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Roles of periostin in symptom manifestation and airway remodeling in a murine model of allergic rhinitis.

Hur DG, Khalmuratova R, Ahn SK, Ha YS, Min YG - Allergy Asthma Immunol Res (2012)

Bottom Line: No differences in the expression of MMP-2 or TIMP-1 were found in the knockout group.However, after a month of allergen challenge, type I collagen in the nasal tissue was lower in the knockout group than in the control group.The number of eosinophils and the symptom score were also lower in the knockout group.

View Article: PubMed Central - PubMed

Affiliation: Department of Otorhinolaryngology, School of Medicine, Gyeongsang National University, Jinju, Korea.

ABSTRACT

Purpose: Periostin was originally identified as a secreted factor during screening of a mouse osteoblastic library. In a recent study, periostin was found to directly regulate eosinophil accumulation in allergic mucosal inflammation. Chronic eosinophilic inflammation is related to the development of remodeling. The present study examined the expression of periostin and evaluated its role in the inflammatory process and remodeling associated with allergic rhinitis.

Methods: A murine model of allergic rhinitis was established in periostin knockout mice. We analyzed the expression of periostin, manifestation of nasal symptoms, eosinophilic inflammation, and subepithelial fibrosis as well as the expression of MMP-2, TIMP-1, and type 1 collagen in nasal tissue.

Results: Periostin was mainly distributed in the subepithelial tissue of the nasal mucosa. The subepithelial tissue was thinner in the knockout group than in the control group. No differences in the expression of MMP-2 or TIMP-1 were found in the knockout group. However, after a month of allergen challenge, type I collagen in the nasal tissue was lower in the knockout group than in the control group. The number of eosinophils and the symptom score were also lower in the knockout group.

Conclusions: Periostin is expressed in nasal tissues of murine models of allergic rhinitis. Periostin deficiency may affect the remodeling of nasal tissue with reduced subepithelial fibrosis, and lead to less eosinophilic inflammation.

No MeSH data available.


Related in: MedlinePlus

Protocol for induction of the murine AR model. Three groups of mice were used in these experiments, and each group contained three subgroups, according to the day of sacrifice.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout; W, week; M, month.
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Figure 1: Protocol for induction of the murine AR model. Three groups of mice were used in these experiments, and each group contained three subgroups, according to the day of sacrifice.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout; W, week; M, month.

Mentions: Ovalbumin (OVA; Sigma, St. Louis, MO, USA)-induced airway inflammation was performed in mice as described previously.19 Male mice (C57BL/6J or B6;129-Postntm1Jmol/J) at 4 weeks of age were sensitized by intraperitoneal injection of 25 µg OVA/2 mg aluminum hydroxide gel on days 0 and 5, followed by daily intranasal challenge (from day 12 to day 19) with 3% OVA diluted in 40 µL phosphate buffered saline (PBS). Prolonged inflammation was induced by subsequent nasal exposure to 3% OVA three times a week after day 19 until the mice were sacrificed after 1 or 3 months. The B6;129-Postntm1Jmol/J strain mice were called the KO group, and the C57BL/6J strain mice were called the OVA group. Data were obtained from five mice per group. The control mice (C57BL/6J) received saline injections and saline intranasal challenges instead of the OVA solution and were called the PBS group (Fig. 1).


Roles of periostin in symptom manifestation and airway remodeling in a murine model of allergic rhinitis.

Hur DG, Khalmuratova R, Ahn SK, Ha YS, Min YG - Allergy Asthma Immunol Res (2012)

Protocol for induction of the murine AR model. Three groups of mice were used in these experiments, and each group contained three subgroups, according to the day of sacrifice.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout; W, week; M, month.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3378929&req=5

Figure 1: Protocol for induction of the murine AR model. Three groups of mice were used in these experiments, and each group contained three subgroups, according to the day of sacrifice.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout; W, week; M, month.
Mentions: Ovalbumin (OVA; Sigma, St. Louis, MO, USA)-induced airway inflammation was performed in mice as described previously.19 Male mice (C57BL/6J or B6;129-Postntm1Jmol/J) at 4 weeks of age were sensitized by intraperitoneal injection of 25 µg OVA/2 mg aluminum hydroxide gel on days 0 and 5, followed by daily intranasal challenge (from day 12 to day 19) with 3% OVA diluted in 40 µL phosphate buffered saline (PBS). Prolonged inflammation was induced by subsequent nasal exposure to 3% OVA three times a week after day 19 until the mice were sacrificed after 1 or 3 months. The B6;129-Postntm1Jmol/J strain mice were called the KO group, and the C57BL/6J strain mice were called the OVA group. Data were obtained from five mice per group. The control mice (C57BL/6J) received saline injections and saline intranasal challenges instead of the OVA solution and were called the PBS group (Fig. 1).

Bottom Line: No differences in the expression of MMP-2 or TIMP-1 were found in the knockout group.However, after a month of allergen challenge, type I collagen in the nasal tissue was lower in the knockout group than in the control group.The number of eosinophils and the symptom score were also lower in the knockout group.

View Article: PubMed Central - PubMed

Affiliation: Department of Otorhinolaryngology, School of Medicine, Gyeongsang National University, Jinju, Korea.

ABSTRACT

Purpose: Periostin was originally identified as a secreted factor during screening of a mouse osteoblastic library. In a recent study, periostin was found to directly regulate eosinophil accumulation in allergic mucosal inflammation. Chronic eosinophilic inflammation is related to the development of remodeling. The present study examined the expression of periostin and evaluated its role in the inflammatory process and remodeling associated with allergic rhinitis.

Methods: A murine model of allergic rhinitis was established in periostin knockout mice. We analyzed the expression of periostin, manifestation of nasal symptoms, eosinophilic inflammation, and subepithelial fibrosis as well as the expression of MMP-2, TIMP-1, and type 1 collagen in nasal tissue.

Results: Periostin was mainly distributed in the subepithelial tissue of the nasal mucosa. The subepithelial tissue was thinner in the knockout group than in the control group. No differences in the expression of MMP-2 or TIMP-1 were found in the knockout group. However, after a month of allergen challenge, type I collagen in the nasal tissue was lower in the knockout group than in the control group. The number of eosinophils and the symptom score were also lower in the knockout group.

Conclusions: Periostin is expressed in nasal tissues of murine models of allergic rhinitis. Periostin deficiency may affect the remodeling of nasal tissue with reduced subepithelial fibrosis, and lead to less eosinophilic inflammation.

No MeSH data available.


Related in: MedlinePlus