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B/Rel Transcription Factors: c-Rel Promotes Airway Hyperresponsiveness and Allergic Pulmonary Inflammation1
*
Pulmonary and
Renal Divisions, Brigham and Women’s Hospital, Boston, MA 02115;
Cornell University Medical College, New York, NY 10021; and
§
Departments of Medicine and Pathology, Harvard Medical School, Boston, MA 02115
The NF-
B/Rel family of transcription factors induces many genes
involved in immune and inflammatory responses. Mice with germline
deletions of individual NF-B/Rel subunits have different phenotypes,
suggesting that the NF-B/Rel transcription factors have different
functions. We tested whether c-Rel promotes allergic asthma using a
murine model of allergen-induced pulmonary inflammation and airway
hyperresponsiveness. Our investigation focused on c-Rel, which is
expressed in lymphoid cells and is important for lymphocyte activation.
In response to allergen sensitization and challenge, c-Rel-deficient
mice did not develop increases in pulmonary inflammation,
bronchoalveolar lavage fluid eosinophilia, or total serum IgE. c-Rel
deficiency also prevented the induction of airway hyperresponsiveness.
Allergen-treated wild-type mice had increased DNA binding to an NF-B
consensus site. Chemokine expression was altered in allergen-treated
c-Rel-deficient mice. Monocyte chemoattractant protein-1, which is
regulated by NF-B, was decreased in allergen-treated c-Rel-deficient
mice relative to wild-type controls. The increase in NF-B/Rel
transcription factors after allergen challenge in wild-type mice and
the decrease in allergen reactivity found in c-Rel-deficient mice
indicate that c-Rel promotes allergic inflammation. Alteration of
pulmonary chemokine expression in c-Rel-deficient mice may inhibit
allergen-induced pulmonary inflammation and airway
hyperresponsiveness.
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