1992
DOI: 10.1016/0022-4804(92)90025-u
|View full text |Cite
|
Sign up to set email alerts
|

A role for ELAM-1 in the pathogenesis of MOF during septic shock

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
16
0

Year Published

1995
1995
2022
2022

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 52 publications
(16 citation statements)
references
References 22 publications
0
16
0
Order By: Relevance
“…IL-8 levels are increased in sputum from COPD patients compared with those in sputum of control subjects (nonsmokers, cigarette smokers without disease, or asthmatic patients) (78). A similar increase in the expression of intercellular adhesion molecule 1 (ICAM-1) has been observed in asthma, chronic bronchitis, ARDS, and COPD (79,80). ICAM-1 promotes immunologic and inflammatory reactions such as leukocyte diapedesis within the lung.…”
Section: Role Of Ros/rns In Inflammatory Respiratory Disease Expressimentioning
confidence: 74%
“…IL-8 levels are increased in sputum from COPD patients compared with those in sputum of control subjects (nonsmokers, cigarette smokers without disease, or asthmatic patients) (78). A similar increase in the expression of intercellular adhesion molecule 1 (ICAM-1) has been observed in asthma, chronic bronchitis, ARDS, and COPD (79,80). ICAM-1 promotes immunologic and inflammatory reactions such as leukocyte diapedesis within the lung.…”
Section: Role Of Ros/rns In Inflammatory Respiratory Disease Expressimentioning
confidence: 74%
“…LQGV treatment was also associated with a significant reduction of neutrophil accumulation in the liver [23]. Endothelial activation, characterized by increased expression of adhesion molecules [E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and subsequent tissue infiltration by neutrophils is an early event in septic shock and a crucial step towards the development of organ failure [20,25,26]. E-selectin blockage has been shown to protect against neutrophil-induced tissue injury during endotoxaemia in mice [27].…”
Section: Discussionmentioning
confidence: 99%
“…5,6 Consequently, E-selectin expression, which is absent in control livers, can be up-regulated under inflammatory conditions in experimental animals [7][8][9][10] and humans. [11][12][13] Although there appear to be some variations in E-selectin expression depending on the disease state, the general consensus from these studies is that E-selectin is most strongly expressed on endothelial cells of portal tract vessels and hepatic venules and to a lesser degree on sinusoidal lining cells.…”
mentioning
confidence: 99%