Isotype commitment of B cells and dissemination of the primed state after mucosal stimulation with Mycoplasma pulmonis

Rose, Faina V.; Cebra, J J

doi:10.1128/iai.49.2.428-434.1985

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…The appearance of M. pulmonis-specific antibody in serum was similar in both strains of mice after infection and consistent with previous studies (5,27,28). IgM was the first antibody to be detected, at 7 days; this was followed by IgG and IgA, which were detected at 14 and 21 days, respectively.…”

Section: Discussionsupporting

confidence: 92%

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

et al. 1995

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Mycoplasma pneumoniae is a leading, worldwide cause of death and disability due to pneumonia. Mycoplasma pulmonis infection in mice is an invaluable model for the study of host defenses against respiratory mycoplasmas in vivo. C3H/HeN mice are much more susceptible to acute inflammatory lung disease due to M. pulmonis than C57BL/6N mice, but little is known about the chronic disease in these mouse strains. We infected C3H/HeN and C57BL/6N mice with 10 4 CFU of M. pulmonis UAB CT and evaluated them at weekly intervals by quantitative mycoplasma culture of nasal passages, trachea, and lungs, assessment of lesion severity in nasal passages, trachea, and lungs, and determination of serum immunoglobulin classes and subclasses by enzyme-linked immunosorbent assay. We found that C3H/HeN mice had 2 to 5 logs more organisms in their lungs and far more severe lung disease than C57BL/6N mice through 63 days postinfection. Although both strains of mice developed the same classes of antibody, C3H/HeN mice had much greater anti-M. pulmonis immunoglobulin G (IgG) responses in the IgG1 and IgG2a subclasses than C57BL/6N mice. These results suggest that adaptive immunity does not effect resolution of chronic mycoplasma infection and disease in the lungs.

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Section: Discussionsupporting

confidence: 92%

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

et al. 1995

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“…Limiting dilution analysis. Lymphocytes were isolated from the lungs of B6C3 mice by mild enzymatic treatment (34) or from the spleens of mice by mechanical dispersion and were analyzed in limiting dilution microcultures (in the absence of dendritic cells) as previously described (36). Supernatants were collected after 7 days of culture and analyzed by ELISA for the production of anti-FHA antibodies.…”

Section: Methodsmentioning

confidence: 99%

Mucosal immunization with filamentous hemagglutinin protects against Bordetella pertussis respiratory infection

1992

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Mucosal immunization of mice with purified BordeteUla pertussis filamentous hemagglutinin (FHA), by either the respiratory or the gut route, was found to protect against B. pertussis infection of the trachea and lungs. Intranasal immunization of BALB/c and (C57BL/6 x C3H/HeN)Fl adult female mice with FHA prior to B. pertussis aerosol challenge resulted in a 2 to 3 log reduction in number of bacteria recovered from the lungs and the tracheas of immunized mice in comparison to unimmunized controls. Intraduodenal immunization of adult mice with FEIA before infection also resulted in approximately a 2 log reduction in the recovery of bacteria from the lungs and the tracheas of immunized mice in comparison to unimmunized controls. Immunoglobulin A and immunoglobulin G anti-FHA were both detected in bronchoalveolar lavage fluids of mucosally immunized mice. Limiting dilution analysis revealed a 60-fold increase in the frequency of FHA-specific B cells isolated from the lungs of mice immunized intranasally with FHA in comparison to unimmunized control mice. These data suggest that both gut and respiratory mucosal immunization with a major adhesin ofB. pertussis generates a specific immune response in the respiratory tract that may serve as one means of mitigating subsequent B. pertussis respiratory infection.

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“…However, Ab production does not help the animal to recover from the respiratory disease but can protect it, if given before the infection (Williamson et al 1986). In mice, exposure to M-pulmonis leads to a specific Tcell dependent B-cell response in which the majority of the secreting clones produce IgGl (Rose & Cebra 1985). The specific response to M. pulmonis could be increased by the simultaneous administration of dextran sulfate (Kishima et al 1987).…”

Section: Mycoplasma Effects On Lymphocytes In Vivomentioning

confidence: 99%

Interactions between Mycoplasmas and the Immune System

Ruuth

Praz

1989

Immunological Reviews

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Mycoplasmas are a heterogenous group of prokaryotic organisms causing a wide variety of diseases, including autoimmune disorders. Thus, it is not surprising that various mycoplasmas strains, including Mycoplasma arginini, M. arthritidis, M. neurolyticum and M. pulmonis, are able to regulate the immune response. Though some of the studies of the immunomodulatory action of mycoplasmas have been done in vivo, the majority of the investigations have been conducted in vitro. This has led to the recognition that mycoplasmas are polyclonal activators of both B and T cells from several species, acting through MHC-restricted or -unrestricted pathways. Mycoplasma activation not only induces T-cell proliferation but also leads but to the formation of cytotoxic T cells. We, as well as others, have shown that mycoplasma-mediated B-cell activation induces proliferation as well as Ig secretion, and also that mycoplasma stimulation of lymphocytes may result in the production of cytokines. We communicate here our investigations into the effects of an M. arginini strain on the growth and maturation of preactivated B cells. After an initial biological characterization of the M. arginini effects in vitro, we established the protein nature of the growth-supporting activity and proceeded further on to isolate and identify the responsible proteins. The use of lipid- and lipoglycan-free extracts has allowed us to further extend our studies on the biological activities of the proteins from M. arginini and to compare these results with the effects obtained using live organisms. Furthermore, the study was extended to include a characterization of the in vivo-induced effects of live M. arginini. Altogether, the results from these experiments allow us to conclude that M. arginini is a T-cell independent polyclonal B-cell mitogen, mediated by five identified proteins, inducing growth and Ig secretion of both resting and preactivated B cells.

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Isotype commitment of B cells and dissemination of the primed state after mucosal stimulation with Mycoplasma pulmonis

Cited by 10 publications

References 23 publications

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

Mucosal immunization with filamentous hemagglutinin protects against Bordetella pertussis respiratory infection

Interactions between Mycoplasmas and the Immune System

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