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Infection and Immunity, June 2001, p. 3869-3876, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3869-3876.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Elevated Cytokine and Chemokine Levels and Prolonged Pulmonary Airflow Resistance in a Murine Mycoplasma pneumoniae Pneumonia Model: a Microbiologic, Histologic, Immunologic, and Respiratory Plethysmographic Profile

Robert D. Hardy,1,* Hasan S. Jafri,1 Kurt Olsen,1 Meike Wordemann,1 Jeanine Hatfield,1 Beverly B. Rogers,1 Padma Patel,2 Lynn Duffy,2 Gail Cassell,2 George H. McCracken,1 and Octavio Ramilo1

Departments of Pediatric Infectious Diseases and Pathology, University of Texas Southwestern Medical Center, Dallas, Texas,1 and Diagnostic Mycoplasma Laboratory, University of Alabama, Birmingham, Alabama2

Received 5 February 2001/Returned for modification 6 March 2001/Accepted 26 March 2001

Because Mycoplasma pneumoniae is hypothesized to play an important role in reactive airway disease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was established. BALB/c mice were intranasally inoculated once with M. pneumoniae and sacrificed at 0 to 42 days postinoculation. All mice became infected and developed histologic evidence of acute pulmonary inflammation, which cleared by 28 days postinoculation. By contrast, M. pneumoniae persisted in the respiratory tract for the entire 42 days studied. Tumor necrosis factor alpha, gamma interferon, interleukin-6 (IL-6), KC (functional IL-8), MIP-1alpha , and MCP-1/JE concentrations were significantly elevated in bronchoalveolar lavage samples, whereas IL-4 and IL-10 concentrations were not significantly elevated. Pulmonary airflow resistance, as measured by plethysmography, was detected 1 day postinoculation and persisted even after pulmonary inflammation had resolved at day 28. Serum anti-M. pneumoniae immunoglobulin G titers were positive in all mice by 35 days. This mouse model provides a means to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactive airway disease/asthma.

* Corresponding author. Mailing address: Dept. of Pediatrics, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9063. Phone: (214) 648-3720. Fax: (214) 648-2961. E-mail: Robert.Hardy{at}UTSouthwestern.edu.

Infection and Immunity, June 2001, p. 3869-3876, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3869-3876.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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