Background: Ozone (O 3 ), a common air pollutant, induces exacerbation of asthma and chronic obstructive pulmonary disease. Pulmonary surfactant protein (SP)-D modulates immune and inflammatory responses in the lung. We have shown previously that SP-D plays a protective role in a mouse model of allergic airway inflammation. Here we studied the role and regulation of SP-D in O 3 -induced inflammatory changes in the lung.
Objective and design
To determine whether Finegoldia magna protein L (PL) causes lung inflammation and, if so, whether the response is dependent on its Ig-binding B cell superantigenic property.
Material
Pulmonary inflammatory reactions were analyzed at varying time points after intratracheal administration of PL to various strains of mice.
Results
PL caused peribronchial and perivascular inflammation that peaked at 18–24 hours. Polymorphonuclear cells (PMNs) began to accumulate in bronchoalveolar lavage fluid (BALF) of PL-challenged mice by 4 hours and accounted for >90% of leukocytes by 18–24 hours. Inflammation was marked by the appearance of MIP-2, KC, TNF-α, and IL-6 in the BALF with peak levels attained 4 hours after PL administration. PL-induced pulmonary inflammation was associated with increased airway hyperreactivity following inhalation of methacholine. The inflammatory reaction was unabated in mice lacking B cells and Igs. By contrast, PL-induced inflammation was abrogated in MyD88- deficient mice. PL-induced responses required alveolar macrophages.
Conclusions
These results strongly suggest that PL-induced lung inflammation is dependent on an innate MyD88 dependent pathway rather than the Ig-binding properties of this microbial B cell superantigen. We propose that this pulmonary inflammatory reaction is caused by the interaction of PL with a Toll-like receptor expressed on alveolar macrophages.
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