چکیده (انگلیسی):

Background: The role of interleukin (IL)-23 in asthma pathophysiology is still controversial. We examined
its role in allergic airway inflammation in response to two distinct antigens using IL-23-deficient
mice.
Methods: Allergic airway inflammation was evaluated in wild-type and IL-23p19
/
mice. Mice were
sensitized to ovalbumin (OVA) or house dust mite (HDM) by intraperitoneal injection of antigen and their
airways were then exposed to the same antigen. Levels of antigen-specific immunoglobulins in serum as
well as cytokines in bronchoalveolar or peritoneal lavage fluid and lung tissue were determined by
enzyme-linked immunosorbent assay and/or quantitative polymerase chain reaction.
Results: Deficiency of IL-23p19 decreased eosinophils and Th2 cytokines in bronchoalveolar lavage fluid
(BALF) of OVA-treated mice, while it increased BALF eosinophils of HDM-treated mice. Peritoneal injection
of OVA with alum, but not of HDM, induced local synthesis of IL-6, IL-10, and IL-23. Systemic
production of antigen-specific IgG1 was partially dependent on IL-23. In contrast, airway exposure to
HDM, but not to OVA, induced IL-23p19 mRNA expression in the lungs. In IL-23p19-deficient mice, HDMexposed
lungs did not exhibit the induction of IL-17A, which negatively regulates eosinophilic
inflammation.
Conclusions: Different antigens induced IL-23 at different part of the body in our similar asthma models.
Endogenous IL-23 production at the site of antigen sensitization facilitates type-2 immune responses,
whereas IL-23 production and subsequent IL-17A synthesis in the airways suppresses allergic
inflammation.