Limits...
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

Allergen-induced nasal symptoms. The numbers of (A) sneezes and (B) rubbings for 10 min immediately after the allergen challenge were counted. The OVA group had a higher symptom score than the PBS group at all time points, *P<0.05; The KO group had a lower sneeze score than the OVA group at 1 and 3 months of allergen challenge. The KO group had a lower rubbing score than the OVA group at 3 months of allergen challenge, **P<0.05. Data are expressed as mean±SE.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3378929&req=5

Figure 8: Allergen-induced nasal symptoms. The numbers of (A) sneezes and (B) rubbings for 10 min immediately after the allergen challenge were counted. The OVA group had a higher symptom score than the PBS group at all time points, *P<0.05; The KO group had a lower sneeze score than the OVA group at 1 and 3 months of allergen challenge. The KO group had a lower rubbing score than the OVA group at 3 months of allergen challenge, **P<0.05. Data are expressed as mean±SE.

Mentions: Sneezing and nose rubbing, predominant features in this model after allergen challenge, were used as symptom parameters for AR. Fig. 8 shows the changes in allergen-induced nasal symptoms. The number of sneezes was lower in the KO group than in the OVA groups after 1 and 3 months of allergen challenge (P<0.05). The number of rubbings was lower in the KO group than in the OVA groups after 3 months of allergen challenge (P<0.05). The average numbers of sneezes and rubbings were higher in the OVA group than the PBS group at all recorded time points (P<0.05), and the numbers gradually increased over time. The average number of sneezes seemed higher in the PBS group than the KO group, and rubbings showed the opposite pattern, although this was statistically nonsignificant. The allergen-induced nasal symptoms were maintained during the prolonged allergen challenge.


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)

Allergen-induced nasal symptoms. The numbers of (A) sneezes and (B) rubbings for 10 min immediately after the allergen challenge were counted. The OVA group had a higher symptom score than the PBS group at all time points, *P<0.05; The KO group had a lower sneeze score than the OVA group at 1 and 3 months of allergen challenge. The KO group had a lower rubbing score than the OVA group at 3 months of allergen challenge, **P<0.05. Data are expressed as mean±SE.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 8: Allergen-induced nasal symptoms. The numbers of (A) sneezes and (B) rubbings for 10 min immediately after the allergen challenge were counted. The OVA group had a higher symptom score than the PBS group at all time points, *P<0.05; The KO group had a lower sneeze score than the OVA group at 1 and 3 months of allergen challenge. The KO group had a lower rubbing score than the OVA group at 3 months of allergen challenge, **P<0.05. Data are expressed as mean±SE.
Mentions: Sneezing and nose rubbing, predominant features in this model after allergen challenge, were used as symptom parameters for AR. Fig. 8 shows the changes in allergen-induced nasal symptoms. The number of sneezes was lower in the KO group than in the OVA groups after 1 and 3 months of allergen challenge (P<0.05). The number of rubbings was lower in the KO group than in the OVA groups after 3 months of allergen challenge (P<0.05). The average numbers of sneezes and rubbings were higher in the OVA group than the PBS group at all recorded time points (P<0.05), and the numbers gradually increased over time. The average number of sneezes seemed higher in the PBS group than the KO group, and rubbings showed the opposite pattern, although this was statistically nonsignificant. The allergen-induced nasal symptoms were maintained during the prolonged allergen challenge.

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