Member of the Association of American Physicians
His primary areas of investigation include Immunology, Cytokine, Lung, Chemokine and Tumor necrosis factor alpha. The Immunology study combines topics in areas such as Bronchoalveolar lavage and In vivo. Theodore J. Standiford combines subjects such as Alveolar macrophage, Legionella pneumophila and Monocyte with his study of Cytokine.
His studies deal with areas such as Fibrosis, Pathology, Fibroblast and Immunosuppression as well as Lung. Theodore J. Standiford has researched Chemokine in several fields, including Aspergillus fumigatus, Innate immune system and Human disease. His Tumor necrosis factor alpha study integrates concerns from other disciplines, such as Lipopolysaccharide and Macrophage.
His main research concerns Immunology, Cytokine, Lung, Inflammation and Chemokine. His works in Immune system, Tumor necrosis factor alpha, Innate immune system, Proinflammatory cytokine and Sepsis are all subjects of inquiry into Immunology. His Tumor necrosis factor alpha research integrates issues from Molecular biology, Cell biology and Alveolar macrophage.
His Cytokine study incorporates themes from Lipopolysaccharide and Macrophage. His Lung study combines topics from a wide range of disciplines, such as Pathology, In vivo and Pneumonia. Theodore J. Standiford works mostly in the field of Inflammation, limiting it down to topics relating to Monocyte and, in certain cases, Chemotaxis, as a part of the same area of interest.
Immunology, Sepsis, Inflammation, Microbiology and Lung injury are his primary areas of study. His biological study spans a wide range of topics, including Lung and Pneumonia. His study in Lung is interdisciplinary in nature, drawing from both Fibrosis and Epithelium.
His Sepsis research incorporates themes from Bioinformatics, Transcriptome, Immune system, Neuroinflammation and Human brain. His studies in Microbiology integrate themes in fields like Legionella pneumophila, Interferon, Matricellular protein, Pseudomonas aeruginosa and Proinflammatory cytokine. His Lung injury research includes elements of Psychological intervention, Cancer research, In vitro, Interleukin and Complement receptor.
Theodore J. Standiford mostly deals with Immunology, Sepsis, Lung, Immune system and Inflammation. His Cytokine, Chemokine and Virus study in the realm of Immunology connects with subjects such as Trichostatin A. His work carried out in the field of Sepsis brings together such families of science as Precision medicine, Systems biology, Bioinformatics and Proteomics.
As a part of the same scientific study, Theodore J. Standiford usually deals with the Lung, concentrating on Pneumonia and frequently concerns with Respiratory disease, Respiratory system and Interleukin. The concepts of his Immune system study are interwoven with issues in Lung cancer and Primary tumor. The various areas that Theodore J. Standiford examines in his Inflammation study include mir-223, Epithelium, In vitro and Gene expression.
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Interleukin-8 gene expression by a pulmonary epithelial cell line. A model for cytokine networks in the lung.
T J Standiford;S L Kunkel;M A Basha;S W Chensue.
Journal of Clinical Investigation (1990)
Interleukin-8 (IL-8): The Major Neutrophil Chemotactic Factor in the Lung
Steven L. Kunkel;Theodore Standiford;Keita Kasahara;Robert M. Strieter.
Experimental Lung Research (1991)
Balance of inflammatory cytokines related to severity and mortality of murine sepsis.
Keith R. Walley;Nicholas W. Lukacs;Theodore J. Standiford;Robert M. Strieter.
Infection and Immunity (1996)
Pre-B-cell colony-enhancing factor as a potential novel biomarker in acute lung injury.
Shui Q. Ye;Brett A. Simon;James P. Maloney;April Zambelli-Weiner.
American Journal of Respiratory and Critical Care Medicine (2005)
The Pseudomonas aeruginosa autoinducer N-3-oxododecanoyl homoserine lactone accelerates apoptosis in macrophages and neutrophils.
Kazuhiro Tateda;Yoshikazu Ishii;Manabu Horikawa;Tetsuya Matsumoto.
Infection and Immunity (2003)
Alveolar macrophage-derived cytokines induce monocyte chemoattractant protein-1 expression from human pulmonary type II-like epithelial cells.
T J Standiford;S L Kunkel;S H Phan;B J Rollins.
Journal of Biological Chemistry (1991)
Neutralization of IL-10 increases survival in a murine model of Klebsiella pneumonia
M. J. Greenberger;R. M. Strieter;S. L. Kunkel;J. M. Danforth.
Journal of Immunology (1995)
MCP-1 protects mice in lethal endotoxemia.
David A. Zisman;Steven L. Kunkel;Robert M. Strieter;Wan C. Tsai.
Journal of Clinical Investigation (1997)
Neutralization of IL-10 increases lethality in endotoxemia. Cooperative effects of macrophage inflammatory protein-2 and tumor necrosis factor.
T J Standiford;R M Strieter;N W Lukacs;S L Kunkel.
Journal of Immunology (1995)
Neutralization of Macrophage Inflammatory Protein-2 Attenuates Neutrophil Recruitment and Bacterial Clearance in Murine Klebsiella Pneumonia
Marc J. Greenberger;Robert M. Strieter;Steven L. Kunkel;Jean M. Danforth.
The Journal of Infectious Diseases (1996)
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