scholarly journals Is the intercellular adhesion molecule-1/leukocyte function associated antigen 1 pathway of leukocyte adhesion involved in the tissue damage of alcoholic hepatitis?

Gut ◽  
1992 ◽  
Vol 33 (2) ◽  
pp. 268-271 ◽  
Author(s):  
P Burra ◽  
S G Hubscher ◽  
J Shaw ◽  
E Elias ◽  
D H Adams
Keyword(s):  
Adhesion Molecule ◽  
Tissue Damage ◽  
Alcoholic Hepatitis ◽  
Leukocyte Adhesion ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Leukocyte Function

Immune complexes alter cerebral microvessel permeability: roles of complement and leukocyte adhesion

2006 ◽  
Vol 291 (2) ◽  
pp. H694-H704 ◽  
Author(s):  
Karyn J. Lister ◽  
Michael J. Hickey
Keyword(s):  
Adhesion Molecule ◽  
Immune Complexes ◽  
Inflammatory Responses ◽  
Leukocyte Adhesion ◽  
Intercellular Adhesion ◽  
Microvascular Permeability ◽  
Intercellular Adhesion Molecule ◽  
Complement Pathway ◽  
Intercellular Adhesion Molecule 1 ◽  
Peripheral Tissues

Immune complexes (ICs) are potent inflammatory mediators in peripheral tissues. However, very few studies have examined the ability of ICs to induce inflammatory responses in the brain. Therefore, using preformed ICs or the reverse passive Arthus (RPA) model to localize ICs to the pial microvasculature of mice, we aimed to investigate the ability of ICs to induce an inflammatory response in the cerebral (pial) microvasculature. Application of preformed ICs immediately increased pial microvascular permeability, with a minimal change in leukocyte adhesion in pial postcapillary venules. In contrast, initiation of the RPA response in the pial microvasculature induced changes in cerebral microvascular permeability and increased leukocyte adhesion in pial postcapillary venules. The RPA response induced deposition of C3 in perivascular regions adjacent to sites of IC formation. Depletion of C3 abrogated RPA-induced microvascular permeability and leukocyte adhesion, indicating that the complement pathway was critical for this response. Inhibition of leukocyte adhesion via CD18 blockade also reduced IC-induced microvascular permeability. However, this did not require intercellular adhesion molecule-1, inasmuch as blockade of intercellular adhesion molecule-1 did not alter RPA-induced microvascular permeability and adhesion. These findings demonstrate that ICs are capable of rapidly inducing inflammatory responses in the cerebral microvasculature, with the complement pathway and leukocyte recruitment playing critical roles in microvascular dysfunction.

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