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Sepsis-induced leukocyte adhesion in the pulmonary microvasculature in vivo is mediated by CD11a andCD11b.

Wang, Yongzhi LU ; Roller, Jonas LU ; Menger, Michael D and Thorlacius, Henrik LU (2013) In European Journal of Pharmacology 702(1-3). p.135-141
Abstract
Leukocyte accumulation is a rate-limiting step in inflammatory lung injury. The aim of this study was to define the role of CD11a/CD18 and CD11b/CD18 in sepsis-induced leukocyte rolling and adhesion in lung arterioles, capillaries and venules in male C57BL/6 mice using intravital fluorescence microscopy. Cecal ligation and puncture (CLP) markedly increased leukocyte rolling in arterioles and venules but not in capillaries in the lung. Immunoneutralization of CD11a, but not CD11b, decreased CLP-provoked leukocyte rolling in lung arterioles. Inhibition of CD11a or CD11b abolished CLP-induced arteriolar and venular leukocyte adhesion. Immunoneutralization of CD11a and CD11b reduced sepsis-induced leukocyte sequestration in pulmonary... (More)
Leukocyte accumulation is a rate-limiting step in inflammatory lung injury. The aim of this study was to define the role of CD11a/CD18 and CD11b/CD18 in sepsis-induced leukocyte rolling and adhesion in lung arterioles, capillaries and venules in male C57BL/6 mice using intravital fluorescence microscopy. Cecal ligation and puncture (CLP) markedly increased leukocyte rolling in arterioles and venules but not in capillaries in the lung. Immunoneutralization of CD11a, but not CD11b, decreased CLP-provoked leukocyte rolling in lung arterioles. Inhibition of CD11a or CD11b abolished CLP-induced arteriolar and venular leukocyte adhesion. Immunoneutralization of CD11a and CD11b reduced sepsis-induced leukocyte sequestration in pulmonary capillaries. Moreover, blocking CD11a or CD11b function improved microvascular blood flow in the lung of CLP animals. Considered together, our novel findings show that CD11a and CD11b mediate leukocyte adhesion in both arterioles and venules as well as trapping in capillaries in the lung. In addition, our data demonstrate that CD11a but not CD11b supports leukocyte rolling in pulmonary arterioles. Thus, these findings elucidate the molecular mechanisms behind leukocyte-endothelium interactions in the lung during systemic inflammation. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
European Journal of Pharmacology
volume
702
issue
1-3
pages
135 - 141
publisher
Elsevier
external identifiers
  • wos:000317153100018
  • pmid:23380685
  • scopus:84874398826
ISSN
1879-0712
DOI
10.1016/j.ejphar.2013.01.024
language
English
LU publication?
yes
id
77d10f2a-6f82-4859-88e7-6cf62715f47d (old id 3560229)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/23380685?dopt=Abstract
date added to LUP
2013-03-01 12:28:24
date last changed
2019-10-23 01:16:31
@article{77d10f2a-6f82-4859-88e7-6cf62715f47d,
  abstract     = {Leukocyte accumulation is a rate-limiting step in inflammatory lung injury. The aim of this study was to define the role of CD11a/CD18 and CD11b/CD18 in sepsis-induced leukocyte rolling and adhesion in lung arterioles, capillaries and venules in male C57BL/6 mice using intravital fluorescence microscopy. Cecal ligation and puncture (CLP) markedly increased leukocyte rolling in arterioles and venules but not in capillaries in the lung. Immunoneutralization of CD11a, but not CD11b, decreased CLP-provoked leukocyte rolling in lung arterioles. Inhibition of CD11a or CD11b abolished CLP-induced arteriolar and venular leukocyte adhesion. Immunoneutralization of CD11a and CD11b reduced sepsis-induced leukocyte sequestration in pulmonary capillaries. Moreover, blocking CD11a or CD11b function improved microvascular blood flow in the lung of CLP animals. Considered together, our novel findings show that CD11a and CD11b mediate leukocyte adhesion in both arterioles and venules as well as trapping in capillaries in the lung. In addition, our data demonstrate that CD11a but not CD11b supports leukocyte rolling in pulmonary arterioles. Thus, these findings elucidate the molecular mechanisms behind leukocyte-endothelium interactions in the lung during systemic inflammation.},
  author       = {Wang, Yongzhi and Roller, Jonas and Menger, Michael D and Thorlacius, Henrik},
  issn         = {1879-0712},
  language     = {eng},
  number       = {1-3},
  pages        = {135--141},
  publisher    = {Elsevier},
  series       = {European Journal of Pharmacology},
  title        = {Sepsis-induced leukocyte adhesion in the pulmonary microvasculature in vivo is mediated by CD11a andCD11b.},
  url          = {http://dx.doi.org/10.1016/j.ejphar.2013.01.024},
  volume       = {702},
  year         = {2013},
}