Cory Hogaboam | Cedars-Sinai Medical Center (original) (raw)

Papers by Cory Hogaboam

Blood, 2013

NPM-ALK induces a metabolic shift toward biomass production.

American Journal of Respiratory and Critical Care Medicine, Dec 20, 2012

Allergy Frontiers: Future Perspectives, 2010

ABSTRACT Allergic and asthmatic diseases stubbornly plague a growing number of Americans and the ... more ABSTRACT Allergic and asthmatic diseases stubbornly plague a growing number of Americans and the clinical cost of treating these diseases shows no sign of abating. Persistent peribronchial inflammation (consisting primarily of eosinophils and mononuclear cells) and airway hyperresponsiveness to various stimuli (either antigen-specific or nonspecific) are key features of asthma. Despite concerted efforts in this regard, the mechanisms that lead to the initiation and chronicity of allergic airway inflammation during asthma remain poorly understood. Consequently, the development of inflammation-specific therapeutic interventions for this disorder have proved challenging, but necessary, in light of the fact that the anti-inflammatory effects of corticosteroids diminish with continual use and may not eliminate the airway remodeling features associated with asthma. Recent clinical and basic research suggests that targeting chemokines and/or chemokine receptors shows promise in the treatment of asthma and asthma-like diseases.

Lung Diseases - Selected State of the Art Reviews, 2012

American Journal of Physiology Lung Cellular and Molecular Physiology, Jun 1, 2001

6 other HighWire hosted articles, the first 5 are: This article has been cited by [PDF] [Full Tex... more 6 other HighWire hosted articles, the first 5 are: This article has been cited by [PDF] [Full Text] [Abstract] , March 4, 2002; 195 (5): 583-592. [PDF] [Full Text] [Abstract] , December 15, 2002; 100 (13): 4291-4297. Blood gene array analysis Stem cell factor induces eosinophil activation and degranulation: mediator release and [PDF] [Full Text] [Abstract] , December 15, 2002; 169 (12): 7063-7070. An Aspirin-Triggered Lipoxin A4 Stable Analog Displays a Unique Topical [PDF] [Full Text] [Abstract] , January 1, 2005; 171 (1): 35-39. Am. J. Respir. Crit. Care Med. A. A. Berlin and N. W. Lukacs Responses Treatment of Cockroach Allergen Asthma Model with Imatinib Attenuates Airway [PDF] [Full Text] [Abstract] , April 1, 2007; 81 (4): 1111-1119. J. Leukoc. Biol. V. Dolgachev, M. Thomas, A. Berlin and N. W. Lukacs production and survival Stem cell factor-mediated activation pathways promote murine eosinophil CCL6 on the following topics: http://highwire.stanford.edu/lists/artbytopic.dtl can be found at Medline items on this article's topics Physiology .. Mice Medicine .. Airway Physiology .. Bronchi Physiology .. Mast Cells Biophysics .. Tumor Necrosis Factor Oncology .. Leukotrienes including high-resolution figures, can be found at: Updated information and services http://ajplung.physiology.org/cgi/content/full/280/6/L1242 at: can be found AJP -Lung Cellular and Molecular Physiology about Additional material and information http://www.the-aps.org/publications/ajplung This information is current as of December 8, 2008 .

The Journal of Immunology, Dec 1, 1999

Cytokines are a family of soluble secreted mediators produced by cells that effect the functionin... more Cytokines are a family of soluble secreted mediators produced by cells that effect the functioning of the same or other cells. Aspergillus fumigatus is a potent stimulator of cytokine and chemokine production by a variety of cells present in the inflamed lung. Substantial research interest has focused upon the cytokine responses to fungal colonization of the lung. Models of fungal

The Journal of Clinical Investigation, Oct 15, 1999

Amer J Respir Crit Care Med, 2007

Rationale: Prostaglandin (PG) E 2 , a cyclooxygenase-derived lipid mediator, is a potent down-reg... more Rationale: Prostaglandin (PG) E 2 , a cyclooxygenase-derived lipid mediator, is a potent down-regulator of fibroblast activation in normal lung fibroblasts. Although fibroblasts from patients with idiopathic pulmonary fibrosis are known to exhibit a defect in PGE 2 synthesis, there is little information about their responsiveness to this lipid mediator. Objectives: To compare responses to PGE 2 in normal, usual interstitial pneumonia (UIP), and other diffuse parenchymal lung disease (DPLD) fibroblasts. Methods: Fibroblasts were grown in vitro from well characterized control (n 5 7), UIP (n 5 17), or other DPLD (n 5 13) lung tissue. The effects of PGE 2 on fibroblast proliferation and collagen expression were determined. Measurements and Main Results: Only 3 of 12 UIP fibroblast lines exhibited PGE 2 -mediated inhibition of both collagen synthesis and cell proliferation, as opposed to 6 of 6 nonfibrotic control cell lines. The degree of PGE 2 resistance in DPLD fibroblasts was quite variable, with UIP cells exhibiting the greatest degree of resistance to PGE 2 , whereas other DPLD fibroblasts manifested a degree of resistance intermediate to control and UIP. The resistance to suppression of collagen expression correlated with worse lung function. Molecular mechanisms for resistance included altered E prostanoid receptor profiles and diminished expression of the downstream kinase, protein kinase A. Conclusions: The recognition that UIP fibroblasts manifest variable refractoriness to PGE 2 suppression sheds new light on the activation phenotype of these cells and on the pathogenesis of fibrotic lung disease.

European Respiratory Journal, Sep 1, 2013

Number: 1931 Publication Number: P248 Abstract Group: 3.3. Mechanisms of Lung Injury and Repair K... more Number: 1931 Publication Number: P248 Abstract Group: 3.3. Mechanisms of Lung Injury and Repair Keyword 1: Idiopathic pulmonary fibrosis Keyword 2: COPD -diagnosis Keyword 3: Lung injury

Chemokines in Disease, 1999

A20. EMERGING APPROACHES TO RESPIRATORY INFECTIONS: LATE BREAKING ABSTRACTS, 2011

University of Michigan, Ann Arbor, MI, Keio University School of Medicine, Tokyo, Japan, Universi... more University of Michigan, Ann Arbor, MI, Keio University School of Medicine, Tokyo, Japan, University of Michigan, Medical school, Ann 1 2 ... Arbor, MI, Univ. of Michigan, Dept. of Pathology, Ann Arbor, MI 4 ... RATIONALE: Severe sepsis is a significant human health concern, with ...

A23. IDIOPATHIC PULMONARY FIBROSIS: EPIDEMIOLOGY, BIOMARKERS, AND OUTCOMES, 2010

3916 Taubman Center / University of Michigan, Ann Arbor, MI, United States of America, University... more 3916 Taubman Center / University of Michigan, Ann Arbor, MI, United States of America, University of Michigan, Ann Arbor, MI, United 1 ... States of America, Mayo Clinic, Rochester, MN, United States of America, University of Michigan Health System, Ann Arbor, MI, United 3

Proceedings of the American Thoracic Society, 2012

Patients with idiopathic pulmonary fibrosis (IPF) survive a median of 3 years after diagnosis, bu... more Patients with idiopathic pulmonary fibrosis (IPF) survive a median of 3 years after diagnosis, but a high degree of variability in longitudinal disease progression has been observed. Unfortunately, physiology and clinical parameters determined at the time of diagnosis have proven inaccurate in predicting the rate at which IPF ultimately progresses. A mechanistic explanation for disease progression in patients with IPF is presently unclear, but we have recently shown that hypomethylated CpG DNA drives the rapid progression of fibrotic lung disease through the differentiation of pulmonary fibroblasts into myofibroblasts through a TLR9-dependent mechanism. Furthermore, we recently reported that the clinical progression of IPF might be a consequence of aberrant microRNA processing. Using this framework of data, we are presently addressing the following specific hypothesis: hypomethylated CpG DNA activation in pulmonary fibroblasts leads to aberrant micro RNA processing, thereby promoting the rapid progression of IPF.

Frontiers in Pharmacology, 2014

Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease characte... more Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease characterized by the persistence of activated myofibroblasts resulting in excessive deposition of extracellular matrix proteins and profound tissue remodeling. Myofibroblasts have been shown to arise from interstitial fibroblasts, epithelial to mesenchymal transition of type II alveolar epithelial cells, and the differentiation of recruited fibrocytes. There are many mechanisms that are utilized by these cells for survival, proliferation, and persistent activation including up-regulation of cytokines [i.e., Interleukin 6 (IL-6) and C-C motif chemokine ligand 21 (CCL21)], cytokine receptors [i.e., Interleukin 6Receptor 1 (IL-6R1), Glycoprotein 130 (gp130) and C-C Chemokine Receptor type 7 (CCR7)], and innate pattern recognition receptors [(PRRs; i.e., Toll Like Receptor 9 (TLR9)]. In this review, we will discuss the role of the cytokines IL-6 and CCL21, their receptors and the PRR, TLR9, in fibroblast recruitment, activation, survival, and differentiation into myofibroblasts in IPF.