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09:58
A Reversible, Non-invasive Method for Airway Resistance Measurements and Bronchoalveolar Lavage Fluid Sampling in Mice
Published on: April 13, 2010
Airway eosinophilic inflammation is attenuated in conserved noncoding sequence-1-deficient mice
Takayuki Ohtomo1, Shoichiro Miyatake, Yuichiro Kajiyama
1National Hospital Organization, Sagamihara National Hospital, Clinical Research Center for Allergy and Rheumatology, Sagamihara, Japan.
International Archives of Allergy and Immunology
|June 25, 2008
Summary
Conserved noncoding sequence-1 (CNS-1) regulates T helper 2 cytokine expression. Deleting CNS-1 attenuated allergic airway inflammation and IgE production in mice, indicating its role in vivo.
Area of Science:
- Immunology
- Genetics
- Allergy Research
Background:
- Conserved noncoding sequence-1 (CNS-1) is a key regulatory element for T helper 2 (Th2) cytokine expression.
- Th2 cytokines (IL-4, IL-5, IL-13) and IgE levels are critical in allergic responses.
- CNS-1 knockout (CNS-1-/-) mice exhibit attenuated Th2 cytokine expression and serum IgE levels.
Purpose of the Study:
- To investigate the role of CNS-1 in regulating allergic airway inflammation and Th2 immune responses in vivo.
- To determine if CNS-1 deficiency impacts eosinophilic inflammation and IgE production in a mouse model of allergic asthma.
Main Methods:
- Ovalbumin (OVA)-induced allergic asthma model in CNS-1-/- and wild-type (CNS-1+/+) mice.
- Sensitization with OVA/aluminum followed by antigen challenge.
- Assessment of bronchoalveolar lavage fluid (BALF) eosinophils, Th2 cytokine concentrations, OVA-specific IgE antibody levels, and bronchial responsiveness.
Main Results:
- Single OVA/aluminum sensitization led to significantly attenuated BALF eosinophilia and OVA-specific IgE in CNS-1-/- mice compared to CNS-1+/+ mice.
- Repeated OVA/aluminum sensitization (twice) showed no significant difference in eosinophilia or IgE induction between CNS-1-/- and CNS-1+/+ mice.
- Bronchial responsiveness was not detailed in the provided abstract excerpt.
Conclusions:
- The CNS-1 locus plays a significant role in regulating eosinophilic inflammation in vivo.
- CNS-1 is essential for the development of allergic airway inflammation, particularly under conditions of single antigen exposure.
- The regulatory function of CNS-1 may be influenced by the intensity or duration of antigen exposure.
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