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Mycoplasma pneumoniae Antigens Stimulate Interleukin-8*

Kathryn Chmura, BA; Ryan D. Lutz, BS; Hirofumi Chiba, MD, PhD; Mari S. Numata, MD, PhD; Hee-Jung Choi, MD, PhD; Giamila Fantuzzi, PhD; Dennis R. Voelker, PhD; Edward D. Chan, MD
Author and Funding Information

*From the Department of Medicine (Ms. Chmura, Mr. Lutz, Drs. Chiba, and Numata) and Program in Cell Biology (Dr. Voelker), National Jewish Medical and Research Center; and the Divisions of Pulmonary Sciences and Critical Care Medicine (Dr. Chan) and Infectious Diseases (Dr. Choi and Fantuzzi), University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Edward D. Chan, MD, K613e, Goodman Building, National Jewish Medical and Research Center, 1400 Jackson St, Denver, CO 80206; e-mail: chane@njc.org



Chest. 2003;123(3_suppl):425S. doi:10.1378/chest.123.3_suppl.425S
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Asthma is characterized by the presence of airway inflammation that results in bronchial hyperresponsiveness and symptoms of airway obstruction. Persistent and severe asthma may have an eosinophilic or noneosinophilic infiltration of the airways, the latter characterized by a profusion of neutrophils.1 More recent findings implicate that neutrophils may play a role in the irreversible airflow limitation seen in asthma.23 There is evidence that some chronic asthmatics have an increased incidence of polymerase chain reaction positivity for Mycoplasma pneumoniae and that these patients may have a clinical response to clarithromycin therapy.4 In an animal model of asthma in which BALB/c mice were inoculated intranasally with M pneumoniae, bronchial hyperresponsiveness developed.5 In addition, the resultant inflammation was principally neutrophilic.

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