J
Jeffrey J. Bowden
Researcher at University of California, San Francisco
Publications - 13
Citations - 630
Jeffrey J. Bowden is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Substance P & Neurogenic inflammation. The author has an hindex of 7, co-authored 8 publications receiving 609 citations. Previous affiliations of Jeffrey J. Bowden include Cardiovascular Institute Hospital.
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Journal ArticleDOI
Direct observation of substance P-induced internalization of neurokinin 1 (NK1) receptors at sites of inflammation
Jeffrey J. Bowden,Adella M. Garland,Peter Baluk,Peter M. Lefevre,Eileen F. Grady,Steven R. Vigna,Nigel W. Bunnett,Donald M. McDonald +7 more
TL;DR: It is suggested that internalization of NK1 receptors by endothelial cells may be one of the mechanisms that limit the amount of plasma leakage at sites of inflammation.
Book ChapterDOI
Neurogenic inflammation. A model for studying efferent actions of sensory nerves.
Donald M. McDonald,Jeffrey J. Bowden,Jeffrey J. Bowden,Peter Baluk,Nigel W. Bunnett,Nigel W. Bunnett,Nigel W. Bunnett +6 more
TL;DR: Studies of neurogenic inflammation have helped to understand the efferent actions of sensory nerves but also have given insight into the mechanism and consequences of inflammatory changes in endothelial cells and in the plasma leakage that follows.
Journal ArticleDOI
Inhibition of Neutrophil and Eosinophil Adhesion to Venules of Rat Trachea by Beta 2-adrenergic Agonist Formoterol
TL;DR: It is concluded that formoterol, acting via beta 2-adrenergic receptors, not only can reduce the amount of plasma leakage but also can reduced the number of neutrophils and eosinophils that adhere to the vascular endothelium at sites of inflammation.
Journal ArticleDOI
Dexamethasone and oxytetracycline reverse the potentiation of neurogenic inflammation in airways of rats with Mycoplasma pulmonis infection
TL;DR: This study addressed the issue of whether the extensive remodeling of the airway mucosa and potentiation of neurogenic inflammation can be reversed once they are established in F344 rats infected with M. pulmonis, and found that dexamethasone, like oxytetracycline, reduced the number of infecting organisms.
Journal ArticleDOI
Upregulation of substance P receptors in angiogenesis associated with chronic airway inflammation in rats.
TL;DR: It is concluded that increased expression of NK1 receptors, which is internalized into endosomes after ligand binding, contributes to the abnormal sensitivity of endothelial cells of angiogenic blood vessels to substance P in the airways of M. pulmonis-infected rats.