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Receptor Interacting Protein 2 (RIP2) Is Dispensable for OVA-Induced Airway Inflammation in Mice.

Kim TH, Park YM, Ryu SW, Kim DJ, Park JH, Park JH - Allergy Asthma Immunol Res (2013)

Bottom Line: Receptor interacting protein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to be associated with the severity of allergic asthma in children.Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels.Our results suggest that RIP2 is not associated with the development of allergic airway inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University, Seoul, Korea.

ABSTRACT

Purpose: Asthma is a pulmonary chronic inflammatory disease characterized by airway obstruction and hyperresponsiveness. Pattern recognition receptors are known to play a key role in the development of allergic diseases as well as host defenses against microbial infection. Receptor interacting protein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to be associated with the severity of allergic asthma in children. In this study, we examined the role of RIP2 in the development of allergic airway inflammation in a mouse model.

Methods: Airway inflammation was induced in mice through intranasal administration of ovalbumin (OVA) after 2 intraperitoneal immunizations with OVA. Lung inflammation and mucus hypersecretion were examined histologically and total cell infiltration in bronchoalveolar (BAL) fluids was determined. Levels of the Th2-related cytokines, IL-5 and IL-13, in lung extracts were measured by ELISA. Serum antigen-specific IgE and IgG1 levels were also assessed.

Results: OVA-induced lung inflammation and mucus hypersecretion were not different between WT and RIP2-deficient mice. The IL-5 and IL-13 levels in the bronchoalveolar (BAL) fluids were also not impaired in RIP2-deficient mice compared to WT mice. Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels.

Conclusions: Our results suggest that RIP2 is not associated with the development of allergic airway inflammation.

No MeSH data available.


Related in: MedlinePlus

Cytokine production in the lung tissue of WT and RIP2-deficient mice. Lung extracts from the right lungs of sacrificed mice. IL-5 (A) and IL-13 (B) levels in lung extracts were measured by ELISA. Data are expressed as means±SD. Coefficients of variations (%) are shown in brackets.
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Figure 3: Cytokine production in the lung tissue of WT and RIP2-deficient mice. Lung extracts from the right lungs of sacrificed mice. IL-5 (A) and IL-13 (B) levels in lung extracts were measured by ELISA. Data are expressed as means±SD. Coefficients of variations (%) are shown in brackets.

Mentions: We examined OVA-induced IL-5 and IL-13 levels in lung extracts of WT and RIP2-deficient mice. Results showed that i.n. challenge with OVA increased the IL-5 and IL-13 levels in the lungs of mice (Fig. 3 A and B). However, RIP2 deficiency did not affect OVA-induced IL-5 and IL-13 levels in lung extracts (Fig. 3 A and B).


Receptor Interacting Protein 2 (RIP2) Is Dispensable for OVA-Induced Airway Inflammation in Mice.

Kim TH, Park YM, Ryu SW, Kim DJ, Park JH, Park JH - Allergy Asthma Immunol Res (2013)

Cytokine production in the lung tissue of WT and RIP2-deficient mice. Lung extracts from the right lungs of sacrificed mice. IL-5 (A) and IL-13 (B) levels in lung extracts were measured by ELISA. Data are expressed as means±SD. Coefficients of variations (%) are shown in brackets.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3936046&req=5

Figure 3: Cytokine production in the lung tissue of WT and RIP2-deficient mice. Lung extracts from the right lungs of sacrificed mice. IL-5 (A) and IL-13 (B) levels in lung extracts were measured by ELISA. Data are expressed as means±SD. Coefficients of variations (%) are shown in brackets.
Mentions: We examined OVA-induced IL-5 and IL-13 levels in lung extracts of WT and RIP2-deficient mice. Results showed that i.n. challenge with OVA increased the IL-5 and IL-13 levels in the lungs of mice (Fig. 3 A and B). However, RIP2 deficiency did not affect OVA-induced IL-5 and IL-13 levels in lung extracts (Fig. 3 A and B).

Bottom Line: Receptor interacting protein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to be associated with the severity of allergic asthma in children.Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels.Our results suggest that RIP2 is not associated with the development of allergic airway inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University, Seoul, Korea.

ABSTRACT

Purpose: Asthma is a pulmonary chronic inflammatory disease characterized by airway obstruction and hyperresponsiveness. Pattern recognition receptors are known to play a key role in the development of allergic diseases as well as host defenses against microbial infection. Receptor interacting protein 2 (RIP2), a serine/threonine kinase, is an adaptor molecule of NOD1 and NOD2, and genetic variation in this receptor is known to be associated with the severity of allergic asthma in children. In this study, we examined the role of RIP2 in the development of allergic airway inflammation in a mouse model.

Methods: Airway inflammation was induced in mice through intranasal administration of ovalbumin (OVA) after 2 intraperitoneal immunizations with OVA. Lung inflammation and mucus hypersecretion were examined histologically and total cell infiltration in bronchoalveolar (BAL) fluids was determined. Levels of the Th2-related cytokines, IL-5 and IL-13, in lung extracts were measured by ELISA. Serum antigen-specific IgE and IgG1 levels were also assessed.

Results: OVA-induced lung inflammation and mucus hypersecretion were not different between WT and RIP2-deficient mice. The IL-5 and IL-13 levels in the bronchoalveolar (BAL) fluids were also not impaired in RIP2-deficient mice compared to WT mice. Moreover, RIP2 deficiency did not affect serum OVA-specific IgG1 and IgE levels.

Conclusions: Our results suggest that RIP2 is not associated with the development of allergic airway inflammation.

No MeSH data available.


Related in: MedlinePlus