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Role of mitogenicity in pathogenicity of mycoplasmas for murine hosts

Annales De Microbiologie
|January 1, 1984
PubMed

Insights

Lewis rats showed more severe lung damage from Mycoplasma pulmonis than Hooded rats. Optimal pneumonia development required co-stimulation of both B- and T-cell mitogens in rat lungs.

Area of Science:

  • Immunology
  • Pathology
  • Microbiology

Background:

  • Mycoplasma pulmonis is a pathogen that can cause respiratory disease in rats.
  • Rat strains exhibit varying susceptibility to M. pulmonis infections.
  • Mitogens, substances that induce cell division, can modulate immune responses.

Purpose of the Study:

  • To compare the mitogenicity and pathogenicity of Mycoplasma pulmonis in Lewis and Hooded rats.
  • To investigate the roles of T-cell and B-cell mitogens in the induction of pneumonia.
  • To determine the necessity of co-stimulation of both lymphocyte types for maximal pneumonia development.

Main Methods:

  • Comparison of M. pulmonis membrane-induced mitogenic and pathologic effects in Lewis and Hooded rats.
  • Intranasal administration of concanavalin A (T-cell mitogen) or M. neurolyticum membranes (B-cell mitogen) to Hooded rats.
  • Intranasal co-administration of both mitogens to Hooded rats.

Main Results:

  • Lewis rats exhibited more severe mitogenic and pathologic responses to M. pulmonis membranes compared to Hooded rats.
  • Individual T-cell and B-cell mitogens independently affected rat lungs.
  • Maximal interstitial lymphocytic pneumonia development necessitated co-stimulation of both B- and T-lymphocytes.

Conclusions:

  • Severity of lung lesions correlates with the degree of mitogenic responses in different rat strains.
  • Both B- and T-cell mitogens play roles in pneumonia induction.
  • Co-stimulation of B- and T-lymphocytes is essential for maximal interstitial lymphocytic pneumonia.

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