J
James H. Fisher
Researcher at Anschutz Medical Campus
Publications - 32
Citations - 3167
James H. Fisher is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Surfactant protein D & Surfactant protein A. The author has an hindex of 25, co-authored 32 publications receiving 3096 citations. Previous affiliations of James H. Fisher include Memorial Sloan Kettering Cancer Center & Rose Medical Center.
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Journal ArticleDOI
Role of Surfactant Proteins A, D, and C1q in the Clearance of Apoptotic Cells In Vivo and In Vitro: Calreticulin and CD91 as a Common Collectin Receptor Complex
R. William Vandivier,Carol Anne Ogden,Valerie A. Fadok,Peter R. Hoffmann,Kevin K. Brown,Marina Botto,Mark Walport,James H. Fisher,Peter M. Henson,Kelly E. Greene +9 more
TL;DR: The results suggest that the entire collectin family of innate immune proteins (including C1q) works through a common receptor complex to enhance removal of apoptotic cells, and that collectins are integral, organ-specific components of the clearance machinery.
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Increased metalloproteinase activity, oxidant production, and emphysema in surfactant protein D gene-inactivated mice.
Susan E. Wert,Mitsuhiro Yoshida,Ann Marie LeVine,Machiko Ikegami,Tracy Jones,Gary F. Ross,James H. Fisher,Thomas R. Korfhagen,Jeffrey A. Whitsett +8 more
TL;DR: Targeted ablation of the surfactant protein D (SP-D) gene caused chronic inflammation, emphysema, and fibrosis in the lungs of SP-D (-/-) mice.
Journal ArticleDOI
Surfactant proteins A and D inhibit the growth of Gram-negative bacteria by increasing membrane permeability
Huixing Wu,Alexander Kuzmenko,Sijue Wan,Lyndsay Schaffer,Alison A. Weiss,James H. Fisher,Kwang Sik Kim,Francis X. McCormack +7 more
TL;DR: Data indicate that SP-A and SP-D are antimicrobial proteins that directly inhibit the proliferation of Gram-negative bacteria in a macrophage- and aggregation-independent manner by increasing the permeability of the microbial cell membrane.
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Distinct effects of surfactant protein A or D deficiency during bacterial infection on the lung.
Ann Marie LeVine,Jeffrey A. Whitsett,Jodie Gwozdz,Theresa R. Richardson,James H. Fisher,Michael S. Burhans,Thomas R. Korfhagen +6 more
TL;DR: The collectins, SP-A and SP-D, play distinct roles during bacterial infection of the lung and bacterial killing was decreased and associated with increased lung inflammation, decreased oxidant production, and decreased macrophage phagocytosis in mice lacking surfactant protein.
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Increased lung endothelin-1 production in rats with idiopathic pulmonary hypertension.
Thomas J. Stelzner,R. F. O'Brien,Masashi Yanagisawa,T. Sakurai,K. Sato,S. Webb,Martin R. Zamora,Ivan F. McMurtry,James H. Fisher +8 more
TL;DR: It is found that there is no increase in lung preproET-1 mRNA or ET-1 levels in adult SDR with an equivalent degree of pulmonary hypertension due to chronic hypoxia, implying that the increases in ET- 1 production in FHR were not a common consequence of all pulmonary hypertensive states.