Studies on the Pathogenesis of Acute Inflammation

Allison, Fred; Smith, Matthew R.; Wood, William B.

doi:10.1084/jem.102.6.669

Cited by 71 publications

(7 citation statements)

References 16 publications

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“…Similarly, the means by which cortisol interferes with granulocyte egress from the blood into inflammatory exudates are unkown. The present demonstration of a decreased cellular content of inflammatory exudates confirms studies in man (7,10,21) and in other species (12-14, 22, 23), but sheds no light on whether this effect is on the granulocytes directly (-24-26), on the vascular endothelium (24,27), or results from an effect on the inflammatory stimulus (28)(29)(30).…”

Section: Resultssupporting

confidence: 72%

Leukokinetic studies

Bishop¹,

Athens²,

Boggs³

et al. 1968

J. Clin. Invest.

263

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Section: Resultssupporting

confidence: 72%

Leukokinetic studies

Bishop¹,

Athens²,

Boggs³

et al. 1968

J. Clin. Invest.

263

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“…It appears certain, therefore, that leucocytic sticking must be caused by some event other than mere vasodilatation. This conclusion, as will be discussed in the next report (18), is of particular significance in view of the fact that cortisone acts as a potent vasoconstrictor (15).…”

Section: Discussionmentioning

confidence: 63%

“…Speculations relating to the cause of leucocytic sticking have included the role of vasodilatation (16), postulated changes in cellular surface charges brought on by "currents of injury" (17), and the deposit of a gelatinous precipitate upon the surface of injured endothelium (8). Since, as reported in the next paper (18), the most striking effect of cortisone in acute inflammation is upon this sticking reaction, its genesis is worthy of particular consideration.…”

Section: Discussionmentioning

confidence: 82%

Studies on the Pathogenesis of Acute Inflammation

Allison

Smith

Wood

1955

The Journal of Experimental Medicine

Self Cite

144

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A special adaptation of the rabbit ear chamber has been devised to study in vivo, under high magnification, the acute inflammatory reaction to thermal injury. Systematic observations of the cellular response have led to the following conclusions. 1. Contrary to the commonly accepted view, vasodilatation does not always precede the adherence of leucocytes to vascular endothelium. 2. The fact that leucocytes often adhere to one another as well as to the endothelium indicates that the increased adhesiveness characteristic of the early stages of inflammation is not limited to the surfaces of the endothelial cells. 3. The sharing of erythrocytes and platelets in this increased stickiness suggests that a "plasma factor" is involved. There is indirect but as yet inconclusive evidence that the plasma factor may concern the clotting mechanism of the blood. 4. The adherence of leucocytes to the endothelium is usually first noted on the side of the vessel closest to the site of injury. This previously undescribed phenomenon of "unilateral sticking" is in keeping with the concept that the vascular reaction is caused by products of cellular damage which diffuse to the vessel from the site of injury. 5. Leucocytes always become adherent to the endothelium before penetrating the vessel wall. They often migrate about for some time on the endothelial surface before undergoing diapedesis. 6. Although no definite stomata are at any time visible in the endothelium, penetrating leucocytes may leave behind temporary defects through which other leucocytes and even erythrocytes may pass. 7. The diapedesis of leucocytes appears to depend primarily upon cellular motility. It may occur in static vessels where there is presumably little if any hydrostatic pressure. 8. The diapedesis of erythrocytes, on the other hand, is a passive process depending upon intravascular pressure. Its occurrence is greatly exaggerated in areas in which intravascular pressure becomes elevated. Such elevations occur as the result of proximal arteriolar dilatation and distal occlusion of vessels. 9. Once they have reached the extravascular tissues the leucocytes move about more or less at random, apparently uninfluenced by any compelling chemotactic force. Their resultant migration, however, is toward the site of injury around which they eventually tend to congregate. 10. The histiocytes normally present in the connective tissue appear to play no role in the type of acute inflammatory reaction produced in these experiments.

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“…Similarly, the enhanced phagocytic capacity of leukocytes during "surface phagocytosis" on filter paper may reflect the necessity of leukocytes to adhere well to surfaces in order to move and ingest organisms efficiently (12). Leukocyte margination is one of the first demonstrable changes in the inflammatory process but is greatly suppressed by corticosteroids (13). After demonstration that corticosteroids suppressed leukocyte adhesion to glass (personal observation) and that hyperosmolality, which suppressed leukocyte delivery to renal medullary tissues, also suppressed the leukocyte adhesiveness per se (14), it appeared likely that the property of granulocyte adhesiveness might significantly affect delivery and local function of leukocytes in the infectious or immunologically mediated inflammatory process.…”

Section: Discussionmentioning

confidence: 99%