Search PubMed⌕ Search

Biomedical subjects

C J Howard

Publications and source records attributed to C J Howard.

At least 163 records · Page 9Linked to original sources
PubMed1981

Protection of mice against Mycoplasma pulmonis infection using purified mouse immunoglobulins: comparison between protective effect and biological properties of immunoglobulin classes.

Purified mouse immunoglobulins with specific activity against Mycoplasma pulmonis were examined for their ability to protect mice against intranasal (i.n.) infection with this organism. The survival of mycoplasmas in the respiratory tract of mice inoculated i.n. with M. pulmonis mixed with either IgG1, IgGa, IgG2b or IgA antibodies was less than that seen in control animals inoculated with mycoplasmas mixed with normal mouse serum. The ways in which the immunoglobulin fractions could have mediated resistance were examined in vitro. IgG1, IgG2a and IgG2b antibody fractions killed M. pulmonis in the presence of guinea-pig complement, and also promoted the phagocytosis of M. pulmonis by mouse lung macrophages. In contrast, IgA antibody did not appear to be either mycoplasmacidal or opsonic.

Animals↗
PubMed1980

Interaction of Mycoplasma pulmonis with mouse peritoneal macrophages and polymorphonuclear leucocytes.

Mouse peritoneal macrophages and polymorphonuclear leucocytes were examined for their ability to kill Mycoplasma pulmonis in vitro. Killing of mycoplasmas was shown to require specific antibody, suggesting that antibody-dependent phagocytosis may be involved in resistance to infection. Convalescent mouse serum appeared to be less effective than rabbit antiserum in promoting the killing of mycoplasmas by phagocytic cells. Moreover, mycoplasmas recovered directly from the respiratory tract of infected mice were more resistant to killing by macrophage cultures than organisms grown in vitro. The possibility that these observations may contribute to an understanding of the persistent nature of M. pulmonis infections in mice is discussed.

Animals↗
PubMed1980

Class-specific antibody responses to Mycoplasma pulmonis in sera and lungs of infected and vaccinated mice.

Class-specific antibodies were measured by a solid-phase microradioimmunoassay in the sera and lung washings of mice after intranasal or intravenous inoculation with live Mycoplasma pulmonis and after systemic, intranasal, or combined vaccination with Formalin-inactivated mycoplasmas. After intranasal or intravenous inoculation with live organisms, serum antibodies were first detected in immunoglobulin M (IgM) followed by IgG2, IgG1, and IgA classes, but significant levels of IgA developed only in those mice inoculated intranasally. The appearance of antibodies in lung washings was later than in serum, but again these were predominantly IgG2 and IgG1. After inoculation with killed organisms, serum antibodies were predominantly IgG1, although IgG2, IgM, and, in intranasally vaccinated mice, IgA were also present. Only IgG1 was detected in lung washings from mice vaccinated systemically, but IgA and IgG2 were present in addition in animals vaccinated intranasally. Immunofluorescence studies indicated that some antibody in lung washings from the latter group of animals was produced locally. A comparison of the levels of various class-specific antibodies and resistance to intranasal challenge suggested that local antibody of any immunoglobulin class is capable of mediating resistance in the lungs to M. pulmonis infection.

Administration, Intranasal↗
PubMed1980

Variation in the susceptibility of bovine mycoplasmas to killing by the alternative complement pathway in bovine serum.

All but one of nine Acholeplasma strains were susceptible to killing by gnotobiotic-calf serum while all but one of fifteen Mycoplasma strains were resistant. The mechanism of killing was examined using inhibitors of complement, viz. EDTA. MgEGTA. epsilon-amino caproic acid, and also by desalting serum and adding MgCl2 and CaCl2. The results indicated that, when strains were killed by serum from gnotobiotic calves it was by the alternative complement pathway. However, experiments with mycoplasmas and Escherichia coli indicated that the effect of MgEGTA was not identical for bovine and human sera. Sensitivity to killing by the alternative complement pathway in bovine serum appeared to be a property of avirulent strains and resistance to killing may be regarded as a virulence determinant of mycoplasmas.

Acholeplasma↗
PubMed1980

Immunity to Mycoplasma bovis infections of the respiratory tract of calves.

Calves were inoculated intramuscularly with formalin killed Mycoplasma bovis with adjuvant and after 14 days intratracheally with killed organisms without adjuvant. Seven days later they were challenged intratracheally and 21 days after challenge they were found to have significantly fewer M bovis in their lungs than control calves. Two intramuscular or two intratracheal inoculations of killed M bovis were not found to induce resistance but imunity could be stimulated by three subcutaneous inoculations of inactivated mycoplasmas with adjuvant. Immunity was correlated with antibody detectable in lung washings by the single radial haemolysis technique. Combined intramuscular and intratracheal administration of killed M bovis induced a better antibody response in lung washings than two intramuscular or two intratracheal inoculations. Antibody was also detected in lung washings from calves inoculated three times subcutaneously but in this case it was thought to be derived from serum. The antibody detected in lung washings by single radial haemolysis was found to be IgG by radioimmunoassay.

Animals↗
PubMed1980

Surface receptors for immunoglobulin on bovine polymorphonuclear neutrophils and macrophages.

Surface receptors for rabbit immunoglobulin (Ig) and bovine IgG1 were detected on bovine alveolar macrophages by the rosette technique. Receptors for bovine IgG2 were either absent from, or present at a low level on, the surface of these cells. In contrast, polymorphonuclear neutrophils from peripheral blood and milk were shown to have surface receptors for bovine IgG2 but not for bovine IgG1 or rabbit Ig.

Animals↗
PubMed1979

The effect of an intramammary infusion of endotoxin on experimentally induced mycoplasmal mastitis.

The infusion of 10 microgram of endotoxin lipopolysaccharide from Escherichia coli into the mammary gland of four cows 16 h before inoculation with ureaplasmas did not prevent, or even diminish, the subsequent ureaplasmal mastitis. There was no reduction in the severity or duration of the inflammatory cell response in milk or in the clinical appearance of the resulting mastitis. Also, the excretion of ureaplasmas was not reduced. A similar experiment with Mycoplasma dispar in two cows demonstrated that endotoxin was again ineffective in preventing the mastitis. Furthermore, there was some indication that the proliferation and excretion of this mycoplasma was enhanced in endotoxin-treated quarters.

Animals↗
PubMed1979

Variation in the virulence of strains of Mycoplasma pulmonis related to susceptibility to killing by macrophages in vivo.

The virulence of five strains of Mycoplasma pulmonis, as judged by their ability to survive in the respiratory tract and induce pneumonia in CBA mice, was related to the ability of viable organisms to persist in the peritoneal cavity. This appeared to be the result of differences in the ability of the strains to resist killing by peritoneal macrophages in vivo. It is suggested that resistance to phagocytosis by macrophages is an important determinant of virulence for M. pulmonis.

Animals↗
PubMed1979

Pathogenicity of some Mycoplasma and Acholeplasma species in the lungs of gnotobiotic calves.

Cloned cultures of 16 strains, representing nine different species of Mycoplasma and Acholeplasma, were inoculated intratracheally into gnotobiotic calves. Strains of M bovirhinis, M canadense, M verecundum, A axanthum and A modicum did not produce visible pneumonic lesions and were not reisolated from the lungs. Strains of M alkalescens and M arginini colonised the lower respiratory tract but failed to produce visible pneumonia. M bovigenitalium (strain M991/70) and M dispar (strain Gri226) both colonised the respiratory tract and induced pneumonic lesions estimated to involve up to 8 per cent (M bovigenitalium) and 17 per cent (M dispar) of the lung. Histologically M bovigenitalium produced a cuffing pneumonia and M dispar produced a interstitial alveolitis.

Acholeplasma↗
PubMed1978

The effect of pneumonia induced in mice with Mycoplasma pulmonis on resistance to subsequent bacterial infection and the effect of a respiratory infection with Sendai virus on the resistance of mice to Mycoplasma pulmonis.

The effect of pneumonia induced by Mycoplasma pulmonis in mice on the resistance of the lung to additional bacterial infection was examined. The effect of pneumonia induced by Sendai virus on the resistance of mice to M. pulmonis was also investigated and compared with the effect of Sendai virus on resistance to Staphylococcus aureus. Sendai virus infection decreased subsequent resistance to M. pulmonis in proportion to the virus dose. Decreased resistance to subsequent S. aureus and M. pulmonis infection was greatest at about the same time after inoculation of virus and was related to virus-induced lesions. Besides affecting the resistance of mice to subsequent mycoplasma infection, Sendai virus could enhance an existing mycoplasma infection. Pneumonia induced by M. pulmonis did not decrease resistance to subsequent bacterial infection. The mechanism whereby Sendai virus decreases host resistance is therefore similar for bacteria and mycoplasmas, but pneumonia induced by mycoplasmas does not have the same effect.

Animals↗
PubMed1977

Protective effect of vaccines on Mycoplasma pulmonis-induced respiratory disease of mice.

Mice inoculated intranasally with either a virulent or an avirulent strain of live Mycoplasma pulmonis were resistant to respiratory disease induced by a subsequent intranasal challenge with virulent organisms. Similarly, mice inoculated intravenously with the virulent strain were resistant to intranasal challenge with the same strain. In contrast, mice inoculated intravenously with avirulent M. pulmonis were not resistant to intranasal challenge with the virulent mycoplasma strain. Studies on mice inoculated intravenously with the two strains of M. pulmonis indicated that persistance of mycoplasmas in the respiratory tract may be important in inducing resistance to intranasal challenge with M. pulmonis. These observations, together with the lack of correlation between the level of serum antibodies and resistance to M. pulmonis-induced respiratory disease, suggested that local immune mechanisms were important in resistance. It is proposed that an effective vaccination schedule to protect mice against M. pulmonis-induced respiratory disease may be one that stimulates both systemic and local immune defenses. This suggestion is supported by the observation that systemic followed by local administration of inactivated M. pulmonis was more effective in inducing resistance in mice to intranasal challenge with live organisms than was systemic administration alone. In addition, mice inoculated solely by the intranasal route with inactivated mycoplasmas were resistant to M. pulmonis-induced respiratory disease. These studies indicate the importance of local defense mechanisms in the induction of resistance to M. pulmonis-induced respiratory disease in mice.

Administration, Intranasal↗
PubMed1976

Experimental mycoplasma mastitis in mice.

Thirteen strains of mycoplasma representing six different species, Acholeplasma laidlawii, Mycoplasma dispar, M. bovirhinis, M. bovigenitalium, M. agalactiae subsp. bovis, and M. mycoides subsp. mycoides, were inoculated into the mammary glands of mice, and the number of mycoplasmas present in the glands three days after inoculation was determined. The predominant response included involution of inoculated glands and a neutrophil infiltration. With the exception of M. dispar, the pathogenicity of the six species for mice was found to be similar to their pathogenicity for cattle.

Acholeplasma laidlawii↗
PubMed1976

Interaction of Mycoplasma dispar and Mycoplasma agalactiae subsp. bovis with bovine alveolar macrophages and bovine lacteal polymorphonuclear leukocytes.

Mycoplasma dispar and Mycoplasma agalactiae subsp. bovis survived or grew in cultures of bovine lacteal polymorphonuclear leukocytes or bovine alveolar macrophages. In the presence of specific bovine antibody, macrophages and polymorphonuclear leukocytes appeared to kill both species of mycoplasma. Specific rabbit antisera also promoted the killing of these mycoplasmas by bovine macrophages but had no demonstrable activity for bovine polymorphonuclear leukocytes. It is suggested that phagocytosis of these mycoplasmas by bovine cells occurs only in the presence of specific antibody. The experiments also indicate that differences exist between bovine polymorphonuclear leukocytes and macrophages with regard to their receptor sites for immunoglobulins.

Animals↗