Immune Responses to Tyrophagus putrescentiae–Induced Airway Inflammation in Mice

Journal of Investigational Allergology and Clinical Immunology

J-J Tsai¹  S-C Yin³  C-M Ho²  E-C Liao³ 

[1] College of Life Sciences, National Chung Hsing University, Taichung, Taiwan;Department of Parasitology, National Yang-Ming University, Taipei, Taiwan;Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan

关键词: IL-17F;    Airway inflammation;    Mouse model;    Tyrophagus putrescentiae;    Storage mites;   

Others  :  1183839

【 摘 要 】

Background: Storage mites are a source of aeroallergens that affect patients with allergic rhinitis and asthma. Tyrophagus putrescentiae is a causative factor of airway hypersensitivity, but the mechanisms and pathogenesis ofT putrescentiae–induced allergy are not well understood.

Objective: This study aimed to develop a murine model of T putrescentiae–induced allergic asthma.

Methods: Immune responses and physiologic variations in immunoglobulins (Ig), leukocyte subpopulations, cytokines, gene expression, pulmonary function, and lung pathology were evaluated after intraperitoneal sensitization and intratracheal challenge with crude extract of T putrescentiae.

Results: After sensitization with aluminum hydroxide and challenge with T putrescentiae in mice, levels of T putrescentiae–specific IgE and IgG1 in sera increased significantly compared to the normal saline group (P<.01). Values for inflammatory leukocytes (neutrophils and eosinophils) and cytokines (interleukin [IL] 4, IL-5, and IL-13) increased significantly after sensitization. In terms of pulmonary function, pause values were significantly enhanced in T putrescentiae–sensitized mice after intratracheal challenge with T putrescentiae (P<.05). Expression of type 2 helper T cell (TH2)–related genes (IL4, IL5, IL13, and RANTES), TH2-specific transcription factor (GATA-3), and proinflammatory
genes (IL6), and TH17-related genes (IL17F) increased significantly after airway challenge. Sensitization withT putrescentiaecrude extract led to inflammation of lung tissue, thickening of the tracheal wall, and tracheal rupture.

Conclusions: Intraperitoneal sensitization followed by intratracheal challenge with crude extract of T putrescentiae can induce airway inflammation in BALB/c mice. The symptoms observed in a mouse model of allergic asthma, in terms of immune and clinical parameters, are reminiscent of the symptoms of allergic asthma in humans. A mouse model can be used to evaluate the therapeutic effectiveness of drugs on T putrescentiae–induced airway inflammation in humans.