{'fraction_non_alphanumeric': 0.025477707006369428, 'fraction_numerical': 0.0018198362147406734, 'mean_word_length': 4.882352941176471, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Amphiregulin is not essential for ovalbumin-induced acute airway inflammation in mice.

BACKGROUND
The number of amphiregulin (AR)-positive mast cells in the bronchial mucosa and the levels of AR in sputum from asthmatic patients have been reported to be increased. In addition, AR can promote mucin gene expression in human epithelial cells, suggesting that AR contributes to the pathogenesis of allergic asthma.


METHODS
To elucidate the role of AR in the pathogenesis of asthma, we immunized AR-deficient mice with ovalbumin (OVA) and then induced airway inflammation in them after OVA inhalation. The OVA-induced airway inflammation was assessed on the basis of the lung histology, number of leukocytes in the bronchoalveolar lavage (BAL) fluid, Th2 cytokine levels in the BAL fluid and OVA-specific IgG1 and IgE levels in the serum and compared between AR-sufficient and -deficient mice.


RESULTS
The OVA-induced airway inflammation was comparable in the AR-sufficient and -deficient mice.


CONCLUSIONS
Amphiregulin is not essential for induction of acute airway inflammation by OVA in mice.