Vascular Events in Inflammation

Gm, Böhm

doi:10.1007/978-3-0348-7290-4_4

Inflammation: Mechanisms and Their Impact on Therapy 1977

DOI: 10.1007/978-3-0348-7290-4_4

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Vascular Events in Inflammation

Böhm Gm¹

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Cited by 3 publications

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“…Two important characteristics of the acute inflammatory response are an increased microvascular permeability to plasma proteins and the extravascular accumulation of polymorphonuclear leukocytes (PMN's). The permeability and response to inflammation varies in different segments of the microcirculation (ll, 29) and with the type and intensity of the stimulus (3). The accumulation of PMN's at the site of inflammation commonly involves the diapedesis of leukocytes across the endothelium of postcapillary venules and frequently the emigration of PMN's across a second epithelium.…”

mentioning

confidence: 99%

Epithelial permeability and the transepithelial migration of human neutrophils.

Milks¹,

Brontoli²,

Cramer³

1983

The Journal of Cell Biology

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Although polymorphonuclear leukocytes (PMN's) can migrate through every epithelium in the body regardless of its permeability, very little is known about the effect of epithelial permeability on PMN migration and the effect of emigrating PMN's on the permeability of the epithelium. In an in vitro model system of transepithelial migration, human PMN's were stimulated by 0.1 #m fMet-Leu-Phe to traverse confluent, polarized canine kidney epithelial monolayers of varying permeabilities. Epithelial permeability was determined by both conductance measurement and horseradish peroxidase (HRP) tracer studies. As epithelial permeability increased, the number of PMN invasion sites as well as the number of PMN's that traversed the monolayer increased. The effect of PMN migration on epithelial permeability was examined using the ultrastructural tracers HRP and lanthanum nitrate. PMN's traversing the monolayer made close cell-to-cell contacts with other invading PMNs and with adjacent epithelial cells. These close contacts appeared to prevent leakage of tracer across invasion sites. Following PMN emigration, epithelial junctional membranes reapproximated and were impermeable to the tracers. These results indicated that, in the absence of serum and connective tissue factors, (a) the number of PMN invasion sites and the number of PMN's that traversed an epithelium were a function of the conductance of the epithelium and (b) PMN's in the process of transepithelial migration maintained close cell-cell contacts and prevented the leakage of particles (>5 nm in diameter) across the invasion site.Two important characteristics of the acute inflammatory response are an increased microvascular permeability to plasma proteins and the extravascular accumulation of polymorphonuclear leukocytes (PMN's). The permeability and response to inflammation varies in different segments of the microcirculation (ll, 29) and with the type and intensity of the stimulus (3). The accumulation of PMN's at the site of inflammation commonly involves the diapedesis of leukocytes across the endothelium of postcapillary venules and frequently the emigration of PMN's across a second epithelium. In fact, PMN's are able to traverse virtually every epithelium in the body (1, 31), regardless of its permeability (8,14,25). Yet, little is known about the.~effect of epithelial permeability on PMN migration or about the effect of PMN migration on the permeability of the epithelium. To study this, we have devised an in vitro system (10) that enables us to examine, in the absence of serum and connective tissue factors, the ability of human PMN's to traverse an epithelium with different permeabilities and the effect of this migration on epithelial permeability. At present, only kidney (6, 24), lung (21), urinary bladder (19), and mammary gland (2) epithelia have been shown to form zonulae occludentes and produce measurable transepithelial electrical resistance when grown in vitro. Since PMN's traverse kidney epithelium in response to infection as well as other pat...

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mentioning

confidence: 99%

Epithelial permeability and the transepithelial migration of human neutrophils.

Milks¹,

Brontoli²,

Cramer³

1983

The Journal of Cell Biology

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Problems and results in testing the possible general mode of action of glucocorticoids in rat adjuvant arthritis

Hirschelmann

Bekemeier

1986

Agents and Actions

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The antiinflammatory action of dexamethasone in both phases of rat adjuvant arthritis was significantly reduced by injection of the RNA synthesis inhibitor actinomycin D into the inflamed paw. This effect is apparently caused by inhibition of RNA/protein synthesis and not by actinomycin D irritant activity. Thus, the present data support the view of indirect glucocorticoid activity via gene expression also in subacute and chronic adjuvant arthritis. The dexamethasone-induced antiinflammatory protein seems to be synthetized at the site of inflammation.

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Local haemorrhage induced by Bothrops jararaca venom: relationship to neurogenic inflammation

Gonçalves

Mariano

2000

Mediators of Inflammation

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We investigated morphological alterations induced by s.c. injection of 2.5 microg of Bothrops jararaca venom in rats. Intense disorganisation of collagen fibres was observed 1 min after the venom injection, particularly at regions near vessels and nerves. Mast cells were degranulated, and erythrocytes were seen leaving venules throughout the endothelial junctions. At this time, damaged endothelial cells were not observed. In rats envenomed as above, but immediately after cardiorespiratory failure induced by deep ether anaesthesia, alterations in the connective tissue structures, as previously described, were not observed. The mediation of this haemorrhage was investigated by injecting the venom into the foot pad of mice and compared to the mediation of oedema. Local haemorrhage was significantly reduced in mice pre-treated with capsaicin or guanethidine or submitted to a surgical section of sciatic and saphenous nerves. In these animals, oedema was not affected. Groups treated with methysergide or morphine showed both haemorrhage and oedema significantly reduced. Indomethacin or dexamethasone pre-treatments significantly reduced the oedema, but not the haemorrhage. Moreover, in animals treated with promethazine or mepyramine, oedema and haemorrhage were not affected. These data suggest that local haemorrhage induced by Bothrops jararaca venom is partially controlled by serotonin and neurohumoral mediators. Furthermore, results indicate that haemorrhage and oedema are mediated by different pharmacological systems.

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Vascular Events in Inflammation

Cited by 3 publications

References 103 publications

Epithelial permeability and the transepithelial migration of human neutrophils.

Epithelial permeability and the transepithelial migration of human neutrophils.

Problems and results in testing the possible general mode of action of glucocorticoids in rat adjuvant arthritis

Local haemorrhage induced by Bothrops jararaca venom: relationship to neurogenic inflammation

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