Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
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Target Concepts:
Gene/Protein
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Query: UMLS:C0001511 (
Adhesion
)
5,955
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effect of 2 strains of Haemophilus somnus on bovine endothelial cells in cultured arterial segments was investigated and compared with the effects of Escherichia coli and Salmonella typhimurium. In cultures inoculated with either strain of H somnus, there was widespread contraction and desquamation of endothelial cells, exposing large areas of subendothelial collagen. Many bacteria were adherent to endothelial cells and some were in phagosomes within cells. Endothelial changes were milder in arterial cultures inoculated with E coli or S typhimurium than in those inoculated with either strain of H somnus.
Adhesion
of H somnus to vascular endothelial cells followed by exposure of subendothelial collagen may initiate the thrombosis, vasculitis, and ischemic necrosis characteristic of infectious thromboembolic
meningoencephalitis
in cattle. Arterial cultures might be useful in assaying the virulences of different strains of H somnus, and could be used to investigate the mechanism of their action on endothelial cells.
...
PMID:Effect of Haemophilus somnus on bovine endothelial cell in organ culture. 702 Apr 97
The fungal pathogen Cryptococcus neoformans has a predilection for the central nervous system (CNS), resulting in devastating
meningoencephalitis
. At present, it is unclear how C. neoformans traverses the blood-brain barrier (BBB) and causes CNS infection. The present study has examined and characterized the interaction of C. neoformans with human brain microvascular endothelial cells (HBMEC), which constitute the BBB.
Adhesion
of and transcytosis of HBMEC by C. neoformans was inoculum- and time-dependent and occurred with both encapsulated and acapsulated strains. C. neoformans induced marked morphological changes in HBMEC, for example membrane ruffling, irregular nuclear morphology and swelling of the mitochondria and the ER. These findings suggest that C. neoformans induced actin cytoskeletal reorganization of the host cells. In addition, it was observed that the dephosphorylated form of cofilin was increased during cryptococcal adherence to HBMEC, concomitant with the actin rearrangement. Cryptococcal binding to HBMEC was increased in the presence of Y27632, a Rho kinase (ROCK)-specific inhibitor. Since ROCK activates LIM kinase (LIMK), which phosphorylates cofilin (inactive form), this suggests the involvement of the ROCK-->LIMK-->cofilin pathway. In contrast, the phosphatase inhibitor sodium orthovanadate decreased adherence of Cryptococcus to HBMEC, concomitant with the increase of phosphorylation of cofilin. Furthermore, the tight junction marker protein occludin became Triton-extractable, indicating alteration of tight junctions in brain endothelial cells. This is the first demonstration that C. neoformans is able to adhere to and transcytose across the HBMEC monolayer and alter the cytoskeleton morphology in HBMEC. Further characterization of the interactions between C. neoformans and HBMEC should help the development of novel strategies to prevent cryptococcal meningitis and its associated morbidity.
...
PMID:Cryptococcus neoformans induces alterations in the cytoskeleton of human brain microvascular endothelial cells. 1453 40