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Biomedical subjects

C M Pearson

Publications and source records attributed to C M Pearson.

At least 37 records · Page 2Linked to original sources
PubMed1977

Human monocyte-lymphocyte interaction: a new technique.

A rosette-type assay of the physical interaction between lymphocytes and monocytes after treatment with neuraminidase-galactose oxidase (NGAO) is reported. Monocyte-lymphocyte (ML) rosette formation and subsequent lymphocyte proliferation occurred when either lymphocytes or homologous monocytes were treated with NGAO and cultured together. Maximal ML rosette formation took place at 37 degrees C 4 hr after culture in media containing 10% serum at lymphocyte to monocyte ratios of 10:1 to 20:1. The percentage of rosette formation correlated with the extent of thymidine incorporation when increasing concentrations of NGAO were used. When NGAO-treated monocytes were added to untreated T and non-T lymphocytes, they bound preferentially to T lymphocytes and induced proliferation only in the T subpopulation. These results indicate that the ML rosette assay measures a highly specific monocyte-lymphocyte physical interaction after a mitogenic stimulus which is an early event in lymphocyte activation since it reflects the degree of subsequent lymphocyte proliferation.

Cell Separation↗
PubMed1976

Arylamidases in normal and diseased human muscle.

Human skeletal muscle homogenates were found to contain enzymes that catalyze the hydrolysis of beta-naphthylamides of leucine, arginine and lysine, known substrates for neutral and basic arylamidases. They also contained a trace of activity towards alpha-aspartyl-beta-naphthylamide. The muscle arylamidases were found to be inhibited by p-chloromercuribenzoate, Hg2+ and puromycin. Leucyl, arginyl and lysysl arylamidases were slightly activated by cobalt ions. When compared to controls, no significant differences in muscle arylamidase activities were observed in patients with muscular dystrophies and certain denervating diseases.

Aminopeptidases↗
PubMed1976

Lymphocyte depletion in patients with rheumatoid arthritis.

Sixteen patients with severe rheumatoid arthritis, marked inflammation of the synonvial membrane and high rheumatoid titer were cannulated by the thoracic duct for a period rangin between 82 up to 100 days. The patients being not under any medication during that time. Quantitative and qualitative analysis of the lymphocytes were performed, as well as responses to mitogens, rheumatoid factor, circulating antibodies and delayed hypersensitivity. By the 14th day nearly all the patients had a partial or almost complete remission of their disease. No complications were observed. These results will be discussed.

Arthritis, Rheumatoid↗
PubMed1976

Acid, neutral, and alkaline hydrolases in arthritic synovium.

The levels of six lysosomal enzymes (acid phosphatase, beta-acetylglucosaminidase, cathepsin D, beta-galactosidase, arylsulfatase A, and beta-glucuronidase) and four neutral and alkaline hydrolases (esterase, inorganic phyrophosphatase, alkaline phosphatase, and 5'-nucleotidase) were measured in osteoarthritic, rheumatoid and control synovia. All enzyme levels in diseased synovium except esterase values in osteoarthritis were significantly elevated compared with controls. The mean values of the group of acid hydrolases and the group of neutral and alkaline hydrolases in osteoarthritic synovia were 1.9- and 2.0-fold greater than those of control specimens. In rheumatoid synovia, the values were 4.2- and 4.5 fold greater than control for the same enzymes. Levels in rheumatoid synovia were significantly higher than those in osteoarthritic synovia with the exception of 5'-nucleotidase. Only a limited correlation between the extents of inflammation present in the synovia and the levels of a lysosomal marker enzyme (cathepsin D) was observed. These results demonstrate that whatever the mechanism, increased levels of acid hydrolases as well as certain neutral and alkaline hydrolases are present in osteoarthritic and rheumatoid synovia, and these enzymes are probably contained in the synovial lining cells.

Acetylglucosaminidase↗
PubMed1976

Induction of adjuvant arthritis in the rat by various bacterial cell walls and their water-soluble components.

A number of purified cell walls of various gram-positive bacteria had arthritogenic activity in the rat. The water-soluble adjuvant-active component(s), which were isolated from some of these cell walls by utilizing a peptidoglycan-degrading enzyme, did produce severe adjuvant arthritis. However, the components obtained by digestion with glycan-degrading enzymes failed to produce arthritis. Thus, the present finding indicates the importance of a peptidoglycan portion, especially its intact glycan chain, for induction of adjuvant arthritis.

Animals↗
PubMed1976

Reevaluation of inguinal lymph node injection for production of adjuvant arthritis in the rat.

An experiment was designed to compare the efficiency of lymph node injection for the induction of adjuvant arthritis (AA) with that of conventional footpad injection in the rat. Quantitative studies revealed that the minimal dose required for induction of AA by the lymph node route is one fifth of that by the footpad route. Thus, the lymph node route was found to be more efficient than the footpad method in terms of higher incidence and earlier onset of AA. PPD in Freund's incomplete adjuvant was able to produce tuberculin sensitization in the rat. The lymph node route again proved to be superior in terms of consistent appearance of the 24-hour reaction on days 8 and 14 and prolongation of the skin reaction over 48 h. These findings show that the lymph node method is so efficient in the rat that it will be especially useful for the trial induction of AA with various materials of unknown potency as well as for production of delayed hypersensitivity. In addition, this injection method appears to be a simple and efficient technique for assay of other immunological reactions.

Animals↗
PubMed1976

Effect of degradation of the arabinogalactan portionof a water-soluble component from M. tuberculosis wax D on polyarthritis induction in the rat.

In order to explore a possible role of the arabinogalactin (AG) portion of the water-soluble arthritogenic component (WAC) from M. tuberculosis wax D for induction of adjuvant arthritis (AA) in the rat, this component was digested with an AG-degrading enzyme. The enzyme-digested WAC was able to produce AA. The severity of AA was almost comparable to that of the nondigested WAC. This finding suggests that the AG portion of the WAC does not seem to be essential for AA induction and indirectly points the importance of the peptidoglycan portion.

Animals↗
PubMed1976

Preparation of various fractions from Mycobacterium smegmatis, their arthritogenicity and their preventive effect on adjuvant disease.

Cell walls of Mycobacterium smegmatis were able to produce much more severe arthritis in rats than the delipidated cells, whereas cell envelope and cell membrane fractions were unable to produce the disease. The lysozyme-solubilized product was able to produce mild disease with only 30% of incidence with an optimum dose, whereas the higher and the lower doses did not produce the disease. The rats immunized with cell envelope, cell membrane fraction and nonarthritogenic doses of lysozyme-solubilized product were protected against the subsequent homologous and heterologous challenge of delipidated cells. It was discussed that this preventative effect can be the result of antigenic competition between the arthritogenic and nonarthritogenic components of M. smegmatis. On the other hand, all the fractions separated here were able to serve as an immunoadjuvant in terms of inducing delayed hypersensitivity to ovalbumin in guinea pigs.

Animals↗
PubMed1976

Arthritogenicity of Mycobacterium smegmatis subfractions, related to different oil vehicle and different composition.

Arthrigenicity of Mycobacterium smegmatis subfractions appeared to be remarkably potentiated in oil vehicles such as squalane or mineral oil, while water-in-oil emulsions containing Arlacel A appeared to decrease or suppress their arthritogenicity. It seems that Arlacel A can exert a suppressive effect on the arthritogenicity of the subfractions. Poly I:C and acetylated wax D potentiated the arthritogenicity of lysozyme-solubilized product, while cord factor was unable to do so. When given together with either cell membrane fraction or cell envelope, the lysozyme-solubilized product produced much more severe disease than that of lysozyme-solubilized product alone. Cell walls lost much of their arthritogenicity when mixed with lysozyme-solubilized product.

Animals↗
PubMed1976

Synergism of immunogenic and adjuvant-active components of mycobacterial wax D in the induction of adjuvant arthritis.

Two derivatives of wax D, one possessing immunogenicity and the other adjuvant activity, were tested for the possible role in the induction of adjuvant arthritis (AA) in rats. The former, a water-soluble arthritogenic and immunogenic component (WAC), in incomplete Freund's adjuvant, was able to induce delayed hypersensitivity (DH) and mild AA, but failed to function as an adjuvant in rats. The latter, an acetylated wax D (AD) and its subfraction, AD6, did exert adjuvant activity, but were free from immunogenicity and arthritogenicity. The addition of AD or AD6 to the WAC in incomplete Freund's adjuvant, when injected into inguinal lymph nodes, resulted in the production of severe AA with high incidence. Other adjuvants such as pertussis vaccine and lipopolysaccharide could not replace AD6; they failed to enhance AA when combined with the WAC. Also, other mycobacterial antigen, PPD, could not replace wax D-derived WAC; it did not induce AA when coupled with AD6, although it did induce DH to PPD.

Adjuvants, Immunologic↗
PubMed1976

Arylamidase and cathepsin-A activity of normal and dystrophic human muscle.

Human skeletal muscle homogenate has been shown to contain enzymes that catalyze the hydrolysis of L-leucyl p-nitroanilide and carbobenzoxyglutamyl-L-tyrosine, known substrates, respectively, for arylamidase and cathepsin A. The muscle arylamidase was found to be inhibited by p-chloromercuribenzoate. Addition of Co2+ resulted in slight stimulation of its activity. Neither ethylenediamine tetraacetate nor thiol compounds had any appreciable effect on the enzyme. When compared to controls, no significant differences in muscle arylamidase levels were observed in patients with muscular dystrophies and certain selected neuromuscular diseases. Cathepsin A was, however, increased in muscles moderately affected by muscular dystrophy and denervating diseases.

Adolescent↗
PubMed1976

Improvements for consistently inducing experimental allergic encephalomyelitis (EAE) in rats: I. without using mycobacterium. II. inoculating encephalitogen into the ear.

Several methods of inducing experimental allergic encephalomyelitis (EAE) in rats were examined using different (i) rat strains, (ii) combinations of encephalitogen with different adjuvants, and (iii) sites of encephalitogen inoculation. The time course and severity of the ensuing diseases were determined and methods delineated for inducing a disease with limited variability and high incidence. Omitting the mycobacterial component from the adjuvant eliminated the complication of adjuvant arthritis, which may develop after the appearance of EAE. Encephalitogenic emulsions prepared with an equal volume of frozen guinea pig spinal cord (GPSC) and hexadecane or squalene, injected into two inguinal nodes or one foot pad of Lewis rats, provided two quick and easy ways to induce EAE. Emulsions of encephalitogen with Freund's complete adjuvant or hexadecane, injected into the ear, also induced EAE but lengthened the time between the antigen inoculation and clinical symptoms which accompany the onset of EAE disease. However, injection into the ear offers an advantage over the Newbould technique (direct instillation of encaphalitogen in pre-exposed lymph nodes), since the animals can be confidently predosed with drugs which may reduce lymphoid mass. Effects of local inflammation on systemic drug metabolism are also minimized when using the ear route.

Adjuvants, Immunologic↗
PubMed1976

Arthritogenicity in rats of cell walls from several streptococci staphylococci and two other bacteria.

Bacterial cell walls from Str. bovis, Str. lactis, Str. mutans, Str. thermophilus, Str. salivarius, and Str. pyogenes were able to produce polyarthritis in rats but Str. faecalis cell walls were nonarthritogenic. S. aureus cell walls produced extremely severe disease. It was also shown that cell walls from S. epidermidis, B. megaterium, and M. lysodeikticus were nonarthritogenic. A close correlation was observed between development of arthritis and the delayed hypersensitivity to bacterial peptidoglycans but not with the PPD hypersensitivity. It was suggested that the adjuvanticity of bacterial cell walls is needed to induce the disease and that arthritogenicity requires a specific antigen in addition to the presence of an adjuvant-inducing agent.

Animals↗
PubMed1976

Human lymphocyte subpopulations: the effect of pregnancy.

Peripheral blood lymphocytes from pregnant and nonpregnant females were studied for the presence of the following surface receptors: (i) Receptor for heat-aggregated human IgG (AggIgG); (ii) Receptor(s) for complement components; (iii) Receptor for sheep red blood cells (SRBC). Absolute numbers of lymphocytes with receptors for complement and those with receptors for SRBC were present in equal numbers in both groups. However, in the pregnant females there was a significantly lower number of lymphocytes with receptors for AggIgG. It is hypothesized that some of the immunological changes which occur during pregnancy may be mediated partly through changes in the total numbers of certain lymphocyte subpopulations.

B-Lymphocytes↗
PubMed1976

Structural requirements for arthritogenicity of peptidoglycans from Staphylococcus aureus and Lactobacillus plant arum and analogous synthetic compounds.

The comparative studies on the arthritogenicity of chemically well defined peptidoglycans (PG)2 from the cell walls of Staphylococcus aureus (FDA 209P) and Lactobacillus plantarum (ATCC 8014) showed that 1) a polymer of disaccharide-peptide with or without the presence of N-acetylglucosaminyl-ribitol-teichoic acid produced severe arthritis; 2) oligosaccharide-peptides with or without the special structure (N-acetylglucosaminyl-ribitol-teichoic acid in S. aureus, a polymer of rhamnose and glucose in L. plantarum) produced severe disease; 3) disaccharide-heptapeptide-disaccharide with or without the presence of either glucose-ribitol-teichoic acid or a polymer of rhamnose and glucose appeared to be arthritogenic but much less effective for disease production; 4) N-acetylmuramyl-heptapeptide-N-acetylmuramic acid and disaccharide-hexapeptide were non-arthritogenic; 5) none of the synthetic N-acetylmuramyl-peptides, including tetrapeptide, produced the disease. Thus it is concluded that arthritis-inducing activity is related to the peptidoglycan moiety but not to the special structure, and the most important moiety responsible for disease production may be located in a chain length of two or more disaccharide units on PG subunits. However, it is discussed that non-arthritogenicity of peptidoglycans, including synthetic compounds, may be due to a lack of adjuvanticity in rats rather than a lack of antigenic determinant(s) responsible for production of arthritis.

Animals↗