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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

Subepithelial thickness of the nasal mucosa. The subepithelial thickness of the nasal mucosa was measured (yellow arrow). (A) The nasal tissue around the septal cartilage in the PBS group after 3 months of allergen challenge (Masson's trichrome staining, original magnification, ×400). (B) The same area in the OVA group after 3 months of allergen challenge. (C) The same area in the KO group after 3 months of allergen challenge. (D) The subepithelial tissue was thinner in the KO group than in the OVA groups. *P<0.05. The subepithelial thickness increased over time in the OVA group. **P<0.05. Data are expressed as mean±SE.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout.
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Figure 4: Subepithelial thickness of the nasal mucosa. The subepithelial thickness of the nasal mucosa was measured (yellow arrow). (A) The nasal tissue around the septal cartilage in the PBS group after 3 months of allergen challenge (Masson's trichrome staining, original magnification, ×400). (B) The same area in the OVA group after 3 months of allergen challenge. (C) The same area in the KO group after 3 months of allergen challenge. (D) The subepithelial tissue was thinner in the KO group than in the OVA groups. *P<0.05. The subepithelial thickness increased over time in the OVA group. **P<0.05. Data are expressed as mean±SE.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout.

Mentions: Fig. 4 shows changes in the thickness of the subepithelial tissue of the nasal mucosa. It was significantly thinner in the KO group than in the OVA group (P<0.05), in which it increased gradually and peaked at 3 months (P<0.05).


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)

Subepithelial thickness of the nasal mucosa. The subepithelial thickness of the nasal mucosa was measured (yellow arrow). (A) The nasal tissue around the septal cartilage in the PBS group after 3 months of allergen challenge (Masson's trichrome staining, original magnification, ×400). (B) The same area in the OVA group after 3 months of allergen challenge. (C) The same area in the KO group after 3 months of allergen challenge. (D) The subepithelial tissue was thinner in the KO group than in the OVA groups. *P<0.05. The subepithelial thickness increased over time in the OVA group. **P<0.05. Data are expressed as mean±SE.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Subepithelial thickness of the nasal mucosa. The subepithelial thickness of the nasal mucosa was measured (yellow arrow). (A) The nasal tissue around the septal cartilage in the PBS group after 3 months of allergen challenge (Masson's trichrome staining, original magnification, ×400). (B) The same area in the OVA group after 3 months of allergen challenge. (C) The same area in the KO group after 3 months of allergen challenge. (D) The subepithelial tissue was thinner in the KO group than in the OVA groups. *P<0.05. The subepithelial thickness increased over time in the OVA group. **P<0.05. Data are expressed as mean±SE.PBS, phosphate buffered saline; OVA, ovalbumin; KO, knockout.
Mentions: Fig. 4 shows changes in the thickness of the subepithelial tissue of the nasal mucosa. It was significantly thinner in the KO group than in the OVA group (P<0.05), in which it increased gradually and peaked at 3 months (P<0.05).

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