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1 Dept of Paediatrics, National Jewish Medical and Research Center, Denver, CO, USA. 2 Okayama University Medical School, Okayama, Japan.
CORRESPONDENCE: E. W. Gelfand, 1400 Jackson Street, Denver, CO 80206, USA. Fax: 1 3032702105. E-mail: gelfande{at}njc.org
Keywords: Airway hyperresponsiveness, eosinophils, neutrophils, S-carboxymethylcysteine
Received: July 30, 2004
Accepted June 10, 2005
S-carboxymethylcysteine (S-CMC) has been used as a mucoregulator in respiratory diseases. However, the mechanism of action of S-CMC on allergic airway inflammation has not yet been defined.
In the present study, BALB/c mice were initially sensitised and challenged to ovalbumin (OVA) and, weeks later, re-challenged with OVA (secondary challenge). S-CMC (5100 mg·kg1) was administered from 2 days before the secondary challenge through to the day of assay.
Mice developed airway hyperresponsiveness (AHR) 6 h after the secondary challenge and increased numbers of neutrophils were present in the bronchoalveolar lavage (BAL) fluid. At 72 h after secondary challenge, mice again developed AHR, but the BAL fluid contained large numbers of eosinophils. S-CMC treatment was found to reduce AHR and neutrophilia at 6 h, as well as eosinophilia and AHR at 72 h. These effects appeared to be dose dependent. Goblet cell hyperplasia, observed at 72 h, was reduced by S-CMC. In BAL fluid, increased levels of interferon-
In conclusion, the data indicate that S-carboxymethylcysteine is effective in reducing airway hyperresponsiveness and airway inflammation at two distinct phases of the response to the secondary allergen challenge in sensitised mice.
, interleukin (IL)-12 and IL-10 and decreased levels of IL-5 and IL-13 were detected.
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