Endogenous interleukin-10 suppresses allergen-induced airway inflammation and nonspecific airway responsiveness
Article first published online: 24 DEC 2001
Clinical & Experimental Allergy
Volume 30, Issue 6, pages 775–783, June 2000
How to Cite
Tournoy, Kips and Pauwels (2000), Endogenous interleukin-10 suppresses allergen-induced airway inflammation and nonspecific airway responsiveness. Clinical & Experimental Allergy, 30: 775–783. doi: 10.1046/j.1365-2222.2000.00838.x
- Issue published online: 24 DEC 2001
- Article first published online: 24 DEC 2001
- Cited By
- airway inflammation;
- airway responsiveness;
The airway inflammation observed in asthma is orchestrated by activated Th-2 lymphocytes relevant for the induction of altered airway responsiveness. An increasing body of evidence is accumulating that not only the pro-inflammatory cytokines interleukin (IL)-4 and IL-5 but also the immunomodulating cytokines IL-12 and possibly IL-10 are crucial for regulating the allergic airway inflammation.
Since IL-10 is capable of downregulating a broad spectrum of pro-inflammatory cytokines, we wanted to address the role of endogenously produced IL-10 in vivo in allergic asthma.
Knockout (IL-10−/−) mice (C57BL/6-IL10tm1Cgn) and wild-type (WT) counterparts were immunized (day 0) and exposed (day 14–21) to ovalbumin (OVA). Airway inflammation and reactivity (AR), serum allergen-specific IgE responses and cytokine profiles in the bronchoalveolar lavage fluid (BALF) were studied.
The IL-10−/− mice had more eosinophilic airway inflammation but comparable levels of allergen-specific serum IgE compared to the WT mice after allergen challenge. The AR was comparably increased in the OVA challenged WT and IL-10−/− mice vs sham-exposed WT, but not vs sham-exposed IL-10−/− mice since these showed a higher baseline AR. IFN γ, IL-4 and IL-13 were comparable and IL-5 was even lower in the BALF of the in IL-10−/− mice compared to the similarly exposed WT mice.
These results indicate that IL-10 plays an important and possibly direct role in the control of airway inflammation and responsiveness in an in vivo mouse model of allergy.