Literature DB >> 3397188

Clearance of different strains of Mycoplasma pulmonis from the respiratory tract of C3H/HeN mice.

M K Davidson1, J K Davis, J R Lindsey, G H Cassell.   

Abstract

Pathogen-free C3H/HeN mice were exposed by aerosol to Mycoplasma pulmonis PG34(ASH), UAB 5782C, M1, UAB T, or UAB CT, and clearance of mycoplasmas from the nasal passages, trachea, and lungs was determined during the first 72 h postinoculation (PI). There were differences among strains of mycoplasmas in physical removal of organisms and in killing by nonspecific factors in the nasal passages and trachea. The avirulent strain, PG34(ASH), was quickly removed from the nasal passages and trachea. Physical removal of the other mycoplasmal strains occurred slowly, with 60 to 89% of the radioactive label remaining in the nasal passages and trachea even after 72 h. There were significant differences in killing among mycoplasmal strains by nonspecific host mechanisms in the nasal passages, trachea, and lungs. Strain UAB T was quickly killed at all levels of the respiratory tract. Strains UAB 5782C and M1 were killed at all three sites by 2 to 4 h PI. The most virulent strain, UAB CT, was killed much more slowly than the other strains. However, there was no statistical difference in the relative numbers of mycoplasmas present in the lungs at 72 h PI among strains UAB CT, UAB 5782C, and M1. These studies showed that the different mycoplasmal strains were cleared from the respiratory tract by different mechanisms and suggest that the differences in virulence among the mycoplasma strains can be explained, in part, by the differences in elimination of the organisms from the respiratory tract by nonspecific host defense mechanisms.

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Year:  1988        PMID: 3397188      PMCID: PMC259539          DOI: 10.1128/iai.56.8.2163-2168.1988

Source DB:  PubMed          Journal:  Infect Immun        ISSN: 0019-9567            Impact factor:   3.441


  20 in total

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Journal:  J Exp Med       Date:  1964-01-01       Impact factor: 14.307

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  12 in total

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Authors:  M K Davidson; S E Ross; J R Lindsey; G H Cassell
Journal:  Infect Immun       Date:  1988-08       Impact factor: 3.441

4.  Cyclophosphamide decreases nitrotyrosine formation and inhibits nitric oxide production by alveolar macrophages in mycoplasmosis.

Authors:  J M Hickman-Davis; J R Lindsey; S Matalon
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5.  Upper respiratory tract disease in the gopher tortoise is caused by Mycoplasma agassizii.

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6.  Interleukin-17A Exacerbates Disease Severity in BALB/c Mice Susceptible to Lung Infection with Mycoplasma pulmonis.

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8.  A novel IL-17-dependent mechanism of cross protection: respiratory infection with mycoplasma protects against a secondary listeria infection.

Authors:  Amy N Sieve; Karen D Meeks; Sheetal Bodhankar; Suheung Lee; Jay K Kolls; Jerry W Simecka; Rance E Berg
Journal:  Eur J Immunol       Date:  2009-02       Impact factor: 5.532

9.  Toll-like receptor 2 (TLR2) plays a major role in innate resistance in the lung against murine Mycoplasma.

Authors:  Wees Love; Nicole Dobbs; Leslie Tabor; Jerry W Simecka
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10.  NK cells interfere with the generation of resistance against mycoplasma respiratory infection following nasal-pulmonary immunization.

Authors:  Sheetal Bodhankar; Mathew D Woolard; Xiangle Sun; Jerry W Simecka
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