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W B WOOD

Publications and source records attributed to W B WOOD.

At least 55 records · Page 3Linked to original sources
PubMed1955

Studies on the pathogenesis of acute inflammation. I. The inflammatory reaction to thermal injury as observed in the rabbit ear chamber.

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.

Animals↗
PubMed1955

Studies on the pathogenesis of acute inflammation. II. The action of cortisone on the inflammatory response to thermal injury.

The anti-inflammatory action of cortisone upon the acute cellular response to thermal injury has been systematically studied in the rabbit ear chamber. The hormone has been shown to suppress the reaction of acute inflammation in its earliest recognizable phase; i.e., that involving vasodilatation and the adherence of leucocytes to the vascular endothelium. Evidence has been presented that the anti-inflammatory effect of the hormone cannot be explained on the basis of its vasoconstrictive properties alone. The experimental observations support the hypothesis that cortisone exerts a direct protective action upon endothelial cells and leucocytes, and that in so doing, it renders them refractory to the tissue products which initiate inflammation.

Animals↗
PubMed1955

Studies on the pathogenesis of fever. II. Identification of an endogenous pyrogen in the blood stream following the injection of typhoid vaccine.

Further studies have been made of a pyrogenic substance which appears in the circulation of rabbits during the course of experimental fever induced by injection of typhoid vaccine. With the use of a passive transfer method and pyrogen-tolerant recipients, the biological properties of this substance have been differentiated from those of the uncleared vaccine in the circulation. The newly identified factor resembles leucocytic pyrogen in the rapidity with which it produces fever and in its failure to exhibit cross-tolerance with bacterial pyrogen. This striking similarity of properties suggests that the circulating factor is of endogenous origin and may arise from cell injury. A close correlation between its presence in the circulation and the existence of fever has been demonstrated. The possible relationship of these findings to the pathogenesis of fever is evident.

Animals↗
PubMed1955

Studies on the pathogenesis of fever. I. The presence of transferable pyrogen in the blood stream following the injection of typhoid vaccine.

The rate of clearance of intravenously injected typhoid vaccine was studied in unsensitized, sensitized, and pyrogen-tolerant rabbits by means of a passive transfer technique. The blood of unsensitized rabbits which had not been previously exposed to bacterial pyrogen remained pyrogenic for normal recipients throughout a period of 2 hours following the injection. In contrast, rabbits sensitized by having received either one or two injections of the vaccine at least 3 weeks prior to the experiment cleared their blood of the test vaccine within 30 minutes despite the fact that they exhibit the same febrile response as unsensitized rabbits. After 1 hour, however, a transferable pyrogenic substance was again demonstrable in the sera of this group. Reasons are discussed for believing that this newly appearing substance may be of endogenous origin and may be the factor which directly affects the thermoregulatory centers of the brain. Rabbits which are made tolerant by repeated daily injections of vaccine have a characteristically depressed febrile response. Not only were the blood streams of such animals cleared of the injected vaccine within less than 5 minutes, but samples of their sera obtained 1 and 2 hours after the injection also failed to contain demonstrable quantities of the secondary pyrogen observed in sensitized animals. The latter observation is in keeping with the suggestion that the secondary pyrogen may play a critical role in the production of fever.

Animals↗
PubMed1955

Studies on the antipyretic action of cortisone in pyrogen-induced fever.

The mode of action of cortisone as an antipyretic has been studied in rabbits challenged with intravenous injections of bacterial pyrogens. The fever induced by pyromen or dextran was found to be markedly suppressed when cortisone was administered in liberal amounts (25 mg. twice daily) for 3 days prior to the challenge. Although the cortisone effectively blocked the febrile response to both pyrogens, it failed to influence the transient but marked leucopenia which characteristically precedes the onset of fever. The antipyretic action of the drug also was shown to bear no relation to the activity of the serum factor recently demonstrated by Farr, Grant, and others to be involved in the production of pyrogen-induced fever. In preliminary experiments with typhoid vaccine as the inciting pyrogen, the presence of serum factor activity in normal blood and its absence in the blood of pyrogen-tolerant rabbits was confirmed. Subsequently the blood of rabbits treated with antipyretically effective doses of cortisone was shown to contain just as much serum factor activity as that of normal rabbits. In addition, previous incubation of the pyrogen with serum factor failed to influence the antipyretic effect of the drug. It is concluded from these findings that in suppressing pyrogen fever, cortisone acts neither upon the leucopenic reaction nor upon the fever-accelerating factor of the serum. By exclusion it would appear that the drug must influence some later stage of the fever-producing process. The mechanisms involved in the later stages of the response to exogenous pyrogen remain undefined, and the need for determining whether they are related to the prefebrile leucopenia is emphasized.

Animals↗
PubMed1954

The mechanisms by which macrophages phagocyte encapsulated bacteria in the absence of antibody.

EVIDENCE HAS BEEN PRESENTED: (1) that macrophages from experimentally produced inflammatory exudates are capable of phagocyting fully encapsulated Type I pneumococci and group A Friedländer's bacilli in the absence of antibody, (2) that the principal mechanisms involved are those of surface phagocytosis, and (3) that the majority of pneumococci ingested by macrophages in antibody-free preparations are ultimately destroyed. The relationship of these phenomena to the mechanism of recovery in pneumococcal and Friedländer's bacillus infections has been briefly discussed.

Antibodies↗
PubMed1951

Studies on the cellular immunology of acute bacteremia. I. Intravascular leucocytic reaction and surface phagocytosis.

Evidence has been presented that the introduction of large numbers of bacteria into the blood stream causes a widespread intravascular reaction, characterized by the sticking of leucocytes to the endothelium of capillaries, arterioles, and venules. The adherent granulocytes promptly become motile and thus potentially phagocytic. This intravascular leucocytic response affords a rapid and efficient mobilization of a vast number of active phagocytes within the blood stream. In some of the smaller vessels of both the systemic and pulmonary circulation the reaction is accompanied by the deposition of what appears to be intravascular fibrin. Direct observation by the rabbit ear chamber technique has revealed that leucocytes thus mobilized in small peripheral vessels are capable of phagocyting fully encapsulated Friedländer's bacilli in the absence of antibody. Ingestion of the encapsulated blood-borne bacteria results from surface phagocytosis and occurs primarily in those vessels in which the flow of blood is either slowed or has temporarily stopped altogether. Leucocytes can be seen to phagocyte the organisms by first trapping them against the walls of the vessels or against adjacent leucocytes. Bacteria caught in the interstices of the intravascular "fibrin" may likewise be immobilized and readily phagocyted. Thus granulocytes, without the aid of opsonins, are able to ingest and destroy encapsulated blood-borne bacteria by the same mechanisms that operate in extravascular tissues. It is concluded from these studies that intravascular surface phagocytosis by polymorphonuclear leucocytes supplements the well known phagocytic activities of the reticulo-endothelial cells and therefore serves as an important defense of the host in acute infections caused by encapsulated bacteria and complicated by bacteriemia.

Antibodies↗