Abstract
The function of NCR1 was studied in a model of experimental asthma, classified as a type 1 hypersensitivity reaction, in mice. IgE levels were significantly increased in the serum of OVA immunized NCR1 deficient (NCR1gfp/gfp) mice in comparison to OVA immunized wild type (NCR1+/+) and adjuvant immunized mice. Histological analysis of OVA immunized NCR1gfp/gfp mice revealed no preservation of the lung structure and overwhelming peribronchial and perivascular granulocytes together with mononuclear cells infiltration. OVA immunized NCR+/+ mice demonstrated preserved lung structure and peribronchial and perivascular immune cell infiltration to a lower extent than that in NCR1gfp/gfp mice. Adjuvant immunized mice demonstrated lung structure preservation and no immune cell infiltration. OVA immunization caused an increase in PAS production independently of NCR1 presence. Bronchoalveolar lavage (BAL) revealed NCR1 dependent decreased percentages of eosinophils and increased percentages of lymphocytes and macrophages following OVA immunization. In the OVA immunized NCR1gfp/gfp mice the protein levels of eosinophils’ (CCL24) and Th2 CD4+ T-cells’ chemoattractants (CCL17, and CCL24) in the BAL are increased in comparison with OVA immunized NCR+/+ mice. In the presence of NCR1, OVA immunization caused an increase in NK cells numbers and decreased NCR1 ligand expression on CD11c+GR1+ cells and decreased NCR1 mRNA expression in the BAL. OVA immunization resulted in significantly increased IL-13, IL-4 and CCL17 mRNA expression in NCR1+/+ and NCR1gfp/gfp mice. IL-17 and TNFα expression increased only in OVA-immunized NCR1+/+mice. IL-6 mRNA increased only in OVA immunized NCR1gfp/gfp mice. Collectively, it is demonstrated that NCR1 dampens allergic eosinophilic airway inflammation.
Highlights
Allergic asthma, classified as type 1 hypersensitivity reaction, is a chronic inflammatory disease of the airways characterized by reversible airflow obstruction, bronchial hyper-responsiveness, airway inflammation and production of allergy specific immunoglobulin E (IgE) [1, 2]
In the normalized summary of the two experiments, NCR1gfp/gfp mice demonstrated increased levels of total serum IgE following OVA immunization compared to adjuvant immunized NCR1+/+ and NCR1gfp/gfp mice
To further understand the role of Natural killer (NK) cells in allergic inflammation we studied the role of NCR1 in a model of experimental asthma, classified as type 1 hypersensitivity reaction, in mice
Summary
Allergic asthma, classified as type 1 hypersensitivity reaction, is a chronic inflammatory disease of the airways characterized by reversible airflow obstruction, bronchial hyper-responsiveness, airway inflammation and production of allergy specific immunoglobulin E (IgE) [1, 2]. Studies of airway inflammation in the lungs of asthmatic individuals have revealed the accumulation of a large number of inflammatory cells (predominantly eosinophils), increased mucus production and sub-mucosal mucus glands hyperplasia/metaplasia, epithelial shedding, and smooth muscle cell hypertrophy leading to structural changes that in turn exacerbate the hyper-responsiveness observed in this disease. Chemokines released by mast cells direct the recruitment of inflammatory cells that contribute to the late allergic response. The importance of Th2 cytokines to the allergic induced AHR is inconclusive since neutralization of IL-4 / IL-13 failed to improve the allergic status in human clinical trials [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
