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[Effects of budesonide on airway inflammation and airway remodeling in the ovalbumin sensitized and challenged mice].
Zhonghua Jie He He Hu Xi Za Zhi. 2005 Mar; 28(3):154-9.ZJ

Abstract

OBJECTIVE

To investigate the effects of budesonide (BUD) used in an early phase or delayed phase on the airway inflammation and airway remodeling in ovalbumin (OVA) sensitized and challenged mice.

METHODS

Forty mice were divided into 5 groups (8 in each group) including group A [ovalbumin (OVA) sensitized/challenged mice], group B (saline sensitized/challenged mice), group C (OVA sensitized/challenged mice treated by BUD in the early phase), group D (OVA-sensitized/challenged mice treated by BUD in the late phase) and group E (OVA-sensitized/challenged mice following saline challenge for 18 days). Mice were sensitized on days 0 and 14 by OVA and challenged from days 24 to 41 by OVA repeatedly to establish a murine model of asthma characterized by airway inflammation and airway remodeling. To assess the effects of BUD on the development of airway remodeling and on established airway remodeling, animals were treated with aerosolized BUD (0.5 mg/ml per day) from day 1 before OVA challenge (group C) and from day 18 following first OVA challenge (group D). The outcome measurements included airway inflammatory indices, eosinophils (EOS) count and amount of collagen deposition around the bronchus, area of airway smooth muscle, the degree of mucus secretion in the lumens and depth of airway smooth muscle (ASM) in different grade bronchus by HE, PAS and Masson's staining. The bronchoalveolar lavage fluids (BALF) were assayed for IL-5 and IFN-gamma levels.

RESULTS

In repeatedly OVA-challenged mice (group A), EOS counts in BALF increased significantly [(57.460 +/- 11.060) x 10(4)/ml] when compared with group B [(0.050 +/- 0.020) x 10(4)/ml, P < 0.01]. The IL-5 level increased significantly [(52.9 +/- 2.8) pg/ml vs (16.8 +/- 1.5) pg/ml, < 0.01] and IFN-gamma decreased significantly [(39.5 +/- 3.2) pg/ml vs (63.8 +/- 3.3) pg/ml, < 0.01]. Repeatedly OVA-challenged animals (group A) also developed an increase in EOS counts around bronchus [(1 018 +/- 118)/mm(2)] when compared with group B [(7 +/- 3)/mm(2), < 0.01], goblet cell hyperplasia [(46.0 +/- 5.8)% vs (1.8 +/- 0.5)%, < 0.01] and mucus hypersecretion [(score 2.98 +/- 0.23) vs (score 0.13 +/- 0.06), < 0.01], airway smooth muscle hypertrophy [(30.2 +/- 2.2)/microm(2)/microm vs (13.1 +/- 1.0) microm(2)/microm, < 0.01], enhanced collagen deposition of reticular basement membrane (RBM) [(24.9 +/- 1.3) microm(2)/microm vs (4.3 +/- 0.6) microm(2)/microm, all < 0.01]. Early treatment with BUD significantly reduced EOS counts in BALF [(7.140 +/- 1.250) x 10(4)/ml] as compared with group A [(57.460 +/- 11.060) x 10(4)/ml], < 0.01]. Early BUD treatment also significantly reduced EOS counts around bronchus [(214 +/- 26)/mm(2)], allergen-induced structural changes including goblet cell hyperplasia [(16.1 +/- 2.5)%] and mucus hypersecretion (1.10 +/- 0.15), airway smooth muscle hypertrophy [(14.0 +/- 0.7) microm(2)/microm], and RBM collagen deposition [(12.6 +/- 1.3) microm(2)/microm]. In group E, EOS counts in BALF [(1.250 +/- 0.330) x 10(4)/ml] were decreased significantly when compared with group A (< 0.01), but airway smooth muscle hypertrophy [(32.4 +/- 1.8) microm(2)/microm], and RBM collagen deposition [(22.8 +/- 1.7) microm(2)/microm] showed no reduction as compared with group A (all P > 0.05). Delayed BUD treatment significantly reduced EOS counts in BALF [(0.800 +/- 0.170) x 10(4)/ml], goblet cell hyperplasia [(29.3 +/- 4.3)%] and mucus hypersecretion (1.63 +/- 0.17, < 0.05 or < 0.01), but had no effects on OVA-induced airway smooth muscle hypertrophy [(30.1 +/- 1.8) microm(2)/microm] and RBM collagen deposition [(23.7 +/- 1.4) microm(2)/microm] as compared with group A (P > 0.05).

CONCLUSIONS

Early treatment with BUD inhibited the development of airway inflammation of airway remodeling. However, delayed use with BUD inhibited airway inflammation, but only partially reversed airway remodeling in a murine model of asthma.

Authors+Show Affiliations

Department of Respiratory Medicine, Second Hospital, Medical College of Zhejiang University, Zhejiang University Institute of Respiratory Diseases, Hangzhou 310009, China.No affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

15854408

Citation

Shen, Hua-hao, and Shao-bin Wang. "[Effects of Budesonide On Airway Inflammation and Airway Remodeling in the Ovalbumin Sensitized and Challenged Mice]." Zhonghua Jie He He Hu Xi Za Zhi = Zhonghua Jiehe He Huxi Zazhi = Chinese Journal of Tuberculosis and Respiratory Diseases, vol. 28, no. 3, 2005, pp. 154-9.
Shen HH, Wang SB. [Effects of budesonide on airway inflammation and airway remodeling in the ovalbumin sensitized and challenged mice]. Zhonghua Jie He He Hu Xi Za Zhi. 2005;28(3):154-9.
Shen, H. H., & Wang, S. B. (2005). [Effects of budesonide on airway inflammation and airway remodeling in the ovalbumin sensitized and challenged mice]. Zhonghua Jie He He Hu Xi Za Zhi = Zhonghua Jiehe He Huxi Zazhi = Chinese Journal of Tuberculosis and Respiratory Diseases, 28(3), 154-9.
Shen HH, Wang SB. [Effects of Budesonide On Airway Inflammation and Airway Remodeling in the Ovalbumin Sensitized and Challenged Mice]. Zhonghua Jie He He Hu Xi Za Zhi. 2005;28(3):154-9. PubMed PMID: 15854408.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Effects of budesonide on airway inflammation and airway remodeling in the ovalbumin sensitized and challenged mice]. AU - Shen,Hua-hao, AU - Wang,Shao-bin, PY - 2005/4/28/pubmed PY - 2006/12/23/medline PY - 2005/4/28/entrez SP - 154 EP - 9 JF - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases JO - Zhonghua Jie He He Hu Xi Za Zhi VL - 28 IS - 3 N2 - OBJECTIVE: To investigate the effects of budesonide (BUD) used in an early phase or delayed phase on the airway inflammation and airway remodeling in ovalbumin (OVA) sensitized and challenged mice. METHODS: Forty mice were divided into 5 groups (8 in each group) including group A [ovalbumin (OVA) sensitized/challenged mice], group B (saline sensitized/challenged mice), group C (OVA sensitized/challenged mice treated by BUD in the early phase), group D (OVA-sensitized/challenged mice treated by BUD in the late phase) and group E (OVA-sensitized/challenged mice following saline challenge for 18 days). Mice were sensitized on days 0 and 14 by OVA and challenged from days 24 to 41 by OVA repeatedly to establish a murine model of asthma characterized by airway inflammation and airway remodeling. To assess the effects of BUD on the development of airway remodeling and on established airway remodeling, animals were treated with aerosolized BUD (0.5 mg/ml per day) from day 1 before OVA challenge (group C) and from day 18 following first OVA challenge (group D). The outcome measurements included airway inflammatory indices, eosinophils (EOS) count and amount of collagen deposition around the bronchus, area of airway smooth muscle, the degree of mucus secretion in the lumens and depth of airway smooth muscle (ASM) in different grade bronchus by HE, PAS and Masson's staining. The bronchoalveolar lavage fluids (BALF) were assayed for IL-5 and IFN-gamma levels. RESULTS: In repeatedly OVA-challenged mice (group A), EOS counts in BALF increased significantly [(57.460 +/- 11.060) x 10(4)/ml] when compared with group B [(0.050 +/- 0.020) x 10(4)/ml, P < 0.01]. The IL-5 level increased significantly [(52.9 +/- 2.8) pg/ml vs (16.8 +/- 1.5) pg/ml, < 0.01] and IFN-gamma decreased significantly [(39.5 +/- 3.2) pg/ml vs (63.8 +/- 3.3) pg/ml, < 0.01]. Repeatedly OVA-challenged animals (group A) also developed an increase in EOS counts around bronchus [(1 018 +/- 118)/mm(2)] when compared with group B [(7 +/- 3)/mm(2), < 0.01], goblet cell hyperplasia [(46.0 +/- 5.8)% vs (1.8 +/- 0.5)%, < 0.01] and mucus hypersecretion [(score 2.98 +/- 0.23) vs (score 0.13 +/- 0.06), < 0.01], airway smooth muscle hypertrophy [(30.2 +/- 2.2)/microm(2)/microm vs (13.1 +/- 1.0) microm(2)/microm, < 0.01], enhanced collagen deposition of reticular basement membrane (RBM) [(24.9 +/- 1.3) microm(2)/microm vs (4.3 +/- 0.6) microm(2)/microm, all < 0.01]. Early treatment with BUD significantly reduced EOS counts in BALF [(7.140 +/- 1.250) x 10(4)/ml] as compared with group A [(57.460 +/- 11.060) x 10(4)/ml], < 0.01]. Early BUD treatment also significantly reduced EOS counts around bronchus [(214 +/- 26)/mm(2)], allergen-induced structural changes including goblet cell hyperplasia [(16.1 +/- 2.5)%] and mucus hypersecretion (1.10 +/- 0.15), airway smooth muscle hypertrophy [(14.0 +/- 0.7) microm(2)/microm], and RBM collagen deposition [(12.6 +/- 1.3) microm(2)/microm]. In group E, EOS counts in BALF [(1.250 +/- 0.330) x 10(4)/ml] were decreased significantly when compared with group A (< 0.01), but airway smooth muscle hypertrophy [(32.4 +/- 1.8) microm(2)/microm], and RBM collagen deposition [(22.8 +/- 1.7) microm(2)/microm] showed no reduction as compared with group A (all P > 0.05). Delayed BUD treatment significantly reduced EOS counts in BALF [(0.800 +/- 0.170) x 10(4)/ml], goblet cell hyperplasia [(29.3 +/- 4.3)%] and mucus hypersecretion (1.63 +/- 0.17, < 0.05 or < 0.01), but had no effects on OVA-induced airway smooth muscle hypertrophy [(30.1 +/- 1.8) microm(2)/microm] and RBM collagen deposition [(23.7 +/- 1.4) microm(2)/microm] as compared with group A (P > 0.05). CONCLUSIONS: Early treatment with BUD inhibited the development of airway inflammation of airway remodeling. However, delayed use with BUD inhibited airway inflammation, but only partially reversed airway remodeling in a murine model of asthma. SN - 1001-0939 UR - https://www.unboundmedicine.com/medline/citation/15854408/[Effects_of_budesonide_on_airway_inflammation_and_airway_remodeling_in_the_ovalbumin_sensitized_and_challenged_mice]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=1001-0939&amp;year=2005&amp;vol=28&amp;issue=3&amp;fpage=154 DB - PRIME DP - Unbound Medicine ER -