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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

Expression of type I collagen in the KO group visualized by immunohistochemistry. (A) Original magnification, ×20. (B) Original magnification, ×400. Type I collagen was identified in the subepithelial tissue (asterisk in B) of the nasal mucosa, regardless of periostin deficiency. The graph depicts the ratio of collagen type I to β-actin from nasal tissue lysates. The KO group showed a trend toward decreased type I collagen expression after 1 and 3 months of allergen challenge compared to the OVA group by immunoblotting. Two representative results of immunoblotting (n=5) over time are shown.OVA, ovalbumin; KO, knockout.
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Figure 5: Expression of type I collagen in the KO group visualized by immunohistochemistry. (A) Original magnification, ×20. (B) Original magnification, ×400. Type I collagen was identified in the subepithelial tissue (asterisk in B) of the nasal mucosa, regardless of periostin deficiency. The graph depicts the ratio of collagen type I to β-actin from nasal tissue lysates. The KO group showed a trend toward decreased type I collagen expression after 1 and 3 months of allergen challenge compared to the OVA group by immunoblotting. Two representative results of immunoblotting (n=5) over time are shown.OVA, ovalbumin; KO, knockout.

Mentions: Collagen deposition is an important pathological feature of subepithelial fibrosis. The presence of type I collagen in the nasal tissue of the KO group was determined using immunohistochemistry (Fig. 5). Despite the deficiency of periostin, type I collagen was expressed around the subepithelial area as a matrix protein of subepithelial fibrosis. Immunoblotting was performed to evaluate the quantity of type I collagen expression in the nasal mucosa of different groups (Fig. 5). The KO group showed less type I collagen expression after 1 and 3 months of allergen challenge than the OVA group.


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)

Expression of type I collagen in the KO group visualized by immunohistochemistry. (A) Original magnification, ×20. (B) Original magnification, ×400. Type I collagen was identified in the subepithelial tissue (asterisk in B) of the nasal mucosa, regardless of periostin deficiency. The graph depicts the ratio of collagen type I to β-actin from nasal tissue lysates. The KO group showed a trend toward decreased type I collagen expression after 1 and 3 months of allergen challenge compared to the OVA group by immunoblotting. Two representative results of immunoblotting (n=5) over time are shown.OVA, ovalbumin; KO, knockout.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Expression of type I collagen in the KO group visualized by immunohistochemistry. (A) Original magnification, ×20. (B) Original magnification, ×400. Type I collagen was identified in the subepithelial tissue (asterisk in B) of the nasal mucosa, regardless of periostin deficiency. The graph depicts the ratio of collagen type I to β-actin from nasal tissue lysates. The KO group showed a trend toward decreased type I collagen expression after 1 and 3 months of allergen challenge compared to the OVA group by immunoblotting. Two representative results of immunoblotting (n=5) over time are shown.OVA, ovalbumin; KO, knockout.
Mentions: Collagen deposition is an important pathological feature of subepithelial fibrosis. The presence of type I collagen in the nasal tissue of the KO group was determined using immunohistochemistry (Fig. 5). Despite the deficiency of periostin, type I collagen was expressed around the subepithelial area as a matrix protein of subepithelial fibrosis. Immunoblotting was performed to evaluate the quantity of type I collagen expression in the nasal mucosa of different groups (Fig. 5). The KO group showed less type I collagen expression after 1 and 3 months of allergen challenge than the OVA group.

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