Ona E. Bloom, PhD
Lab Director
Assistant Investigator
Phone: (516) 562-3839
Fax: (516) 562-2953
E-mail: obloom@nshs.edu

Academic Degrees:
B.A. in History, 1992, Barnard College
Ph.D., in Neurobiology, 2001, The Rockefeller University

Research Overview:

We investigate the contributions of inflammation in diseases or injuries that affect the nervous system. One of the most important concepts in science that has been translated into medical practice was pioneered by scientists at The Feinstein Institute and elsewhere: the proteins that cause inflammation, called cytokines, which are made by the body in response to infection or injury, are important in low levels to fight infection and help wound healing, while high levels of these same proteins can cause lasting damage to tissues and organs.

Spinal cord injury affects more than 10,000 Americans each year, often in the earliest phases of adulthood. It is well known that physical trauma to the spinal cord causes damage to nerves and other cells at the injury site. Over minutes to days, cells of the immune system are activated and release factors that cause inflammation, which is thought to play a pivotal role in tissue damage. One major focus of our lab is on understanding inflammation in spinal cord injury with the goal of learning how to support a less toxic environment to nerve cells after injury.

Another major project in the lab is to perform pre-clinical studies based on discoveries from Feinstein colleague Dr. Betty Diamond’s laboratory on the causes of lupus. Lupus is a chronic autoimmune disease that affects approximately 1.5 million Americans. The disease is characterized by the presence of antibodies against the patient, which can lead to inflammation in multiple organs, and is often accompanied by many symptoms, including those affecting the nervous system. This project, pursued together with Dr. Diamond and Feinstein colleague Dr. Yousef Al-Abed, aims to develop novel therapeutic agents for the treatment of lupus.

In addition to these pathological settings, we are also interested in understanding the molecules that the nervous and immune systems use to relay information under normal conditions.

Research Description:

Research in the laboratory focuses on the impact of inflammation in the nervous system, in both acute and chronic settings. 

The role of cytokines in spinal cord injury and regeneration
Spinal cord injury (SCI) is a devastating condition that affects more than a quarter of a million Americans (www.spinalcord.uab.edu). Immediately after spinal cord injury, local and recruited immune cells produce high levels of pro-inflammatory cytokines. The resulting inflammation is thought to inhibit functional recovery.  Thus, current acute treatment for SCI aims to dampen inflammation, via the administration of steroids, which remains a controversial treatment recommendation due its failure to improve lasting functional recovery.  We are investigating the role of immune cells and their products such as cytokines on spinal cord injury and recovery. Neutralizing cytokines lessens inflammation in multiple disease models and therefore, in collaboration with Feinstein colleagues Dr. Yousef Al-Abed and Dr. Christine Metz, we are investigating the impact of modulating cytokine activity on SCI. We are studying the cellular and molecular pathways of cytokine expression during SCI and regeneration, and the impact of specifically modulating these pathways on the extent and time course of recovery after SCI. 

Rational Drug Design in Lupus:

Lupus is a chronic autoimmune disease characterized by the presence of autoantibodies, many of which are directed against DNA and may cross-react with other antigens. These autoantibodies circulate as immune complexes, and activate immune cells or deposit in various organs where they mediate chronic inflammation leading to organ damage. In addition to severe kidney disease, 20-80% of lupus patients are subject to a variety of neuropsychiatric symptoms including depression, cognitive impairment, and seizures. Dr. Betty Diamond’s lab recently showed that a high proportion of anti-DNA antibodies present in lupus that cause kidney symptoms also recognize the NMDA receptor and therefore may contribute to neuropsychiatric symptoms.  In collaboration with Dr. Diamond and Feinstein colleague Dr. Yousef Al-Abed, we are investigating the molecular nature of the antigen-antibody recognition process of lupus autoantibodies in order to promote rational drug design of novel therapeutics for lupus.

Name:   Angelo Papatheodorou
Position:   Research Assistant 
Email:   apapaathe@nshs.edu

Dr. Betty Diamond
Dr. Yousef Al-Abed
Dr. Christine Metz
Dr. Matthew Bank
Dr. Adam Stein
Dr. Todd Slesinger

Bloom O, Unternaehrer J, Jiang A, Shin J-S, Delamarre L, Allen P, Mellman I. Spinophilin participates in information transfer at immunological synapses, J. Cell Biol. 2008 April 14; 181: 203-211.

Jiang A, Bloom O, Ono S, Cui W, Unternaehrer J, Jiang S, Whitney JA, Connolly J, Banchereau J, Mellman I. Disruption of E-cadherin-mediated adhesion induces a functionally distinct pathway of dendritic cell maturation. Immunity 2007 October 26; 27: 610-624.

Evergren, E., Tomilin, N., Vasylieva, E., Sergeeva, V., Bloom, O., Gad, H., Capani, F., Shupliakov, O. (2003) A pre-embedding immunogold approach for detection of synaptic endocytic proteins in situ. J.Neurosci. Methods 2004 May 30;135(1-2):169-74.

Bloom O, Evergren E, Tomilin N, Kjaerulff O, Low P, Brodin L, Pieribone VA, Greengard P, Shupliakov O. Colocalization of synapsin and actin during synaptic vesicle recycling. J Cell Biol. 2003 May 26;161(4):737-47.

Shupliakov O, Bloom O, Gustafsson JS, Kjaerulff O, Low P, Tomilin N, Pieribone VA, Greengard P, Brodin L. Impaired recycling of synaptic vesicles after acute perturbation of the presynaptic actin cytoskeleton. Proc Natl Acad Sci U S A. 2002 Oct 29; 99(22):14476-81.

Andersson U, Wang H, Palmblad K, Aveberger A, Bloom O, Erlandsson-Harris H, Janson A, Kokkola R, Yang H, Tracey K.J. HMG-1 Stimulates Proinflammatory Cytokine Synthesis in Human Monocytes. Journal of Experimental Medicine 2000 21; 192(4):5657.

Wang H, Vishnubhakat JM, Bloom O, Zhang M, Ombrellino M, Sama A, Tracey KJ.
Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes. Surgery. 1999. 126:389-392.

Wang H, Bloom O, Zhang M, Vishnubhakat JM, Ombrellino M, Che J, Frazier A, Yang H, Ivanova S, Borovikova L, Manogue KR, Faist E, Abraham E, Andersson J, Andersson U, Molina PE, Abumrad NN, Sama A, Tracey KJ. HMG-1 as a late mediator of endotoxin lethality in mice. Science. 1999. 285:248-251.

Bloom O, Wang H, Ivanova S, Vishnubhakat JM, Ombrellino M, Tracey KJ. Hypophysectomy, high tumor necrosis factor levels, and hemoglobinemia in lethal endotoxemic shock. Shock. 1998. 10:395-400.

Meistrell ME 3rd, Botchkina GI, Wang H, Di Santo E, Cockroft KM, Bloom O, Vishnubhakat JM, Ghezzi P, Tracey KJ. Tumor necrosis factor is a brain damaging cytokine in cerebral ischemia. Shock. 1997. 8:341-348.

Cockroft KM, Meistrell M 3rd, Zimmerman GA, Risucci D, Bloom O, Cerami A, Tracey KJ. Cerebroprotective effects of aminoguanidine in a rodent model of stroke. Stroke. 1996. 27:1393-1398.

Bianchi M, Bloom O, Raabe T, Cohen PS, Chesney J, Sherry B, Schmidtmayerova H, Calandra T, Zhang X, Bukrinsky M, Ulrich P, Cerami A, Tracey KJ. Suppression of proinflammatory cytokines in monocytes by a tetravalent guanylhydrazone. Journal of Experimental Medicine. 1996. 183:927-936.

Zimmerman GA, Meistrell M 3rd, Bloom O, Cockroft KM, Bianchi M, Risucci D, Broome J, Farmer P, Cerami A, Vlassara H, Tracey KJ. Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine. Proceedings of the National Academy of Sciences U. S. A. 1995. 92:3744-3748.

Bianchi M, Ulrich P, Bloom O, Meistrell M 3rd, Zimmerman GA, Schmidtmayerova H, Bukrinsky M, Donnelley T, Bucala R, Sherry B, et al. An inhibitor of macrophage arginine transport and nitric oxide production (CNI-1493) prevents acute inflammation and endotoxin lethality. Molecular Medicine. 1995. 1:254-266.