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Plasmin system regulation in an ovalbumin-induced rat model of asthma.
Int Arch Allergy Immunol. 2008; 147(3):190-6.IA

Abstract

BACKGROUND

So far studies showing the role of the plasmin system in airway remodelling have been conducted using in vitro models. The aim of the present study was to determine plasmin system regulation in an in vivo rat model of asthma.

METHODS

Asthma in Wistar rats was induced by ovalbumin (OVA) sensitization followed by an OVA challenge (OVA/OVA, n = 6). Control groups were saline-sensitized challenged with OVA (VEH/OVA, n = 6) and OVA-sensitized challenged with saline (OVA/VEH, n = 6). Plasmin system components were determined in the plasma by ELISA. Plasminogen activator inhibitor-1 (PAI-1) was localized by an immunohistochemical reaction.

RESULTS

Sensitization and challenge with OVA caused thickening of the airway wall, hypertrophy of smooth muscle cells, infiltration of inflammatory cells, subepithelial fibrosis, epithelial and endothelial lesions. Serum total IgE was significantly higher in OVA-sensitized rats as compared to VEH-sensitized control groups. Tissue plasminogen activator activity was significantly decreased in asthmatic animals (4.48 +/- 0.4 vs. 6.7 +/- 0.3 ng/ml for OVA/OVA and OVA/VEH; p < 0.05), and PAI-1 activity was statistically significantly higher in asthma rats (0.8 +/- 0.05 vs. 0.5 +/- 0.03 ng/ml for OVA/OVA vs. OVA/VEH; p < 0.05). alpha2-Antiplasmin was higher in rats receiving OVA sensitization than in those that were sham sensitized (p < 0.05). Immunohistochemical staining for PAI-1in the lungs of asthmatic animals showed very strong PAI-1 expression in lung inflammatory cells.

CONCLUSIONS

We have demonstrated for the first time the existence of PAI-1 in lung inflammatory cells of rats with asthma. This finding was consistent with the superiority of plasmin system inhibition over activation in plasma.

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Authors+Show Affiliations

Kucharewicz I
Department of Allergology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland.
Mogielnicki A
No affiliation info available
Kasacka I
No affiliation info available
Buczko W
No affiliation info available
Bodzenta-Łukaszyk A
No affiliation info available

MeSH

AnimalsAsthmaDisease Models, AnimalFibrinolysinHumansInflammationLungMaleOvalbuminPlasminogen Activator Inhibitor 1RatsRats, WistarTissue Plasminogen ActivatorUp-Regulationalpha-2-Antiplasmin

Pub Type(s)

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

Language

eng

PubMed ID

18594148

Citation

Kucharewicz, I, et al. "Plasmin System Regulation in an Ovalbumin-induced Rat Model of Asthma." International Archives of Allergy and Immunology, vol. 147, no. 3, 2008, pp. 190-6.
Kucharewicz I, Mogielnicki A, Kasacka I, et al. Plasmin system regulation in an ovalbumin-induced rat model of asthma. Int Arch Allergy Immunol. 2008;147(3):190-6.
Kucharewicz, I., Mogielnicki, A., Kasacka, I., Buczko, W., & Bodzenta-Łukaszyk, A. (2008). Plasmin system regulation in an ovalbumin-induced rat model of asthma. International Archives of Allergy and Immunology, 147(3), 190-6. https://doi.org/10.1159/000142041
Kucharewicz I, et al. Plasmin System Regulation in an Ovalbumin-induced Rat Model of Asthma. Int Arch Allergy Immunol. 2008;147(3):190-6. PubMed PMID: 18594148.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Plasmin system regulation in an ovalbumin-induced rat model of asthma. AU - Kucharewicz,I, AU - Mogielnicki,A, AU - Kasacka,I, AU - Buczko,W, AU - Bodzenta-Łukaszyk,A, Y1 - 2008/07/02/ PY - 2007/10/17/received PY - 2008/02/19/accepted PY - 2008/7/3/pubmed PY - 2008/11/11/medline PY - 2008/7/3/entrez SP - 190 EP - 6 JF - International archives of allergy and immunology JO - Int Arch Allergy Immunol VL - 147 IS - 3 N2 - BACKGROUND: So far studies showing the role of the plasmin system in airway remodelling have been conducted using in vitro models. The aim of the present study was to determine plasmin system regulation in an in vivo rat model of asthma. METHODS: Asthma in Wistar rats was induced by ovalbumin (OVA) sensitization followed by an OVA challenge (OVA/OVA, n = 6). Control groups were saline-sensitized challenged with OVA (VEH/OVA, n = 6) and OVA-sensitized challenged with saline (OVA/VEH, n = 6). Plasmin system components were determined in the plasma by ELISA. Plasminogen activator inhibitor-1 (PAI-1) was localized by an immunohistochemical reaction. RESULTS: Sensitization and challenge with OVA caused thickening of the airway wall, hypertrophy of smooth muscle cells, infiltration of inflammatory cells, subepithelial fibrosis, epithelial and endothelial lesions. Serum total IgE was significantly higher in OVA-sensitized rats as compared to VEH-sensitized control groups. Tissue plasminogen activator activity was significantly decreased in asthmatic animals (4.48 +/- 0.4 vs. 6.7 +/- 0.3 ng/ml for OVA/OVA and OVA/VEH; p < 0.05), and PAI-1 activity was statistically significantly higher in asthma rats (0.8 +/- 0.05 vs. 0.5 +/- 0.03 ng/ml for OVA/OVA vs. OVA/VEH; p < 0.05). alpha2-Antiplasmin was higher in rats receiving OVA sensitization than in those that were sham sensitized (p < 0.05). Immunohistochemical staining for PAI-1in the lungs of asthmatic animals showed very strong PAI-1 expression in lung inflammatory cells. CONCLUSIONS: We have demonstrated for the first time the existence of PAI-1 in lung inflammatory cells of rats with asthma. This finding was consistent with the superiority of plasmin system inhibition over activation in plasma. SN - 1423-0097 UR - https://www.unboundmedicine.com/medline/citation/18594148/Plasmin_system_regulation_in_an_ovalbumin_induced_rat_model_of_asthma_ L2 - https://www.karger.com?DOI=10.1159/000142041 DB - PRIME DP - Unbound Medicine ER -