Abstract
BackgroundAllergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress. Interleukin (IL)-22, which is derived from lymphocytes, acts on epithelial cells and play a role in the chronic airway inflammation. However, the actual role of IL-22 in allergic asthma is still unclear. Therefore, we explored the effect of IL-22 on allergic airway inflammation and airway hyperresponsiveness (AHR) in an ovalbumin (OVA)-induced asthma mouse model.MethodsTo evaluate the effect of IL-22 in an allergic asthma model, BALB/c mice were sensitized and challenged with OVA; then the recombinant mouse IL-22 was administered intranasally 24 h prior to each challenge. The IL-22 levels in lung homogenates and bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay, respectively. AHR was evaluated through indicators including airways resistance (Rrs), elastance (Ers) and compliance (Crs); the inflammatory cell infiltration was assessed by quantification of differential cells counts in BALF and lung tissues stained by hematoxylin and eosin (H&E); IL-22 specific receptors were determined by immunohistochemistry staining.ResultsThe concentration of IL-22 was significantly elevated in the OVA-induced mice compared with the control mice in lung homogenates and BALF. In the OVA-induced mouse model, IL-22 administration could significantly attenuate AHR, including Rrs, Ers and Crs, decrease the proportion of eosinophils in BALF and reduce inflammatory cell infiltration around bronchi and their concomitant vessels, compared with the OVA-induced group. In addition, the expression of IL-22RA1 and IL-10RB in the lung tissues of OVA-induced mice was significantly increased compared with the control mice, while it was dramatically decreased after the treatment with IL-22, but not completely attenuated in the IL-22-treated mice when compared with the control mice.ConclusionInterleukin-22 could play a protective role in an OVA-induced asthma model, by suppressing the inflammatory cell infiltration around bronchi and their concomitant vessels and airway hyperresponsiveness, which might associate with the expression of its heterodimer receptors. Thus, IL-22 administration might be an effective strategy to attenuate allergic airway inflammation.
Highlights
Allergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress
Cytokines are involved in asthmatic chronic airway inflammation, especially those derived from the lymphocyte, which acts on epithelial cells, such as cytokine interleukin (IL)-22
It functions as a bridge by binding to its type 2-cytokine receptor, which is composed of a heterodimer of IL-22 receptor A1 (IL-22RA1) and IL-10RB; the former is expressed on non-hematopoietic cells, especially epithelial cells, but not immune cells [10, 11], while the latter is expressed on hematopoietic and non-hematopoietic cells [11]
Summary
Allergic asthma is a chronic airway inflammatory disease with a number of cytokines participating in its pathogenesis and progress. Interleukin (IL)-22, which is derived from lymphocytes, acts on epithelial cells and play a role in the chronic airway inflammation. Interleukin-22 is a member of the IL-10 family, and predominately derives from innate and adaptive immune cells, including αβ T cells, γδ T cells, natural killer T cells and group 3 innate lymphoid cells (ILC3s) [6,7,8,9] It functions as a bridge by binding to its type 2-cytokine receptor, which is composed of a heterodimer of IL-22 receptor A1 (IL-22RA1) and IL-10RB; the former is expressed on non-hematopoietic cells, especially epithelial cells, but not immune cells [10, 11], while the latter is expressed on hematopoietic and non-hematopoietic cells [11]. IL22-binding protein (IL-22BP), known as IL-22RA2, is a soluble form of the IL-22 receptor homolog, which binds IL-22 with high affinity and neutralizes the activity of IL-22 in vitro [13, 14]
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