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Biomedical subjects

D G Colley

Publications and source records attributed to D G Colley.

At least 181 records · Page 10Linked to original sources
PubMed1975

Alternate complement pathway induction of aggregation and release of 5-hydroxytryptamine and adenosine diphosphate by rabbit platelets.

The present studies investigated patterns of rabbit platelet aggregation and release of 5-hydroxytryptamine (5HT) utilizing nine variables: three different types of challenge, soluble antigen and antibody (AG-AB), zymosan (Z), an agent known to activate the alternate complement pathway (ACP), and Z preincubated in lightly heparinized plasma so as to become coated with complement (ZC); three different types of platelet-rich plasma (PRP), lightly heparinized PRP in which both complement pathways are active, ethylene glycol tetraacetic acid-PRP (EGTA-PRP) in which only the ACP is active, and ethylene diamine tetraacetic acid PRP (EDTA-PRP), which inhibits both complement pathways; three different types of inhibitors, cobra venom factor (CoF), which causes activation of C3 proactivator (C3PA) to C3 activator (C3A) and fluid phase decomplementation of C3 and C5 through C9, adenosine monophosphate (AMP), a specific antagonist of ADP, and tosyl arginine methyl ester (TAME), an inhibitor thought to act not only on the first component of complement, but also on a platelet membrane site of mediating complement-induced platelet injury as well as on C3PAse. In heparinized PRP, both AG-AB and Z produced biphasic aggregation and prompt and extensive 5HT release. A brief lag period noted with both AG-AB and Z challenge was not observed with ZC challenge, indicating that this lag period represented time required for generation of the necessary complement-dependent membrane-injuring activity. Prior decomplementation by CoF entirely prevented both aggregation and release by either AG-AB or Z but by ZC, indicating first that fluid-phase ACP activation did not produce platelet injury, and second that ZC had on its surface an activity capable of producing immediate biphasic aggregation and prompt 5HT release without the further participation of later acting complement components. Both AMP and TAME eliminated the second phase of aggregation and diminished or eliminated 5HT release with all three challenges, suggesting that both inhibitors might be operative on similar or identical platelet membrane receptors mediating complement-dependent platelet injury. In EGTA-PRP, AG-AB and Z produced delayed monophasic aggregation and delayed and diminished 5HT release, whereas ZC produced immediate although monophasic aggregation but delayed and diminished 5HT release. This suggested that all three challenges were capable of producing ACP-mediated platelet injury.

Adenosine Diphosphate↗
PubMed1973

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. I. Eosinophilia and immunologic responses to a schistosomal egg preparation.

Chronic murine schistosomiasis is characterized by a host cell-mediated immune response to schistosomal egg antigens. This response is manifested in vitro by lymphocyte blastogenic reactivity to a soluble schistosomal egg antigen preparation (SEA) and in vivo by delayed dermal hypersensitivity to SEA. In addition, mice develop reaginic, agglutinating, and early dermal reactive antibodies to SEA and a characteristic pattern of peripheral blood eosinophilia. In this study, depletion of thymus-dependent lymphocytes abolished the anti-SEA lymphocyte blastogenic response and delayed dermal reactivity, reaginic antibody response and the major peak of peripheral blood eosinophilia, which in normal mice occurs at the same time as SEA-induced blastogenesis. Antibodies mediating the early dermal reaction to SEA and agglutinins for SEA-coated particles were not inhibited by T-lymphocyte depletion. The experimental group did not develop the normally observed granulomatous response, but rather suffered focal hepatic and mucosal liquefactive necrosis, bacteremia and accelerated mortality.

Agglutination↗
PubMed1973

Schistosoma mansoni infection in mice depleted of thymus-dependent lymphocytes. II. Pathology and altered pathogenesis.

Murine schistosomiasis mansoni is a more rapidly fatal disease in hosts deprived of their cell-mediated immune capabilities. Analysis of the histopathology of the disease under these circumstances indicates that rather than the hepatic granulomata characteristic of the normal infection, the host develops zones of liquefactive necrosis in the liver and intestinal mucosa. These lesions are associated with severe parenchymal cell destruction. Such hepatic and mucosal damage, with subsequent toxemia and septicemia, is presumed central to the altered course of the disease.

Animals↗
PubMed1972

Complement-dependent platelet injury by staphylococcal protein A.

A new example of complement-mediated platelet injury has been described. Staphylococcal protein A (SPA) causes rabbit platelet injury as manifested by release of platelet 5-hydroxytryptamine (5HT). This reaction is complement-dependent and occurs over a very small range of SPA concentration, larger amounts being inhibitory. Complement fixation by SPA demonstrates the same narrow SPA concentration requirement whereas precipitation of IgG by SPA is roughly proportional to SPA concentration over a wide concentration range. The reaction can be separated into a sensitization step which requires SPA and plasma but not complement, and a release step which does require complement. Complement-mediated platelet damage induced by SPA is a new biologic property of this common component of the cell wall of pathogenic staphylococci which may contribute to the development of inflammatory and thromboembolic reactions complicating intravascular staphylococcal infection.

Animals↗
PubMed1970

Cellular differentiation in the thymus. 3. Surface properties of rat thymus and lymph node cells separated on density gradients.

Young adult rat thymus and lymph node cell subpopulations were obtained by differential flotation on discontinuous BSA density gradients and assayed for properties characteristic of mature thymus-derived lymphocytes. One such subpopulation (C) of thymocytes was enriched in its ability to respond mitotically to a hemiallogeneic MLR stimulus, to localize in the parenchyma of lymph nodes and spleen, and to initiate a GVH reaction in a suitable host. These cells did not respond well to mitotic stimulation by PHA, they were lighter in density than the majority of mature lymph node thymus-derived lymphocytes, and they possessed a thymus-specific antigen (RTA) not present on peripheral lymphoid cells. We conclude that the acquisition of peripheral properties occurs sequentially, during an intrathymic differentiation cycle or shortly after the cells leave the thymus.

Animals↗