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Biomedical subjects

J G Tew

Publications and source records attributed to J G Tew.

At least 145 records · Page 8Linked to original sources
PubMed1979

Immune retention: immunological requirements for maintaining an easily degradable antigen in vivo.

Radioactive human serum albumin (125I-HSA) was injected into the hind foot pads of unimmunized mice, actively immunized mice and mice passively immunized with mouse or rabbit anti-HSA serum. Eleven days later the unimmunized mice had cleared most of the 125I-HSA. In contrast, a high concentration of 125I-HSA was retained in the feet and draining lymph nodes and, to a lesser extent, in the spleen of the actively or passively immunized mice. Although immune retention required specific antibody, it appeared to be independent of T-cells or T-cell factors, since passively immunized nude mice retained antigen as well as actively or passively immunized normal mice. Depletion of the complement system with cobra venom factor (CVF) increased antigen retention in the feet but decreased retention in the spleen. Treatment with CVF did not decrease antigen retention in lymph nodes of actively immunized mice. Such treatment did, however, decrease retention in lymph nodes of passively immunized mice although not to the same extent as in the spleen. Retention of antigen in the feet was not only complement-independent but was also Fc independent, since F(ab')2 fragments of IgG could mediate immune retention. Antigen dose response studies indicated that immune retention in lymph nodes occurred optimally with minute amounts of antigen, whereas optimal retention in the feet required much higher concentrations of antigen. Foot pad injections of non-radiolabelled HSA eliminated 60% of the radioactivity retained in the foot pads of immunized mice. In contrast, non-radioactive egg albumin (EA) had almost no effect on retained HSA. However, if the mice were immunized to both EA and HSA, an injection of EA would displace a significant amount of retained HSA. Complexes of one specificity can apparently displace some retained antigen of a differing specificity.

Animals↗
PubMed1978

Herpes simplex virus vaccine: protection from stomatitis, ganglionitis, encephalitis and latency.

A mouse model system was developed for studying the pathogenesis of oral infection with herpes simplex virus type 1 and the protection offered by prior immunization with a nucleic acid-free vaccine. Of non-immunized mice, 95-100% developed ulcerative lesions 3-5 days following application of virus to abraded oral epithelial surfaces. Infection of the ipsilateral sensory (trigeminal) ganglion and the cerebellum occurred by day 2 and sequentially progressed to the contralateral ganglion by day 4 and to the cerebrum by day 5. Prior immunization of mice with an inactivated virus vaccine, and most importantly, with a vaccine free of nucleic acid, protected mice from subsequent oral virus infection. Protection was demonstrated by: (i) reduction in the incidence and severity of primary oral lesions; (ii) a decrease in the number of mice with acute ganglionic infection or dying of encephalitis; and (iii) a reduction in the incidence of latent trigeminal ganglionic infection.

Animals↗
PubMed1977

A radioimmunoassay for human antibody specific for microbial antigens.

A simple and sensitive method for detecting and quantitating antibody specific for microbial antigens is described. Bacterial, fungal, parasitic or viral antigens attached to bromoacetyl cellulose or the intact cells themselves were added to a series of two-fold dilutions of human serum. After a short incubation period, which allowed human antibody to attach to the antigens, the complex was thoroughly washed and carbon-14 labeled anti-human light chain antibody was added to each dilution. The resulting complex was washed, collected on a filter pad, placed in a scintillation vial and radioassayed. The relationship between radioactivity bound and --log2 of the serum dilution was linear. The endpoint for each assay and a confidence interval was calculated by doing inverse prediction from simple linear regression. Results obtained using this assay indicated the presence of antibody in a pool of normal human sera specific for herpes virus and for both cell surface and intracellular antigens of Streptococcus mutans, Naegleria fowleri, and Cryptococcus neoformans. In general the dominant response was against the intracellular antigens rather than cell surface antigens.

Antibodies, Bacterial↗
PubMed1977

Release of beta-lysin from platelets caused by antigen-antibody complexes, purified enzymes, and platelet-aggregating substances.

The release of beta-lysin, which followed the intravenous injection of antigen-antibody complexes, did not take place when these complexes were added to citrated whole blood but did occur in heparinized blood. beta-Lysin release in heparinized blood was inhibited by citrate but were reversed by the addition of calcium ions that implicated complement reactions. Fourteen different enzymes were added to platelet-rich plasma (PRP). Streptokinase, neuraminidase, papain, phospholipase C, sulfatase, and trypsin caused platelets to release significant quantities of beta-lysin, whereas elastase, phosphatase, protease, ribonuclease A, hyaluronidase, lipase, and pepsin caused little or no increase in the plasma beta-lysin concentration. One enzyme, fibrinolysin, inactivated beta-lysin faster than it was released. The enzyme-induced release of beta-lysin from PRP was often accompanied by a reduction in the number of platelets. The intravenous injection of streptokinase, neuraminidase, and sulfatase caused in vivo releases of beta-lysin into the plasma. The platelet-aggregating substances collagen, arachidonic acid, and adenosine 5'-diphosphate caused beta-lysin to be released from PRP. The platelet-aggregating substances L-epinephrine, zymosan, fibrinogen, reserpine, and serotonin caused little or no release of beta-lysin from platelets. The results of this study indicate that the release of beta-lysin during antigen-antibody-complement reactions, blood coagulation, phagocytosis, and inflammation could be enzyme mediated.

Adenosine Diphosphate↗
PubMed1977

Protection from oral herpes simplex virus infection by a nucleic acid-free virus vaccine.

The effect of immunization with inactivated herpes virus vaccines, including a vaccine free of all nucleic acid, was investigated in a mouse model system. Protection against oral lesions induced by herpes simplex virus type 1 was demonstrated by several criteria: (i) reduction in the incidence and severity of primary oral lesions; (ii) decrease in acute and latent infection of the regional sensory ganglia; and (iii) protection from viral encephalitis and death. The immune response of mice to the vaccine and to subsequent virus challenge was measured by following serum-neutralizing antibody titers.

Animals↗
PubMed1975

Induction and maintenance of the antibody response by different forms of human serum albumin.

Various forms of human serum albumin (HSA) were compared in their ability to induce and maintain the antibody response. In an in vitro model system, antibody synthesis was induced spontaneously during the maintenance phase of the immune response--presumably by persisting antigen. When different lymph nodes (LN) of the same rabbit were primed simultaneously with different forms of HSA, the spontaneous responses obtained in cell cultures prepared from LN primed with high molecular weight forms of HSA were greater than the responses obtained in cell cultures prepared from similar LN primed with lower molecular weight forms of HSA. This difference in response was consistent regardless of the method employed in antigen preparation and persisted for many months. The in vitro results indicating that the antibody response would be maintained at a higher level in animals immunized with high molecular weight forms of antigen and that the method of preparation would not be of major significance were confirmed in vivo in a mouse system.

Animals↗
PubMed1974

Interrelationship between serum beta-lysin, lysozyme, and the antibody-complement system in killing Escherichia coli.

The effects of different serum components alone and in conjunction with each other on Escherichia coli B were investigated. In general, the viability, turbidity, and electron microscope results were compatible with the following conclusions. The most efficient killing and destruction of E. coli B occurred when beta-lysin, lysozyme, and the antibody-complement system functioned in cooperation with each other at the serum concentration in isotonic solutions. The addition of sucrose protected the bacteria from the lethal and lytic action of these agents. Elimination of lysozyme from serum had the least effect on bactericidal activity, even though lysozyme treatment caused the cell wall to separate from the cytoplasmic membrane and caused clear areas to appear in the inner granular layer of the cell wall. Beta-lysin removal had an intermediate effect on the serum bactericidal activity. Beta-lysin treatment caused cell walls to collapse, allowed cytoplasmic contents to leak out of the cells, and stopped the separation of cell wall and cytoplasmic membrane, which normally takes place in 0.5 M sucrose solution. Inactivation of the complement eliminated the serum bactericidal activity against E. coli B. After treatment with antibody and complement, the cell walls became thick and indistinct, a portion of the cytoplasmic contents escaped, and patches of the middle layer of the cell wall appeared in freeze-etch preparations. Beta-lysin damaged the cytoplasmic membrane, lysozyme damaged the inner peptidoglycan layer of the cell wall, and the antibody-complement system damaged both the middle lipopolysaccharide layer of the cell wall and the cytoplasmic membrane.

Animals↗
PubMed1974

Release of beta-lysin from platelets by thrombin and by a factor produced in heparinized blood.

Removal of calcium by either citrate, oxalate, or ethylenediaminetetraacetate inhibited coagulation of blood at an early stage and prevented the release of beta-lysin from platelets. In contrast, heparin caused platelet agglutination and stimulated beta-lysin release in vitro and in vivo. This release was calcium dependent and may have been due to a calcium-dependent reaction in the blood coagulation sequence. Thrombin which by-passed the early calcium-dependent stages of coagulation directly stimulated the release of beta-lysin from platelets. However, thrombin alone or in combination with other plasma factors was not as effective in releasing beta-lysin as the regular coagulation process. Thrombin's platelet degranulating activity correlated with its beta-lysin releasing activity. In contrast to thrombin, staphylococcal coagulase, which also by-passed the calcium-dependent stages of coagulation, coagulated citrated blood without releasing beta-lysin. The release of beta-lysin has been observed previously in the absence of blood coagulation, but this is the first observation of coagulation without beta-lysin release. It is clear that beta-lysin is released from platelets during coagulation by the direct action of thrombin and that it may be released in an earlier calcium-dependent reaction.

Animals↗