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Academic Background

B.S.   (1975)  University of Michigan

M.D.  (1980)   University of Michigan

Internship and Residency, Internal Medicine (1980-1983) 

                         George Washington University Hospital

Infectious Diseases Fellowship (1984-1986)

             University of Wisconsin Hospitals and Clinics

Post-doctoral Fellowship (1986-1988)

             University of Wisconsin Hospitals and Clinics

             (Christian R.H. Raetz, mentor)

Post-doctoral Fellowship (1989-1990)

             Merck Research Laboratories, Rahway, NJ

             (Christian R.H. Raetz, mentor)

Assistant Professor of Medicine and Infectious Diseases (1990- 1995)

             Boston University School of Medicine

Associate Professor of Medicine and Infectious Diseases (1995-1999)

             Boston University School of Medicine

Professor of Medicine and Infectious Diseases (1999-2001)

             Boston University School of Medicine

Professor of Medicine and Infectious Diseases (2001-present)

              UMass Medical School

             Tenure award:  2004

           

Innate immunity and Infectious Diseases.Douglas Golenbock, MD

Dr. Douglas Golenbock is Chief of the Division of Infectious Diseases and Immunology in the Department of Medicine. He holds a joint appointment in the Department of Microbiology and Physiological Systems. The goal of his laboratory is to characterize phagocytic receptors that recognize the presence of microbes in the context of infectious illnesses. As the mechanisms of inflammation in infectious diseases are similar to those associated with sterile inflammation, we also study Alzheimer's Disease.    Virtually all of our work focuses on two groups of receptors: Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in the context of the inflammasome.

 Our entry into the TLR field was heralded by the discovery that TLR4, and MD-2 mediate responses to bacterial endotoxin, a major cause of sepsis. More recently, we have begun to focus on intracellular nucleic acid receptors as regulators of IL-1 production and type I interferons. There are six major projects in the laboratory:

1. Defining the response to bacterial lipopolysaccharide (LPS, endotoxin). LPS immunologically potent amphipathic glycolipid on the surface of Gram-negative bacteria. It is thought to be responsible for Gram-negative sepsis. This project involves detailed studies of TLR4/MD-2 and adapter molecules that transduce an activation signal. The work is funded via an NIH merit award to Dr. Golenbock.

2. Characterizing the role of the LPS receptor system, in pelvic inflammatory disease. This project is based upon the realization that Neisseria gonorrhoeae mediates much of its inflammation via the TLR4/MD-2 signaling pathway and is funded via an NIH U19 award that includes other infectious diseases faculty, including Drs. Peter Rice (program PI) and Sanjay Ram.

3. Defining the innate immune response to P. falciparum malaria. Very little is known about how P. falciparum causes inflammation. We have developed several projects in this area, including basic investigations into nucleic acid receptors and inflammasomes. This is a large project that is a collaboration with two other UMass investigators, Drs. Kate Fitzgerald and Ricardo Gazzinelli. The project is funded via an RO1 to Drs. Golenbock and Fitzgerald.

4. Defining the innate immune response to Group B streptococcus. We have previously demonstrated that Group B streptococcus activates type I interferon production as a result of hemolysin expression, which allows DNA access to the phagocyte cytosolic compartment. Recent studies also implicate hemolysin as a mediator of NLRP3 activation via the effects of bacterial RNA. This project is a three way collaboration with a bacterial genetics group at the Institut Pasteur (France) headed by Dr. Patrick Trieu-Cuot and a cell biology group at the University of Freiburg (Germany) run by Dr. Philipp Henneke, a former Golenbock post-doctoral fellow, and is funded by an RO1 grant to Dr. Golenbock.

5. Defining a role for PSTPIP1. PSTPIP1 is a protein that causes an autoinflammatory disorder known as PAPA syndrome: Pogenic Arthritis, Pyoderma gangrenosum and Acne. The disease is due to dysregulation of IL-1 production that probably results from the activation on pyrin, the gene product associated with Familial Mediterranean Fever. Dr. Donghai Wang, a member of the Golenbock laboratory, has engineered mice that are either deficient in PSTPIP1, or that carry the known lesions of PAPA syndrome. It is funded by an R21 grant to Drs. Wang and Golenbock.

6. Examining the role of the NLRP3 inflammasome in Alzheimers Disease. Alzheimer (AD) is a chronic inflammatory disease that causes premature dementia and death. It appears to be caused, in part, by -amyloid, an insoluble protein that activates the NLRP3 inflammasome in microglial cells, resulting in neuronal cell death.

One of the major goals of the Golenbock lab and the Division of Infectious Diseases is to promote UMass immunology and the field of innate immunity in general. The Division has organized the state of the art meetng in the field of innate immunity. We have now had four Toll meetings: Toll2004 (Taormina, Italy), Toll2006 (Salvador, Brazil; www.toll2006.org), Toll2008 (Cascais, Portugal; www.toll2008.org) and Toll2011 (Riva del Garda, Italy; www.toll2011.org). Virtually all of the research faculty, students and post-docs in Infectious Diseases attend the Toll meetings, which typically involve ~ 600 participants.

For More information on Toll related meetings please see

 http://www.youtube.com/watch?v=2rqQOmkiL5o

For More information on Targeting a new therapy for Alzheimer's pleas see:

 http://www.youtube.com/watch?v=5LXshrNFkXA

 

One or more keywords matched the following items that are connected to Golenbock, Douglas
Item TypeName
Academic Article Cutting edge: recognition of Gram-positive bacterial cell wall components by the innate immune system occurs via Toll-like receptor 2.
Academic Article IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway.
Academic Article Phagocytosis, innate immunity, and host-pathogen specificity.
Academic Article Reduced atherosclerosis in MyD88-null mice links elevated serum cholesterol levels to activation of innate immunity signaling pathways.
Academic Article Expression of functional TLR4 confers proinflammatory responsiveness to Trypanosoma cruzi glycoinositolphospholipids and higher resistance to infection with T. cruzi.
Academic Article Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9.
Academic Article MyD88 is critical for the development of innate and adaptive immunity during acute lymphocytic choriomeningitis virus infection.
Academic Article Comparative toll-like receptor 4-mediated innate host defense to Bordetella infection.
Academic Article MyD88-dependent pathways mediate resistance to Cryptosporidium parvum infection in mice.
Academic Article Toll-like receptor-dependent discrimination of streptococci.
Academic Article A bacterial carbohydrate links innate and adaptive responses through Toll-like receptor 2.
Academic Article Innate immune responses to endosymbiotic Wolbachia bacteria in Brugia malayi and Onchocerca volvulus are dependent on TLR2, TLR6, MyD88, and Mal, but not TLR4, TRIF, or TRAM.
Academic Article Malaria hemozoin is immunologically inert but radically enhances innate responses by presenting malaria DNA to Toll-like receptor 9.
Academic Article The NALP3 inflammasome is involved in the innate immune response to amyloid-beta.
Academic Article Malaria primes the innate immune response due to interferon-gamma induced enhancement of toll-like receptor expression and function.
Academic Article Innate immune recognition of Yersinia pseudotuberculosis type III secretion.
Academic Article LBP, CD14, TLR4 and the murine innate immune response to a peritoneal Salmonella infection.
Academic Article The role of lipopolysaccharide binding protein in resistance to Salmonella infections in mice.
Academic Article Combined action of nucleic acid-sensing Toll-like receptors and TLR11/TLR12 heterodimers imparts resistance to Toxoplasma gondii in mice.
Academic Article Receptor "cross talk" in innate immunity.
Academic Article Lipopolysaccharide binding protein is an essential component of the innate immune response to Escherichia coli peritonitis in mice.
Academic Article Dual role of TLR2 and myeloid differentiation factor 88 in a mouse model of invasive group B streptococcal disease.
Academic Article Innate immune responses to Rhodococcus equi.
Academic Article Negative regulation of Toll-like receptor 4 signaling by the Toll-like receptor homolog RP105.
Academic Article MD-2.
Academic Article Inflammasomes: too big to miss.
Academic Article TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia.
Academic Article TLR3-mediated IFN-? gene induction is negatively regulated by the TLR adaptor MyD88 adaptor-like.
Academic Article MyD88-dependent pathway is essential for the innate immunity to Enterocytozoon bieneusi.
Academic Article Requirement of UNC93B1 reveals a critical role for TLR7 in host resistance to primary infection with Trypanosoma cruzi.
Academic Article Innate immune recognition of an AT-rich stem-loop DNA motif in the Plasmodium falciparum genome.
Academic Article Beyond empiricism: informing vaccine development through innate immunity research.
Academic Article Inflammation in mice ectopically expressing human Pyogenic Arthritis, Pyoderma Gangrenosum, and Acne (PAPA) Syndrome-associated PSTPIP1 A230T mutant proteins.
Academic Article The history of Toll-like receptors - redefining innate immunity.
Concept Immunity, Innate
Academic Article Host-cell sensors for Plasmodium activate innate immunity against liver-stage infection.
Academic Article Innate sensing of malaria parasites.
Academic Article Involvement of Nod2 in the innate immune response elicited by malarial pigment hemozoin.
Academic Article Innate immunity in Alzheimer's disease.
Academic Article Neuroinflammation in Alzheimer's disease.
Academic Article A Common Variant in the Adaptor Mal Regulates Interferon Gamma Signaling.
Academic Article Control of the innate immune response by the mevalonate pathway.
Academic Article Cutting Edge: Plasmodium falciparum Induces Trained Innate Immunity.
Academic Article The immunology of Plasmodium vivax malaria.
Academic Article Clostridioides difficile Toxin A Remodels Membranes and Mediates DNA Entry Into Cells to Activate Toll-Like Receptor 9 Signaling.
Search Criteria
  • Innate Immune Responses