Research Topics
Species | J M ThurmanSummaryAffiliation: University of Colorado Health Sciences Center Country: USA Publications
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Publications
The alternative pathway of complement in disease: opportunities for therapeutic targetingV Michael Holers
Department of Medicine, University of Colorado Health Sciences Center, P O Box B 115, 4200 East Ninth Ave, Denver, CO 80262, USA
Mol Immunol 41:147-52. 2004..It is also expected that several clinically relevant studies will be presented at the XXth International Complement Workshop that will identify additional areas of interest with regard to this pathway...- Alternative complement pathway activation is essential for inflammation and joint destruction in the passive transfer model of collagen-induced arthritisNirmal K Banda
Divisions of Rheumatology, University of Colorado Health Sciences Center, Denver, CO 80262, USA
J Immunol 177:1904-12. 2006..The mechanisms by which these target organ-specific mAbs bypass the requirements for engagement of the classical pathway remain to be defined but do not appear to involve a lack of alternative pathway regulatory proteins... - An allelic variant of Crry in the murine Sle1c lupus susceptibility interval is not impaired in its ability to regulate complement activationSvetlana N Tchepeleva
Department of Medicine, University of Colorado School of Medicine, Aurora, CO 80045, USA
J Immunol 185:2331-9. 2010.... - Inhibition of the alternative complement activation pathway in traumatic brain injury by a monoclonal anti-factor B antibody: a randomized placebo-controlled study in miceIris Leinhase
Department of Trauma and Reconstructive Surgery, Charite University Medical School, Campus Benjamin Franklin, Berlin, Germany
J Neuroinflammation 4:13. 2007..This neutralizing antibody represents a specific and potent inhibitor of the alternative complement pathway in mice... - Reduced neuronal cell death after experimental brain injury in mice lacking a functional alternative pathway of complement activationIris Leinhase
Department of Trauma and Reconstructive Surgery, Charite University Medical School, Campus Benjamin Franklin, 12200 Berlin, Germany
BMC Neurosci 7:55. 2006.... - Treatment with an inhibitory monoclonal antibody to mouse factor B protects mice from induction of apoptosis and renal ischemia/reperfusion injuryJoshua M Thurman
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA, and Department of Pathology, University Hospital Dubrava, Zabreb, Croatia
J Am Soc Nephrol 17:707-15. 2006..Thus, use of an inhibitory mAb to mouse factor B effectively prevented activation of complement in the kidney after I/R and protected the mice from necrotic and apoptotic injury of the tubules... - Altered renal tubular expression of the complement inhibitor Crry permits complement activation after ischemia/reperfusionJoshua M Thurman
Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
J Clin Invest 116:357-68. 2006..Increased C3 mRNA and decreased factor H mRNA were also detected in the outer medulla after I/R, suggesting that altered synthesis of these factors might further contribute to complement activation in this location... - Acute tubular necrosis is characterized by activation of the alternative pathway of complementJoshua M Thurman
Department of Internal Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
Kidney Int 67:524-30. 2005..The purpose of this study was to determine whether alternative pathway activation also occurs during the development of ischemic acute tubular necrosis in the human kidney... - A novel inhibitor of the alternative complement pathway prevents antiphospholipid antibody-induced pregnancy loss in miceJoshua M Thurman
Division of Nephrology and Hypertension, University of Colorado Health Sciences Center, 4200 E 9th Avenue, B 115, Denver, CO 80262, USA
Mol Immunol 42:87-97. 2005..The mAb protects mice in an in vivo model of antiphospholipid antibody syndrome, demonstrating the therapeutic potential for the inhibition of factor B in this disease... - C3a is required for the production of CXC chemokines by tubular epithelial cells after renal ishemia/reperfusionJoshua M Thurman
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA
J Immunol 178:1819-28. 2007..This innate immune system thereby recognizes hypoxic injury and triggers a systemic inflammatory response through the generation of C3a and subsequent activation of the NF-kappaB system... - Peeking into the black box: new biomarkers for acute kidney injuryJ M Thurman
Department of Medicine, Division of Nephrology and Hypertension, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA
Kidney Int 73:379-81. 2008..New biomarkers offer the promise of earlier and more accurate diagnosis of AKI. Before they can be deemed clinically useful, however, they must undergo rigorous validation in multiple cohorts... - Triggers of inflammation after renal ischemia/reperfusionJoshua M Thurman
The University of Colorado Health Sciences Center, Division of Nephrology and Hypertension, 4200 E 9th Avenue, B 115, Denver, CO 80262, USA
Clin Immunol 123:7-13. 2007..A greater understanding of the signals that trigger the inflammatory response may permit the development of effective therapies to ameliorate ischemic ARF... - The alternative pathway of complement is activated in the glomeruli and tubulointerstitium of mice with adriamycin nephropathyAmanda M Lenderink
Department of Medicine, University of Colorado, Denver, USA
Am J Physiol Renal Physiol 293:F555-64. 2007..These results demonstrate that complement activation in this nonimmune complex-mediated model of progressive renal disease requires an intact alternative pathway... - Lack of a functional alternative complement pathway ameliorates ischemic acute renal failure in miceJoshua M Thurman
Division of Nephrology University of Colorado Health Sciences Center, Denver, CO 80262, USA
J Immunol 170:1517-23. 2003..Our results demonstrate that complement activation in the kidney after I/R occurs exclusively via the alternative pathway, and that selective inhibition of this pathway provides protection to the kidneys from ischemic ARF... - The complement inhibitors Crry and factor H are critical for preventing autologous complement activation on renal tubular epithelial cellsBrandon Renner
Department of Medicine, University of Colorado Denver School of Medicine, Denver, CO 80045, USA
J Immunol 185:3086-94. 2010..However, congenital deficiency of Crry or reduced expression of the protein on the basolateral surface of injured cells permits spontaneous complement activation and tubular injury... - Factor B of the alternative complement pathway regulates development of airway hyperresponsiveness and inflammationChristian Taube
Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA
Proc Natl Acad Sci U S A 103:8084-9. 2006..These results demonstrate that in sensitized hosts complement activation through the alternative pathway after allergen exposure is critical to the development of AHR and airway inflammation... - B cell subsets contribute to renal injury and renal protection after ischemia/reperfusionBrandon Renner
Department of Medicine, University of Colorado Denver School of Medicine, Denver, CO 80045, USA
J Immunol 185:4393-400. 2010..However, nonperitoneal B cells attenuate renal injury after I/R, possibly through the production of IL-10... - Targeted inhibition of the complement alternative pathway with complement receptor 2 and factor H attenuates collagen antibody-induced arthritis in miceNirmal K Banda
Division of Rheumatology, University of Colorado Denver, School of Medicine, Aurora, CO 80045, USA
J Immunol 183:5928-37. 2009..The relative potency of CR2-fH in vitro was superior to mAbs to factor B and C5. Thus, CR2-fH specifically targets and inhibits the AP of complement in vitro and is effective in CAIA in vivo... - Alternative pathway of complement in children with diarrhea-associated hemolytic uremic syndromeJoshua M Thurman
Department of Medicine, Division of Nephrology, University of Colorado, Denver School of Medicine, Aurora, CO, USA
Clin J Am Soc Nephrol 4:1920-4. 2009..Therefore, we determined whether plasma levels of markers of activation of the AP are increased in D+HUS and are biomarkers of the severity of renal injury that predict the need for dialysis... - Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndromeGuillermina Girardi
Department of Medicine, Hospital for Special Surgery Weill Medical College, Cornell University, 535 East 70th Street, New York, New York 10021, USA
J Clin Invest 112:1644-54. 2003..Our findings identify the key innate immune effectors engaged by pathogenic autoantibodies that mediate poor pregnancy outcomes in APS and provide novel and important targets for prevention of pregnancy loss in APS... - Oxidative stress renders retinal pigment epithelial cells susceptible to complement-mediated injuryJoshua M Thurman
Department of Medicine, University of Colorado Denver School of Medicine, Denver, Colorado 80045, USA
J Biol Chem 284:16939-47. 2009..These findings link oxidative stress, complement activation, and apical VEGF release, which have all been associated with the pathogenesis of AMD... - Renal inflammation: targeted iron oxide nanoparticles for molecular MR imaging in miceNatalie J Serkova
Department of Anesthesiology, University of Colorado Denver School of Medicine, 1775 N Aurora Ct, M20 3103, Aurora, CO 80045, USA
Radiology 255:517-26. 2010.... - Comparative effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on blood pressure and the kidneyJoshua M Thurman
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA
Am J Med 114:588-98. 2003..The purpose of this paper is to review the mechanisms of action of these two classes of medication, as well as the experimental and clinical evidence that they slow the progression of renal disease... - Acute renal failure after bilateral nephrectomy is associated with cytokine-mediated pulmonary injuryThomas S Hoke
Department of Medicine, University of Colorado at Denver and Health Sciences Center, Denver, CO80262, USA
J Am Soc Nephrol 18:155-64. 2007.... - Urinary concentrating defect in hypothyroid rats: role of sodium, potassium, 2-chloride co-transporter, and aquaporinsMelissa A Cadnapaphornchai
Department of Medicine, University of Colorado School of Medicine, Denver, USA
J Am Soc Nephrol 14:566-74. 2003.... - Effect of primary polydipsia on aquaporin and sodium transporter abundanceMelissa A Cadnapaphornchai
Department of Medicine, University of Colorado School of Medicine, Denver 80262, USA
Am J Physiol Renal Physiol 285:F965-71. 2003..We conclude that the impaired urinary concentrating ability associated with primary POLY in rats is due to impaired osmotic equilibration in the collecting duct that is mediated primarily by decreased AQP-2 protein abundance... - The central role of the alternative complement pathway in human diseaseJoshua M Thurman
Division of Nephrology and Hypertension, University of Colorado Health Sciences Center, Denver, CO 80262, USA
J Immunol 176:1305-10. 2006.... - Pharmacological complement inhibition at the C3 convertase level promotes neuronal survival, neuroprotective intracerebral gene expression, and neurological outcome after traumatic brain injuryIris Leinhase
Department of Trauma and Reconstructive Surgery, Charite University Medical School, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany
Exp Neurol 199:454-64. 2006..These data suggest that pharmacological complement inhibition represents a promising approach for attenuation of neuroinflammation and secondary neurodegeneration after head injury... - Evidence for non-traditional activation of complement factor C3 during murine liver regenerationAmelia Clark
Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, United States
Mol Immunol 45:3125-32. 2008..In vitro analysis raises the possibility that plasmin may contribute to non-traditional complement activation during liver regeneration in vivo... - New approaches to the treatment of dense deposit diseaseRichard J H Smith
Department of Internal Medicine and Otolaryngology, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA
J Am Soc Nephrol 18:2447-56. 2007..As the understanding of DDD increases, novel therapies should be integrated into existing protocols for DDD and evaluated using an open-label Bayesian study design... - The alternative pathway of complement activation is critical for blister induction in experimental epidermolysis bullosa acquisitaSidonia Mihai
Department of Dermatology, University of Lubeck, Lubeck, Germany, and Department of Pediatrics, Laboratory of Developmental Immunology, Massachusetts General Hospital, Boston 02115, USA
J Immunol 178:6514-21. 2007.... - Complement activation induces dysregulation of angiogenic factors and causes fetal rejection and growth restrictionGuillermina Girardi
Autoimmunity and Inflammation Program, Hospital for Special Surgery, Weill Medical College, Cornell University, New York, NY 10021, USA
J Exp Med 203:2165-75. 2006..These studies provide the first evidence linking the complement system to angiogenic factor imbalance associated with placental dysfunction, and identify a new effector of immune-triggered pregnancy complications... - Candidate inhibitors of porcine complementEbbe B Thorgersen
Institute of Immunology, Rikshospitalet Radiumhospitalet Medical Center and University of Oslo, N 0027 Oslo, Norway
Mol Immunol 44:1827-34. 2007..05 mg/mL for all three activators. All candidates tested inhibited porcine complement activation, but in different ways and to different degrees. Of the complement-specific candidates, VCP inhibited all activators completely at low doses...
Research Grants
- Complement Activation and Renal Ischemia/Reperfusion InjuryJOSHUA THURMAN; Fiscal Year: 2007....
- Complement and Ischemic Acute Renal FailureJOSHUA THURMAN; Fiscal Year: 2007..The purpose of these studies is to ameliorate ischemic ARF by blocking these pathogenic events, and to develop strategies for decreasing the morbidity and mortality associated with ischemic ARF in humans. ..