Biomedical subjects

I G Colditz

Publications and source records attributed to I G Colditz.

At least 55 records · Page 3Linked to original sources

PubMed1990

Effect of exogenous prostaglandin E2 and actinomycin D on plasma leakage induced by neutrophil-activating peptide-1/interleukin-8.

Neutrophil accumulation and plasma leakage were measured in rabbit skin at sites stimulated with recombinant human neutrophil activating peptide-1/interleukin-8 (NAP-1/IL-8). Neutrophil accumulation occurred at doses equal to or greater than 10(-11) moles NAP-1/IL-8 per site. Co-injection of prostaglandin E2 (PGE2) extended the threshold of inflammatory activity of NAP-1/IL-8 to less than 10(-13) moles/site and caused approximately three-fold increases in neutrophil accumulation and ten-fold increases in plasma leakage at the higher doses of NAP-1/IL-8 examined. Plasma leakage declined more rapidly than did neutrophil accumulation as lesions aged. It was postulated that an endothelial response may be initiated to limit plasma leakage during ongoing neutrophil emigration at sites stimulated with NAP-1/IL-8. The induction of vasodilatation by injection of PGE2 masked the decline of plasma leakage with time in lesions up to 120 min old. Co-injection of the RNA synthesis inhibitor, actinomycin D, failed to abrogate the decline of plasma leakage with time, suggesting that de novo protein synthetic events such as production of the vasoconstrictor peptide, endothelin, are unlikely to contribute to the mechanism that restricts plasma leakage in older lesions. Although plasma leakage induced by NAP-1/IL-8 is dependent on the emigration of neutrophils, the results indicate that a mechanism, independent of de novo protein synthesis, restricts the rate of plasma leakage per neutrophil as lesions age.

Animals↗

PubMed1988

Kinetics of endotoxin-induced inflammation in ovine mammary gland.

The inflammatory response to stimulation with endotoxin of lactating and nonlactating mammary glands of sheep was examined. Similar numbers of neutrophils and mononuclear cells were recovered from nonlactating glands sampled every 2 h for 8 h and in glands sampled once at 8 h. Thus the inflammatory response was initiated by 2 h and repeated sampling did not modify the time course of the response. In contrast, in lactating ewes, fewer cells were recovered from glands sampled every 2 h than from glands sampled once at 8 h. Fewer neutrophils were also recovered when glands were serially sampled from 4 h to 8 h. Thus, removal of milk and inflammatory exudate modified the time course of the leukocyte influx into lactating glands. Significant accumulation of neutrophils occurred by 2 h in dose-response experiments in nonlactating glands. Peak accumulation of neutrophils occurred between 2 and 6 h, and a marked decline occurred after 8 h. In lactating glands, a slower onset and longer duration of neutrophil accumulation occurred. Twenty- to 30-fold more neutrophils were recovered by 8 h in lactating than nonlactating glands. This difference was not due to a lower threshold of sensitivity to endotoxin. Infusion of milk into nonlactating glands did not modify the intensity or time course of the inflammatory response to endotoxin. Thus, the physiological state of resident cells within the lactating gland, rather than the interaction of inflammatory exudate with milk, can account for the different reaction pattern in lactating glands. Inflammation in the nonlactating gland closely resembles inflammatory responses in skin and provides a convenient model for investigating the initiation and regulation of inflammatory processes.

Animals↗

PubMed1988

Two patterns of early neutrophil accumulation in acute inflammatory lesions.

A model of acute inflammation in the skin of sheep was developed using [111In]oxine-labeled neutrophils to quantify the accumulation of neutrophils in inflammatory lesions. Peak accumulation occurred during the first hour in lesions induced by zymosan-activated sheep plasma (ZAP, 100%) and during the second hour in lesions induced by endotoxin (10(-11) moles) and casein (2 x 10(-8) moles). The accumulation of neutrophils after the final stimulus diminished when lesions were restimulated every 2 h on two or more occasions. Thus desensitization of inflammatory lesions previously observed in rabbit skin is not restricted to that species. The early accumulation of neutrophils in primary and restimulated lesions was measured in lesions from 10 min to 2 h old. In primary lesions, ZAP induced significant neutrophil accumulation by 10 min, whereas 30 to 45 min elapsed before significant neutrophil accumulation occurred in lesions induced with endotoxin and casein. The initial responses in restimulated lesions were not diminished, but there was a failure of neutrophil accumulation to continue for as long as occurred in primary lesions. This finding indicates that regulation of the neutrophil influx into dermal inflammatory lesions may occur at a point after occupancy of the putative tissue receptors in the pathway which leads to accumulation of neutrophils at the injection site. The results indicate that there are at least two patterns of neutrophil accumulation in primary inflammatory lesions. The delayed pattern of neutrophil accumulation induced by casein and endotoxin resembles the enhanced binding of neutrophils to stimulated endothelial cultures in vitro, whereas the basis for the immediate response induced by ZAP remains conjectural. It is proposed that the primary action of chemotactic agents may be to provoke changes in the adhesive properties of endothelium and resident connective tissue cells thus permitting the migration of neutrophils into inflammatory lesions.

Acute Disease↗

PubMed1988

Studies on the inflammatory response during involution of the ovine mammary gland.

Cessation of lactation, initiated by the removal of lambs from their mothers, induced an inflammatory response with elevated numbers of neutrophil leucocytes in mammary secretions being detected within 16 h. Leucocyte numbers were still elevated 7 d later. Infusion of whole milk into non-lactating glands caused no change in leucocyte numbers after 24 h. Involution secretions, however, had the capacity to induce an inflammatory response when infused into non-lactating glands. Daily infusion of endotoxin (100 ng) into non-lactating glands resulted in a marked attenuation of the inflammatory response. Such desensitization did not accompany reinfusion of involution secretion. Responses to involution secretion were enhanced in glands desensitized to endotoxin. The failure of desensitization to develop in glands receiving repeated infusions of involution secretion and the lack of cross-desensitization between involution secretion and endotoxin indicate that a novel mediator of inflammation may be produced during mammary involution in sheep.

Animals↗

PubMed1987

Inflammatory and immunological responses in skin and peripheral lymph of sheep following intracutaneous injection of Staphylococcus aureus.

The cellular response within lesions and in draining lymph was examined in sheep following a primary intracutaneous injection of live or killed S. aureus. Microscopic examination of sections from live S. aureus lesions (12, 24, 48, and 96 h following vaccination) revealed a high ratio of neutrophils to macrophages at all times. This ratio was initially high following inoculation of killed S. aureus but decreased steadily at successive sampling times. Representative sections from lesions were subjected to indirect immunofluorescent staining to identify IgM-, IgG1-, and IgG2-containing cells. The ratio of IgG2- to IgG1-containing cells in lesions produced following live S. aureus vaccination was significantly greater than the ratio in lesions produced by killed staphylococci. Lesions induced by live S. aureus recruited significantly greater numbers of 51Cr-labeled allogeneic neutrophils from blood than did lesions induced by killed S. aureus. During the first 6 h this difference was approx. 20-fold. The volume of lymph and the number of leukocytes draining live S. aureus lesions was considerably greater than from lesions produced by killed staphylococci. The proportion of neutrophils in lymph draining both types of lesions increased markedly during the first two days of the response but was observed to be greater and remained higher for a longer period of time in lymph draining vaccine lesions produced following injection of live staphylococci. The increase in proportion of neutrophils in lymph was accompanied by a concomitant decrease in proportion of lymphocytes and macrophages. No immunoglobulin-containing cells or anti-staphylococcal antibody production was detected in lymph draining either type of lesion. These differences in inflammatory responses may contribute to the documented differences in immune responses to live and killed staphylococcal vaccines.

Animals↗

PubMed1987

Some characteristics of inflammation induced by muramyl dipeptide, endotoxin, and concanavalin A.

Inflammatory reactions induced by muramyl dipeptide (MDP), endotoxin, and concanavalin A (Con A) were examined in the skin of rabbits. The neutrophil influx induced by MDP peaked at 2 h and declined to a low level by 4 h, thus resembling the response induced by endotoxin. MDP and endotoxin exhibited homologous desensitization when extant lesions were restimulated at 6 h. These agents did not, however, induce heterologous desensitization. Con A induced a biphasic influx of neutrophils into inflammatory lesions with peaks at 2 h and 12 h. Neither the first nor second peak exhibited desensitization to homologous restimulation; however, the cell influx in restimulated lesions assumed a monophasic character peaking at 3 h. Con A lesions were not desensitized to restimulation with MDP or endotoxin. The results suggest that these chemotaxinogens rely on different endogenous mediators to induce an inflammatory response. The protracted second period of neutrophil infiltration of Con A-induced lesions and the failure of desensitization of this response to develop suggest that the mediator of Con A-induced inflammation may play an important role in the sustained recruitment of neutrophils in some inflammatory diseases.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1987

The inflammatory activity of activated complement in ovine and bovine mammary glands.

Infusion of zymosan-activated plasma (ZAP), a source of activated complement, induced inflammation in non-lactating mammary glands but not in lactating glands of ewes and cows. Interstitial injection of ZAP in lactating ovine glands also failed to induce inflammation as assessed by the neutrophil content of milk. The inflammatory activity of ZAP in non-lactating glands was inhibited by infusion of whole milk but not by skimmed milk. These results suggest that components of whole milk mask the inflammatory activity of activated complement. In addition, lactating mammary tissue of ewes and cows may lack sensitivity to the inflammatory effect of activated complement. Thus, activated complement cannot be an important mediator of inflammation in the lactating gland.

Animals↗

PubMed1987

Induction of inflammatory responses by endotoxin in the non-lactating ovine mammary gland.

In non-lactating ewes, intramammary infusion of endotoxin provokes an intense but transient inflammatory response as assessed by mammary lavage. The variability of the method for sampling the leucocytes in mammary secretions was examined. Initial lavage with 20 ml pyrogen-free saline recovered 83.0 +/- 2.8 and 84.4 +/- 3.0% of the total leucocyte numbers harvested by three serial washes of quiescent and inflamed glands, respectively. Lavage of glands prior to infusion of endotoxin did not affect the magnitude of the subsequent inflammatory response. Three treatments at 3.5 day intervals with the glucocorticoid, dexamethasone, which inhibits the inflammatory response to intramammary infusion of antigen in systemically immunized ewes, did not affect the inflammatory response to endotoxin. However, the variability of the inflammatory response to activated complement was greatly increased in dexamethasone-treated ewes; this effect was attributed to the induction of lactation which results in loss of sensitivity of the gland to the inflammatory activity of activated complement. The results indicated that the macrophages and lymphocytes which are present in mammary secretions in large numbers, and dexamethasone-sensitive lymphocytes in the gland, played a trivial role in the induction of inflammatory responses to endotoxin.

Animals↗

PubMed1987

Acute inflammation in gram-negative infection: endotoxin, interleukin 1, tumor necrosis factor, and neutrophils.

Experimental bacterial infection of the dermis induced with gram-negative microorganisms is associated with an acute inflammatory reaction, which represents the principal local defense against spread of the infection. When the inflammatory reaction is quantitated with radiolabeled cells and proteins, the kinetics resemble acute inflammation induced with other agents, such as immune complexes or chemotaxins. There is an interrelationship between the components or events of the inflammatory reaction; inasmuch as vascular injury is neutrophil-dependent, neutrophils must migrate to the site where the bacteria multiply. In neutropenic animals there is no such emigration and bacterial multiplication is not inhibited. The microorganisms shed endotoxin, which in turn induces secretion of interleukin 1 (IL 1) and probably tumor necrosis factor. Endotoxin is the most potent agent (10(-15) mol vs. 10(-12) mol of C5ades Arg) capable of inducing a neutrophil influx. Desensitization or tachyphylaxis of the tissues (probably of postcapillary venular endothelium) to IL 1 seems to control cessation of the neutrophil influx (also in vitro evidence). Phagocytosis of the bacteria by neutrophils is associated with release of oxygen radicals and lysosomal proteases from the neutrophils. These are instrumental in eliciting microvascular injury, which is characterized by enhanced vasopermeability, hemorrhage, and thrombosis.

Acute Disease↗

PubMed1987

Desensitization of the acute inflammatory response in skin and mammary gland of sheep.

Desensitization of the inflammatory response was investigated in the mammary glands and skin of sheep. Following twice daily stimulation of non-lactating glands, neutrophil concentrations in inflammatory exudates during the seventh response to endotoxin (1 microgram) and zymosan-activated plasma (1 ml) were 30% and 20% and those in primary responses occurring concurrently in contralateral glands. Cross-desensitization of ZAP was found in non-lactating glands pretreated with endotoxin. In lactating glands, inflammatory responses were examined following daily infusion of endotoxin (1 microgram) and oyster glycogen (50 mg). The neutrophil influx following infusion of each agent declined linearly, with the fourth response being 16% of the first response for both agents. On Day 5, inflammatory responses in contralateral glands receiving an initial challenge were comparable with primary responses on Day 1 in repeatedly stimulated glands. Thus, desensitization was a local phenomenon restricted to the restimulated gland. The return of normal responsiveness to 1 microgram endotoxin occurred after 9 days in glands desensitized by infusion of a single dose of 50 micrograms endotoxin. Accumulation of neutrophils and leakage of plasma were examined in skin sites restimulated with endotoxin and oyster glycogen. Neutrophil accumulation in restimulated lesions was comparable to primary lesions after about 3.5 days for endotoxin and 4.5 days for oyster glycogen. On the other hand, plasma leakage did not return to normal until Day 8 for endotoxin and until after Day 10 for oyster glycogen. The dissociation between neutrophil accumulation and plasma leakage in restimulated skin lesions contrasts with the dependence of plasma leakage on neutrophil migration reported in primary inflammatory lesions. The results suggest that desensitization of the inflammatory response may influence the pathogenesis of bacterial infection.

Acute Disease↗

PubMed1986

The role of interleukin-1 in neutrophil leukocyte emigration induced by endotoxin.

Chemotactic factors induce neutrophil emigration into tissues. Interleukin-1 (IL-1) was found to be several log times more potent in this respect than C5a des Arg, leukotriene B4, and f-Met-Leu-Phe and of comparable potency to endotoxin. Kinetic studies revealed a rapid and transient neutrophil influx, with the peak rate at 30-90 minutes. Cross tachyphylaxis was observed between IL-1 and endotoxin; and this, together with its high potency and rapid onset of action, suggest that IL-1 mediates endotoxin-induced neutrophil emigration.

Animals↗

PubMed1986

Emigration and accumulation of PMN-leukocytes induced by endotoxin, interleukin 1 and other chemotactic substances.

This publication describes polymorphonuclear leukocyte (PMN) emigration and accumulation, which is prerequisite for their defensive function in infected tissues. The extravasated PMNs can kill microorganisms, but in this process they also release proteolytic enzymes and other cell constituents which can alter and even injure the tissues, primarily the microcirculation. In the first part of the paper in vivo quantitation of the acute inflammatory reaction is described with emphasis on PMN emigration and accumulation. With 51Cr-labeled PMNs the kinetics of their emigration induced by a number of chemotaxins and chemotaxinigens was found to be similar, peaking in 1-4 hour old lesions and returning to baseline values thereafter. The most potent substance tested was endotoxin, which induced a PMN influx at a molar concentration a least 3 orders of magnitude lower than the other substances tested, implying the these substances are not the primary endogenous mediators of endotoxin induced inflammation. Next we describe an observation which shed considerable light on the mechanisms underlying PMN emigration. When a chemotaxin or endotoxin was injected intradermally and after varying periods of time reinjected into the same site, the PMN influx into those sites was diminished, compared to sites not previously injected, i. e. injected for the first time. This tachyphylaxis or diminished responsiveness was attributed to a downregulation of receptors, presumably on endothelial cells, coupled to a facilitatory mechanism. Other mechanism proposed to terminate emigration of PMNs during inflammatory reaction were unlikely, based on our experimental findings. Endotoxin is not chemotactic in vitro but it induces PMN emigration when injected intradermally. Hence the third part of the publication deals with PMN emigration induced by interleukin 1 and its significance for endotoxin-induced inflammation. IL 1 is the only chemotaxin which induces PMN accumulation at a concentration comparable to that of endotoxin and considerably lower than the other chemotaxins. There was cross tachyphylaxis between endotoxin and IL 1 and vice versa. The PMN influx into IL 1 sites injected 6 hours earlier with IL 1 or with endotoxin was diminished compared to IL 1 sites injected into normal skin. Sites injected first with IL 1 and then with a low dose of endotoxin also exhibited cross tachyphylaxis. FMLP or LTB4 injected into sites pretreated with endotoxin did not exhibit cross tachyphylaxis, i. e. the PMN influx was similar to sites injected for the first time with these chemotaxins.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1985

Humoral and cellular factors affecting the neutrophil response of the locally immunised mammary gland to staphylococcal infection.

Locally immunising the non-lactating ovine mammary gland by infusing killed Staphylococcus aureus enhances neutrophil accumulation in mammary secretion during subsequent staphylococcal infection. Immunological factors influencing this increased neutrophil response were studied in the present experiments. Glands locally immunised with killed Brucella abortus supported a greater neutrophil response to staphylococcal infection than did glands immunised with killed S. aureus. An enhanced neutrophil response to staphylococcal infection was recorded in 3 of 7 ewes locally immunised with zymosan. Passive immunisation by intramammary infusion of secretions from immunised glands conferred an enhanced neutrophil response during staphylococcal infection. Absence of haemolytic complement in secretions of immunised glands suggested complement was not implicated in the response. Secretions of immunised glands contained elevated concentrations of mononuclear cells. When exudates rich in mononuclear cells were established by infusion of endotoxin into non-immunised glands there was no increase in the neutrophil response to subsequent staphylococcal infection. However, when the mononuclear cell concentration was elevated by intramammary infusion of staphylococcal antigens in systemically immunised ewes there was an increase in the neutrophil response to subsequent infection. Thus humoral and cellular characteristics of the locally immunised mammary gland influence the kinetics of the neutrophil influx during staphylococcal infection.

Animals↗

PubMed1985

The immunophysiological basis for vaccinating ruminants against mastitis.

The roles of humoral and cellular defence mechanisms in protection of the mammary gland against bacterial infection are reviewed. Effective protection depends on opsonisation of pathogens and subsequent phagocytosis by neutrophils. A concomitant requirement for protection is the rapid infiltration of neutrophils into the infected gland. Immunological studies have shown the need to prime animals against antigens expressed by bacteria when they grow in vivo. Vaccination procedures which promote these mammary defence mechanisms are discussed.

Animals↗

PubMed1985

Margination and emigration of leucocytes.

A recurrent conclusion of studies on margination and emigration of leucocytes into acute inflammatory lesions has been that these two processes are the result of different stimuli. The recent description of tachyphylaxis of skin lesions to neutrophil chemotaxins is compared with the purported regulation of acute inflammation by deactivation of neutrophils, inactivation of chemotaxins and inhibition of cell migration. It is concluded that tachyphylaxis might regulate the intensity of the peak neutrophil influx whereas chemotaxin inactivators and migration inhibition factors might regulate the subsequent low grade neutrophil influx into lesions. It is suggested that the chemotaxin receptors which manifest tachyphylaxis may be located on endothelial cells of post-capillary venules. The literature indicates that an alteration in endothelium provides a sufficient stimulus for margination to occur. It is emphasised that attention should be directed towards determining the minimal changes in endothelium necessary to permit or induce margination to proceed. Emigration of marginated neutrophils might then occur in response to chemotaxin diffusing to the vessel wall or by locomotion along a gradient of substratum-bound chemotaxin. The selectivity of the leucocyte infiltration of tissues that occurs in some types of inflammation could be exerted by the stimulus for margination or the stimulus for emigration. It is noted that selective margination of lymphocytes occurs in post-capillary venules of lymphoid tissues. The role of a lymphocyte chemotaxin as the stimulus for emigration in this location is unknown. To encompass the known phenomena, a general theory of leucocyte margination and emigration would predict that leucocytes selectively marginate onto acceptor molecules expressed by endothelium and extravasate in response to a chemotactic stimulus. Endothelium-bound chemotaxins may function as acceptor molecules. A bipartisan model of leucocyte migration to extravascular locations is proposed which contends that leucocyte can be recruited non-specifically as inflammatory cells or they can be recruited specifically as effector cells of immune reactions. It is suggested that tachyphylaxis is a characteristic of inflammatory cell recruitment but not of immunologically driven cell recruitment. The binding of chemotaxins to endothelial cells in vivo, the selectivity of margination, the status of margination in desensitised tissues and the role of chemotaxins in lymphocyte recirculation through lymph nodes are identified as critical questions to resolve the mechanisms of leucocyte margination and emigration.

Capillary Permeability↗

PubMed1985

Kinetics of tachyphylaxis to mediators of acute inflammation.

The kinetics of vascular leakage and tachyphylaxis induced by histamine and bradykinin were examined in rabbit skin and were compared with the kinetics of tachyphylaxis of neutrophil accumulation in lesions induced with the chemotaxin formylmethionyl-leucyl-phenylalanine (FMLP). Maximal leakage of 125I-human serum albumin occurred during the first 5 min after injection of bradykinin and from 10 to 20 min after injection of histamine. Tachyphylaxis developed within 30 min of injection of bradykinin and 1 hr after injection of histamine. For both agents, there was a linear regression of sensitivity with time from 8 hr to 4 days, with normal sensitivity estimated to return at 4.6 days for bradykinin and 4.7 days for histamine. Marked cross-desensitization occurred between the two agents, and lesions initiated with the chemotaxin FMLP were desensitized to restimulation with a mixture of histamine and bradykinin. Initiation of lesions with histamine and bradykinin did not diminish the accumulation of neutrophils when lesions were restimulated with FMLP. The kinetics of tachyphylaxis of neutrophil accumulation in lesions stimulated with FMLP exhibited a linear regression of sensitivity on time between 4 days and 10 days, with estimated resensitization at 11.9 days. Histamine and bradykinin induce enhanced vascular permeability when endothelial cells in post-capillary venules contract following stimulation of their membrane receptors for these agents. We have recently proposed that the migration of neutrophils into acute inflammatory lesions is regulated by a mechanism coupled to chemotaxin receptors which may be similarly located on endothelial cells within the lesions. The present experiments indicate that expression of receptors for vascular permeability agents and the chemotaxin FMLP are independent events with distinct kinetics.

Animals↗

PubMed1984

Chemotactic factor-specific desensitization of skin to infiltration by polymorphonuclear leukocytes.

The accumulation of polymorphonuclear leukocytes (PMNs) was measured in rabbits following single or repeated injections into skin sites of the inflammatory agents, zymosan-activated plasma and formylmethionyl-leucyl-phenylalanine. Fewer cells entered lesions restimulated with the same agent during the subsequent inflammatory response than simultaneously entered skin sites stimulated for the first time. Decreased reactivity of a restimulated site was specific to the initiating stimulus, developed within 2 to 4 h of initial stimulation and persisted for at least 8 h. The results indicate that PMN accumulation in acute inflammatory lesions is regulated locally by a chemotactic factor-specific mechanism which differs from PMN deactivation and concentration gradient mechanisms currently thought to regulate PMN migration in vivo.

Animals↗

PubMed1984

Desensitization of acute inflammatory lesions to chemotaxins and endotoxin.

Desensitization of the neutrophil inflammatory response to intracutaneous injection of chemotaxins and endotoxin was studied in rabbits. When restimulated 6 hr later with the same agent, inflammatory lesions initiated with platelet-activating factor (PAF), leukotriene B4 (LTB4), or endotoxin supported a diminished influx of neutrophils compared with responses in normal skin. In contrast, repeated stimulation of lesions with alpha-casein failed to lead to desensitization. The specificity of desensitization was investigated, and it was found that lesions initiated with formylmethionyl-leucyl-phenylalanine (FMLP) supported a normal response when restimulated with PAF, alpha-casein, or endotoxin. Initiation of lesions with LTB4, however, diminished the subsequent response to zymosan-activated plasma and PAF, but not endotoxin, alpha-casein, or FMLP. This result indicates that LTB4 is not a final common mediator of neutrophil infiltration of acute inflammatory lesions. Desensitization was detected irrespective of the concentration of chemotaxin used to investigate the response. Repeated stimulation of lesions with FMLP abolished the accumulation of neutrophils after the final stimulus, indicating that complete desensitization can occur and the presence of a chemotaxin within an inflammatory lesion is not sufficient stimulus for neutrophil infiltration of the site to proceed. Lesions initiated with endotoxin supported comparable responses when restimulated with a mixture of FMLP and endotoxin or FMLP alone, despite 93% inhibition of the response to restimulation with endotoxin alone. This indicates that a cell-directed inhibitor of neutrophil migration, such as lipomodulin or neutrophil-immobilizing factor, does not produce the diminished responses in desensitized lesions. It is proposed that desensitization occurs due to down-regulation of a receptor-coupled pathway that permits or facilitates neutrophil extravasation in acute inflammatory lesions. The chemotaxin receptors regulating neutrophil extravasation are probably located on endothelial cells of post-capillary venules.

Acute Disease↗