136.5.1680

Pober JS, 1986, J Immunol, 137, 1893, 10.4049/jimmunol.137.6.1893

10.1016/0140-6736(92)91067-I

10.1146/annurev.me.38.020187.001455

10.1378/chest.106.2.535

10.1097/00003246-199509000-00014

10.1146/annurev.ph.57.030195.004143

10.1097/00003246-199712000-00023

10.1164/ajrccm/148.3.785

10.1007/BF01534436

10.1097/00024382-199611000-00007

Weiland JE, 1986, Am Rev Respir Dis, 133, 218

10.1126/science.2749255

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American Journal of Physiology - Lung Cellular and Molecular Physiology

Tập 278 Số 5

L1008-L1017

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