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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

OVA-induced airway inflammation in WT and RIP2-deficient mice. A schematic diagram of the experimental design (A). Mice were sensitized by i.p. administration of OVA mixed with adjuvant at days 0, 1, 7, and 8. On days 14, 15, 21, and 22, mice were challenged with OVA or PBS. Photographs of lung tissues were obtained from H&E-stained sections (B) and histopathological scores were determined semi-quantitatively by microscopic examination (C). Total cell numbers in the BAL fluids were counted (D) and a differential cell count was performed using Diff-Quick staining (E). Data are expressed as means±SD.
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Figure 1: OVA-induced airway inflammation in WT and RIP2-deficient mice. A schematic diagram of the experimental design (A). Mice were sensitized by i.p. administration of OVA mixed with adjuvant at days 0, 1, 7, and 8. On days 14, 15, 21, and 22, mice were challenged with OVA or PBS. Photographs of lung tissues were obtained from H&E-stained sections (B) and histopathological scores were determined semi-quantitatively by microscopic examination (C). Total cell numbers in the BAL fluids were counted (D) and a differential cell count was performed using Diff-Quick staining (E). Data are expressed as means±SD.

Mentions: Protocols are depicted schematically in Fig. 1A. Both WT and RIP2-deficient mice were sensitized with 40 µg OVA (Sigma-Aldrich, St. Louis, MO, USA) and 2 mg of adjuvant (Imject® Alum, Thermo scientific, Rockford, IL, USA) in 200 µL of PBS, or with PBS alone by intraperitoneal (i.p.) injection on days 0, 1, 7, and 8. On days 14, 15, 21, and 22, anesthetized mice were challenged intranasally (i.n.) with 200 µg of OVA in PBS or with PBS alone in a volume of 50 µL. Animals were sacrificed 2 days after the last challenge and bronchoalveolar lavage (BAL) fluids, serum, and lung tissues were collected for analysis.


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)

OVA-induced airway inflammation in WT and RIP2-deficient mice. A schematic diagram of the experimental design (A). Mice were sensitized by i.p. administration of OVA mixed with adjuvant at days 0, 1, 7, and 8. On days 14, 15, 21, and 22, mice were challenged with OVA or PBS. Photographs of lung tissues were obtained from H&E-stained sections (B) and histopathological scores were determined semi-quantitatively by microscopic examination (C). Total cell numbers in the BAL fluids were counted (D) and a differential cell count was performed using Diff-Quick staining (E). 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 1: OVA-induced airway inflammation in WT and RIP2-deficient mice. A schematic diagram of the experimental design (A). Mice were sensitized by i.p. administration of OVA mixed with adjuvant at days 0, 1, 7, and 8. On days 14, 15, 21, and 22, mice were challenged with OVA or PBS. Photographs of lung tissues were obtained from H&E-stained sections (B) and histopathological scores were determined semi-quantitatively by microscopic examination (C). Total cell numbers in the BAL fluids were counted (D) and a differential cell count was performed using Diff-Quick staining (E). Data are expressed as means±SD.
Mentions: Protocols are depicted schematically in Fig. 1A. Both WT and RIP2-deficient mice were sensitized with 40 µg OVA (Sigma-Aldrich, St. Louis, MO, USA) and 2 mg of adjuvant (Imject® Alum, Thermo scientific, Rockford, IL, USA) in 200 µL of PBS, or with PBS alone by intraperitoneal (i.p.) injection on days 0, 1, 7, and 8. On days 14, 15, 21, and 22, anesthetized mice were challenged intranasally (i.n.) with 200 µg of OVA in PBS or with PBS alone in a volume of 50 µL. Animals were sacrificed 2 days after the last challenge and bronchoalveolar lavage (BAL) fluids, serum, and lung tissues were collected for analysis.

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