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The effect of overexpression of endothelial nitric oxide synthase on eosinophilic lung inflammation in a murine model.
Int Immunopharmacol. 2006 Jul; 6(7):1040-52.II

Abstract

The effects of nitric oxide (NO) on allergic inflammation are controversial. In particular, the role of endothelial nitric oxide synthase (eNOS) in asthma remains uncertain. In the present study, we examined the effects of overexpression of eNOS on allergic inflammation using eNOS transgenic (eNOS-Tg) mice, in which eNOS protein is overexpressed in the vascular endothelium and airway epithelium. We found that eNOS-Tg mice showed a reduction of the asthmatic response to allergen challenge. Eosinophilic accumulation in the airspaces, eosinophilic activity, and bronchial responsiveness to acetylcholine were significantly attenuated in eNOS-Tg mice, as compared with wild-type mice following ovalbumin sensitization/challenge, even though the levels of circulating eosinophils were comparable in the wild-type and eNOS-Tg mice. The concentrations of eotaxin in the bronchoalveolar lavage fluid were significantly less in eNOS-Tg mice than in the wild-type mice. In addition, immunohistochemical analysis showed that the expressions of both intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on the pulmonary endothelium of eNOS-Tg mice was decreased compared with the controls. These results suggest that chronic eNOS overexpression contributes to the suppression of allergic inflammation by reducing the production of eotaxin in the airspaces and/or the expression of adhesion molecules in the vascular endothelium.

Authors+Show Affiliations

Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16714207

Citation

Kobayashi, Kazuyuki, et al. "The Effect of Overexpression of Endothelial Nitric Oxide Synthase On Eosinophilic Lung Inflammation in a Murine Model." International Immunopharmacology, vol. 6, no. 7, 2006, pp. 1040-52.
Kobayashi K, Nishimura Y, Yamashita T, et al. The effect of overexpression of endothelial nitric oxide synthase on eosinophilic lung inflammation in a murine model. Int Immunopharmacol. 2006;6(7):1040-52.
Kobayashi, K., Nishimura, Y., Yamashita, T., Nishiuma, T., Satouchi, M., & Yokoyama, M. (2006). The effect of overexpression of endothelial nitric oxide synthase on eosinophilic lung inflammation in a murine model. International Immunopharmacology, 6(7), 1040-52.
Kobayashi K, et al. The Effect of Overexpression of Endothelial Nitric Oxide Synthase On Eosinophilic Lung Inflammation in a Murine Model. Int Immunopharmacol. 2006;6(7):1040-52. PubMed PMID: 16714207.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The effect of overexpression of endothelial nitric oxide synthase on eosinophilic lung inflammation in a murine model. AU - Kobayashi,Kazuyuki, AU - Nishimura,Yoshihiro, AU - Yamashita,Tomoya, AU - Nishiuma,Teruaki, AU - Satouchi,Miyako, AU - Yokoyama,Mitsuhiro, Y1 - 2005/12/01/ PY - 2005/06/08/received PY - 2005/07/27/revised PY - 2005/09/23/accepted PY - 2006/5/23/pubmed PY - 2006/9/2/medline PY - 2006/5/23/entrez SP - 1040 EP - 52 JF - International immunopharmacology JO - Int Immunopharmacol VL - 6 IS - 7 N2 - The effects of nitric oxide (NO) on allergic inflammation are controversial. In particular, the role of endothelial nitric oxide synthase (eNOS) in asthma remains uncertain. In the present study, we examined the effects of overexpression of eNOS on allergic inflammation using eNOS transgenic (eNOS-Tg) mice, in which eNOS protein is overexpressed in the vascular endothelium and airway epithelium. We found that eNOS-Tg mice showed a reduction of the asthmatic response to allergen challenge. Eosinophilic accumulation in the airspaces, eosinophilic activity, and bronchial responsiveness to acetylcholine were significantly attenuated in eNOS-Tg mice, as compared with wild-type mice following ovalbumin sensitization/challenge, even though the levels of circulating eosinophils were comparable in the wild-type and eNOS-Tg mice. The concentrations of eotaxin in the bronchoalveolar lavage fluid were significantly less in eNOS-Tg mice than in the wild-type mice. In addition, immunohistochemical analysis showed that the expressions of both intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on the pulmonary endothelium of eNOS-Tg mice was decreased compared with the controls. These results suggest that chronic eNOS overexpression contributes to the suppression of allergic inflammation by reducing the production of eotaxin in the airspaces and/or the expression of adhesion molecules in the vascular endothelium. SN - 1567-5769 UR - https://www.unboundmedicine.com/medline/citation/16714207/The_effect_of_overexpression_of_endothelial_nitric_oxide_synthase_on_eosinophilic_lung_inflammation_in_a_murine_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(05)00267-5 DB - PRIME DP - Unbound Medicine ER -