To:nigel bates who wrote (523)
From: Miljenko Zuanic
Thursday, Apr 26, 2001 7:19 PM
Respond to of 524
Experimental Allergic Asthma Responds to IL-13 Antiserum
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WESTPORT, CT (Reuters Health) Apr 25 - Immunoneutralization of IL-13 produces significant therapeutic
benefits in mice with allergic asthma induced by Aspergillus fumigatus, according to a report in the April 15th issue
of the Journal of Immunology.
Because IL-13 overexpression in mouse lung produces many of the features seen in clinical asthma, the authors
explain, IL-13 might prove to be an attractive therapeutic target for chronic allergic asthma.
Dr. Kate Blease from University of Michigan Medical School in Ann Arbor, Michigan and colleagues studied the
effect of IL-13 neutralization with IL-13 antiserum on the features of A. fumigatus-induced allergic asthma in mice.
IL-13 levels increased and remained elevated 30 days after A. fumigatus conidia challenge. Moreover, IL-13
receptor expression increased significantly within 7 days of conidia challenge, remained elevated at day 21, and
returned to baseline levels by 30 days, the authors report.
Airway hyperreactivity (AHR) accompanied the fungus-induced asthma, the report indicates, but IL-13
immunoneutralization between days 14 and 30 or between days 30 and 38 after conidia exposure significantly
reduced AHR at day 38.
IL-13 immunoneutralization also markedly inhibited collagen deposition, subepithelial fibrosis, and goblet cell
hyperplasia, the researchers note.
In contrast, IL-13 immunoneutralization did not alter cytokine release from restimulated spleen cells, suggesting, the
investigators say, that IL-13 does not have important systemic immunomodulatory effects.
These results suggest that IL-13 might, indeed, be a reasonable therapeutic target in allergic asthma. "We are
interested in identifying other inhibitors of IL-13," Dr. Blease told Reuters Health. "In particular, targeting of the
IL-13 receptor subunits may provide beneficial effects."
"To neutralize IL-13 at extended time points after the establishment of disease, and indeed [to halt] the progression
of subepithelial lung fibrosis and [inhibit] goblet cell hyperplasia and mucus production would be a major advance
from the current therapeutic regimes available at present," Dr. Blease concluded.
J Immunol 2001;166:5219-5224. |
