Endogenous interleukin‐10 suppresses allergen‐induced airway inflammation and nonspecific airway responsiveness

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Abstract
Background: 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.Objective: 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.Methods: 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.Results: 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.Conclusion: 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.