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Biomedical subjects

L E Glynn

Publications and source records attributed to L E Glynn.

15 recordsLinked to original sources
PubMed1978

Cell-mediated and humoral immunity to chick type II collagen and its cyanogen bromide peptides in guinea-pigs.

Cell-mediated immunity (CMI) to chick type II collagen and its cyanogen bromide (CB) peptides was studied in guinea-pigs using cutaneous delayed hypersensitivity reactions. Responses were largely independent of molecular conformation in animals immunized with either native or denatured collagen, and reactions obtained with CB peptides 8, 9, 10 and 12 suggested that sites in the central regions of collagen chains were recognized in CMI. Antibodies to collagen were detected by haemagglutination and immunofluorescence only in animals immunized with native molecule and not in animals immunized with denatured or CB-digested material. Humoral and CMI responses were similar in that neither recognized the pepsin-labile non-helical regions of the molecule. The responses differed in that humoral reactions were conformation-dependent and type-specific and CMI reactions were not.

Animals↗
PubMed1977

Primary lesion in osteoarthrosis.

The primary disturbance in osteoarthrosis is generally regarded as occurring in the articular cartilage and as resulting from a combination of ageing and mechanical factors. An alternative hypothesis is that the primary disturbance is located in the synovial lining cells. It is suggested that proteolytic enzymes which normally leak from the phagocytic (A type) lining cells are in the healthy joint neutralised by inhibitors synthesised by the B-type lining cells. Osteoarthrosis is the result of an imbalance between leakage of enzymes and provision of inhibitors.

Bone Diseases↗
PubMed1977

Is persisting antigen responsible for the chronicity of experimental allergic arthritis?

Animals were injected intra-articularly with antigen after prior immunization with that antigen in Freund's incomplete adjuvant in order to precipitate immune complexes in the surfaces of menisci, ligaments, and cartilage. On reimmunization with antigen in Freund's complete adjuvant 10 weeks later, generally an arthritis limited to the intercondylar fossa developed; but on intra-articular injection of antigen a second time a widespread arthritis developed in that joint. Thus immune deviation had not occurred and animals were in an immunological condition such as to be capable of developing widespread arthritis given the correct intra-articular stimulus. It is concluded that antigen, persisting as immune complexes, plays no part in maintaining widespread monarthritis, presumably owing to its inability to participate in a delayed hypersensitivity reaction as a result of sequestration.

Animals↗
PubMed1977

Effect of excising Freund's adjuvant granuloma on subsequent development of experimental allergic arthritis.

Rabbits were immunized with antigen in Freund's complete adjuvant. Several weeks later the granuloma which developed was excised one day before joint challenge with antigen. The subsequent development of experimental allergic arthritis (EAA) was not affected, which argues against the chronicity of the disease being maintained by continuous recruitment of mycobacterial debris to EAA joints.

Animals↗
PubMed1977

The role of the plasmalogen in the cross-reaction between group A streptococcus and human myocardium.

Ethanol-soluble mycardial material which reacts with anti-streptococcal sera in a number of immunological tests has been isolated and identified as ethanolamine plasmalogen. The reactions of cardiac plasmalogen with antistreptococcal sera was specific and could be inhibited by streptococcus-derived materials. Guinea-pigs sensitized to streptococci gave positive skin reactions when challenged with myocardial plasmalogen. The pattern of the immunofluorescent staining given by antiplasmalogen sera was very much like that given by antistreptococcal sera. Nevertheless, the plasmalogen failed to compete for tissue-bound myocardial antigens when tried as an inhibitor of the immunofluorescent staining of myocardium either by antistreptococcal sera or by antiplasmalogen sera. A hypothesis of the role of the plasmalogen in the formation of complexes between streptococci and myocardium-derived material in the initiation of autoimmune processes is presented.

Antibodies, Bacterial↗
PubMed1976

Anti-streptococcal antibodies reacting with brain tissue. I. Immunofluourescent studies.

Serum JD from a 14-year old girl with Sydenhams chorea contained antibodies which gave immunofluorescent staining of the limiting membrane of the brain, ependymal tissue and fibrous astrocytes. These antibodies could be completely absorbed by Str. pyogenes type 24 (NCTC 8305) but only partially if at all by type 6 matt (NCTC 8302) or type 6 glossy (NCTC 8709). In contrast, staining by the same serum of the choroid plexus, the periphery of hepatocytes, the periphery of the cells of the gastric mucosa, and tubules in the kidney could be absorbed out by the type 6 matt and type 24 strains (but not by the type 6 glossy or Staph. aureus NCTC 6571). A rabbit anti-streptococcal serum (3/74) raised against disintegrated washed cells of Str. pyogenes type 24 stained and the same structures in the brain to high titre, but not the choroid plexus and not the other structures stained by serum JD. These staining reactions of 3/74 could be absorbed out by Str. pyogenes type 24 but not by Str. pyogenes type 6 matt or type 6 glossy. None of these staining patterns given by serum JD or by 3/74 could be absorbed by human uterine smooth muscle. Serum 3/74 stained heart muscle but this reaction could be absorbed without affecting the brain staining reactions. Sera from 4 other patients with Sydenham's chorea were found to give staining of the ependyma and the limiting membrane, 2 only very weakly.

Adolescent↗
PubMed1975

Persistence of antigen in nonarthritic joints.

The presence of antigen, IgG and C3 was shown by radioautography and immunofluorescence in the collagenous tissues of the joints of animals injected intra-articularly with antigen after having been previously immunized with that antigen in Freund's incomplete adjuvant. Since these joints were shown to be virtually free of inflammatory reactions, we suggest that the persistence of immune complexes activating complement cannot fully explain the chronicity of experimental allergic arthritis.

Animals↗
PubMed1975

The non-passage of mycobacteria from Freund's complete adjuvant granuloma depots to arthritic joints.

The intra-articular injection of antigen after immunization with that antigen in FCA, the mycobacterial component of which consisted of live M. avium or dead 125I-M. tuberculosis, resulted in identical chronic disease, experimental allergic arthritis. In the former case live mycobacteria could be isolated from the subcutaneous granuloma which developed at the injection site, and from arthritic joints into which 10 mug wet weight (equivalent of 2 mug dry weight) had been injected with this antigen. However, no mycobacteria could be isolated from other inflamed or normal joints. With 125I-labelled mycobacteria radioactive counting and radioautography clearly showed M. tuberculosis present in the subcutaneous granuloma but not in either injected or uninjected joints. The quantity of mycobacteria which could have been detected if present was estimated to be less than 1 mug dry weight. These results strongly suggest that mycobacteria do not travel from the granuloma depot to the arthritic joint, and that any mechanism one may consider to explain the chronicity of EAA cannot involve the physical presence of mycobacteria in the knee joint.

Animals↗