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Biomedical subjects

J R Ward

Publications and source records attributed to J R Ward.

At least 145 records · Page 8Linked to original sources
PubMed1973

Detection and characterization of defective mycoplasmacidal antibody produced by rodents against Mycoplasma arthritidis.

A procedure has been developed for the detection of mycoplasmacidal antibody in the serum of rats and mice infected with Mycoplasma arthritidis. Antibody activity can apparently be measured only by using resting mycoplasma cells. The reaction is complement dependent and is usually complete within 3 h. Early antibody (5 days) could be detected only within the immunoglobulin (Ig)M fraction, whereas late antibody (42 days) is found within the IgG fraction. The mycoplasmacidal antibody was highly specific and cross reactions were not observed with other mycoplasma species. Antibody activity could be removed from serum by absorption with either viable or nonviable M. arthritidis. Cidal antibody produced by rats against other mycoplasma species was active against both resting and multiplying cells. Mycoplasmacidal antibody against M. arthritidis was detected in rats 2 days after injection of the organisms and persisted at least through 300 days. Mice usually developed antibodies by 3 days after injection of the organisms and moderate titers have been observed for as long as 487 days. Since viable mycoplasmas can persist in the peripheral circulation in the presence of antibody, it is likely that viable mycoplasma-antibody complexes are also present.

Absorption↗
PubMed1972

Growth of Newcastle disease virus and rubella virus in rheumatoid and nonrehumatoid synovial cell cultures.

Rheumatoid and nonrheumatoid synovial cell cultures were challenged with Newcastle disease virus and rubella virus in an attempt to confirm reports that rheumatoid synovial cells are relatively resistant to infection with these viruses. Newcastle disease virus caused complete cell destruction by day 7 in both rheumatoid and nonrheumatoid cultures, and peak virus titers were similar. Rubella virus replicated in both rheumatoid and nonrheumatoid synovial cell cultures, and no consistent differences in virus titers were detected. Rubella-infected cell lines were observed for up to 28 days and no virus-specific cytopathic effect was seen.

Adolescent↗
PubMed1971

Role of Biological Mimicry in the Pathogenesis of Rat Arthritis Induced by Mycoplasma arthritidis.

Complement fixation (CF), immunofluorescence, and agar gel double-diffusion tests were used to demonstrate an antigenic relationship between rat tissues and Mycoplasma arthritidis. Rabbit antisera against six strains of M. arthritidis exhibited positive reactions in the CF test with an ethyl alcohol-saline extract of rat muscle, whereas only 6 of 18 antisera against other Mycoplasma species were positive. With the use of gel diffusion techniques, absorption of various M. arthritidis antigens with antiserum against rat muscle removed at least one precipitin band when the absorbed mycoplasma antigens were reacted against homologous antisera. Rabbit antiserum against M. arthritidis was conjugated with fluorescein isothiocyanate and reacted against frozen sections of muscle tissues of various animals. As controls, unlabeled normal rabbit serum and rabbit anti-M. arthritidis serum were included to determine the specificity of the reaction. Rat, hamster, and mouse skeletal muscle exhibited specific fluorescence, whereas chicken, beef, frog, and turtle muscles exhibited no specific fluorescence. Mice injected at birth with rat lymphocytes were found to be more susceptible to subsequent infection by M. arthritidis than were normal mice or mice injected at birth with mouse lymphocytes. These results indicate the occurrence of a heterogenetic antigen(s) common to M. arthritidis and rat tissues. Preliminary evidence suggests that this heterogenetic antigen(s) may enable the mycoplasmas to become established in their host.

Journal Article↗
PubMed1971

Chronic proliferative arthritis of mice induced by Mycoplasma arthritidis. I. Induction of disease and histopathological characteristics.

Mice injected intravenously with Mycoplasma arthritidis developed a chronic arthritis which persisted through at least 269 days. Rats similarly treated developed an acute short-term infection. The mouse disease was characterized by periods of remission and exacerbation and was proliferative in nature, gradually spreading to adjacent joints. M. arthritidis strain 158 P10 was found to be less arthritogenic for mice than for rats, but further passage of this strain in mice substantially increased its virulence. Unlike rats, mice appeared to be susceptible to a "toxin" of M. arthritidis and they developed a necrotic spreading abscess after subcutaneous administration of the organisms. Histopathological studies revealed that mice varied greatly in the degree of joint inflammation, destruction, and repair. The disease was characterized by (i) an initial acute phase with infiltration of the articular and periarticular tissues with polymorphonuclear leukocytes and a mild hyperplasia of the synovial membrane; (ii) a mixed acute-chronic phase in which new areas of acute inflammation developed alongside areas of chronic lesions; (iii) a chronic phase followed which was characterized by massive synovial proliferation with mononuclear cell infiltration, irregularity in the articulating cartilage, pannus formation, and "punched out" defects in cortical bone near cartilagenous osseous junctures. The clinical course and histopathological characteristics of the chronic phase of mouse arthritis induced by M. arthritidis closely resembled those of rheumatoid arthritis of man.

Abscess↗
PubMed1971

Chronic proliferative arthritis of mice induced by Mycoplasma arthritidis. II. Serological responses of the lost and effect of vaccines.

Complement-fixing antibodies were first detected in mice 7 days after intravenous injection with Mycoplasma arthritidis. Peak titers were observed at 21 days, and high levels of antibody persisted through 293 days. The metabolism-inhibiting antibody response was minimal. On fractionation of mouse sera, only 7S antibody was detected which first appeared at 12 days after injection and persisted throughout the experiment. In contrast, serum taken from rats injected with M. arthritidis contained predominantly 19S antibodies in the early stages of the disease which were gradually replaced with 7S antibodies. The intravenous injection of mice with M. arthritidis culture supernatant fluid had no effect upon their subsequent susceptibility to the arthritogenic effects of M. arthritidis, but this procedure appeared to delay the onset of abscess formation after the subcutaneous injection of M. arthritidis. Formalin-killed cells of M. arthritidis partially protected mice against the arthritis induced by M. arthritidis. Previous infections with M. arthritidis conferred partial immunity against the arthritogenic effects of the organism. Serum taken from convalescent mice at 41 days had a partial protective effect when used to immunize passively normal mice against M. arthritidis. However, rabbit anti-M. arthritidis serum which possessed higher complement-fixing and metabolism-inhibiting antibodies was without significant protective properties.

Animals↗
PubMed1970

Varicella arthritis.

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Arthritis, Infectious↗
PubMed1970

Effect of Animal Passage on Arthritogenic and Biological Properties of Mycoplasma arthritidis.

Determinations of the ED(50) of cultures of Mycoplasma arthritidis disclosed the existence of great diversity in the arthritogenic properties of the various strains. In most cases, the ED(50) values were lowered after passaging in rats, and a more severe arthritis with a shorter period of onset was observed. Heavy suspensions of arthritogenic M. arthritidis did not appear to induce any toxic symptoms. Prior injections of endotoxin did not enhance the toxicity of M. arthritidis suspensions. The more arthritogenic strains grew more slowly in the basal medium and remained viable for longer periods of time than those with lower arthritogenic properties. All strains were identical on the basis of complement-fixation tests. Minor differences observed between strains during gel-diffusion studies could not be correlated with arthritogenic properties. Arthritogenic strains appeared to be less susceptible to the inhibiting action of rabbit antisera than were the nonarthritogenic strains.

Journal Article↗
PubMed1970

Immunological response of rodents to murine mycoplasmas.

Mycoplasma arthritidis, M. pulmonis, M. neurolyticum, and M. felis strains administered on various immunization schedules induced complement-fixing and agglutinating antibodies in rats, mice, and guinea pigs. Metabolic inhibiting (MI) antibodies against M. felis were produced by guinea pigs, mice, and rats. M. neurolyticum did not induce MI antibody in mice but induced high titers in guinea pigs and rats. M. pulmonis failed to induce MI antibody titers in mice, induced low titers in rats, and induced high titers in guinea pigs. M. arthritidis induced no or very low titers in rats and low titers in mice, but induced high MI titers in guinea pigs. A positive correlation was demonstrated between ability of the mycoplasma to induce disease and lack of MI antibody formation by its natural host. It is suggested that the apparent inability of the various animals to produce MI antibodies against their natural mycoplasmal parasites may enable the mycoplasmas to become established in their hosts. The concept of biological mimicry is brought forward to explain these observations.

Journal Article↗
PubMed1969

Immunological responses of the rat to Mycoplasma arthritidis.

Arthritis was produced in rats by the intravenous injection of Mycoplasma arthritidis. Metabolic inhibiting antibody and indirect hemagglutinating antibody could not be detected in the sera of arthritic or convalescent animals. Nonmurine species of mycoplasma were capable of inducing metabolic inhibiting antibody in the rat. A hypothesis based upon the possible occurrence of heterogenetic antigens common to M. arthritidis and rat tissue was brought forward to explain these findings. Complement-fixing antibody to M. arthritidis was detected 3 to 4 days after injection and subsequently rose to high levels, depending upon the severity of arthritis and number of organisms injected. Animals that had recovered from intravenous or subcutaneous inoculation with M. arthritidis were resistant to subsequent infections by the organism. Immunity could be passively transferred by the intravenous injection of convalescent serum. Adsorption of the convalescent serum with antigen greatly reduced the complement fixation titer but did not significantly alter the protective properties of the serum. The presence of complement-fixing antibody could not be related to the development of immunity. An avirulent strain of M. arthritidis and a strain previously classified as M. hominis type 2 were capable of inducing resistance to subsequent injection by virulent M. arthritidis.

Animals↗