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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

Hyperplasia of goblet cells and mucus hypersecretion in the bronchus of lung tissue. Lung sections were stained with PAS and examined by light microscopy. Areas in the black boxes are shown at a higher magnification on the right of each picture (A). Numbers of PAS-positive cells in the airway epithelium were counted. In each airway studied, the length of the basement membrane (BM) was measured using image analysis software. The results are presented as mean numbers of PAS-positive cells per micrometer of BM (B). Data are expressed as means±SD.
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Figure 2: Hyperplasia of goblet cells and mucus hypersecretion in the bronchus of lung tissue. Lung sections were stained with PAS and examined by light microscopy. Areas in the black boxes are shown at a higher magnification on the right of each picture (A). Numbers of PAS-positive cells in the airway epithelium were counted. In each airway studied, the length of the basement membrane (BM) was measured using image analysis software. The results are presented as mean numbers of PAS-positive cells per micrometer of BM (B). Data are expressed as means±SD.

Mentions: OVA-induced allergic airway inflammation is characterized by hyperplasia of goblet cells and mucus hypersecretion in the bronchus. To determine whether RIP2 deficiency influenced these phenomena, slide sections were stained with PAS and observed under a light microscope. As shown in Fig. 2 A and B, the number of PAS-positive cells as well as mucus secretion in the airway epithelial layer of mice was increased by intranasal challenge with OVA. However, there was no significant difference in the number of PAS-positive cells or mucus secretion between WT and RIP2-deficient mice (Fig. 2 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)

Hyperplasia of goblet cells and mucus hypersecretion in the bronchus of lung tissue. Lung sections were stained with PAS and examined by light microscopy. Areas in the black boxes are shown at a higher magnification on the right of each picture (A). Numbers of PAS-positive cells in the airway epithelium were counted. In each airway studied, the length of the basement membrane (BM) was measured using image analysis software. The results are presented as mean numbers of PAS-positive cells per micrometer of BM (B). Data are expressed as means±SD.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 2: Hyperplasia of goblet cells and mucus hypersecretion in the bronchus of lung tissue. Lung sections were stained with PAS and examined by light microscopy. Areas in the black boxes are shown at a higher magnification on the right of each picture (A). Numbers of PAS-positive cells in the airway epithelium were counted. In each airway studied, the length of the basement membrane (BM) was measured using image analysis software. The results are presented as mean numbers of PAS-positive cells per micrometer of BM (B). Data are expressed as means±SD.
Mentions: OVA-induced allergic airway inflammation is characterized by hyperplasia of goblet cells and mucus hypersecretion in the bronchus. To determine whether RIP2 deficiency influenced these phenomena, slide sections were stained with PAS and observed under a light microscope. As shown in Fig. 2 A and B, the number of PAS-positive cells as well as mucus secretion in the airway epithelial layer of mice was increased by intranasal challenge with OVA. However, there was no significant difference in the number of PAS-positive cells or mucus secretion between WT and RIP2-deficient mice (Fig. 2 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