ACADEMIC DEGREES

• Ph.D., Physiology, (1996). Tulane University School of Medicine

• M.S., Physiology, (1994). Tulane University School of Medicine

• B.Sc. Honors, Biological Sciences (Physiology), (1989). University of Birmingham, UK.

COURSES TAUGHT

• Biology 4251/5251: Immunology

• Biology 6103/8103: Microbiology and Immunology

HONORS, AWARDS AND MEMBERSHIPS

• 1989-1990: Research Assistant, Dept of Hematology, Queen Elizabeth Medical Centre, Birmingham, UK.

• 1990-1993: Science and Engineering Research Council (UK), Overseas Research Scholarship

• 1993-1995: Tulane University Chancellor's Fellowship.

• 1995-1996: American Heart Association Graduate Student Research Fellowship

• 1996-1998: Research Associate, Department of Microbiology and Immunology, Tulane Univ. Med. Center

• 1998: American Association of Immunologist’s Advanced Immunology Course, Berkeley, California

• 1998: Leah Seidman Schaffer Award for Postdoctoral Research, Tulane Univ. Medical Center

• 1998: Chancellor’s Award for Excellence in Research by a Postdoctoral Fellow, Tulane Univ. Medical Center

• 1998-2000: Research Assistant Professor, Department of Biology, Univ. North Carolina at Charlotte, NC

• 1998: Becton Dickinson Immunocytometry Systems Flow Cytometry Training Course, San Jose CA

• 2000-2004: Assistant Professor, Department of Biology, Univ. North Carolina at Charlotte, NC

• 2000-2003: Institutional Animal Care and Use Committee member

• 2002: American Association of Immunologists Pfizer-Showell Travel Award for Early-Career Scientists

• 2003: Departmental Advisory Committee member (2003-present), Dept. Biology, UNC Charlotte

• 2003: American Association of Immunologists Junior Faculty Travel Award.

• 2004-present: Associate Professor, Department of Biology, Univ. North Carolina at Charlotte, NC

• 2004-present: Departmental Review Committee member, Dept. Biology, UNC Charlotte.

• 2005-present: Departmental Review Committee member, Dept. Kinesiology, UNC Charlotte.

• 2006-2008: Coordinator, M.S. Program in Biology, UNC Charlotte.

• 2006-present: Mentor in UNC Charlotte College of Arts and Sciences Faculty Mentorship Program.

• 2008-present: Professor, Department of Biology, Univ. North Carolina at Charlotte, NC

• Editorial board memberships: Journal of Immunology (2002-2006), Current Immunology Reviews (2004-present), Immunopharmacology and Immunotoxicology (2007-present).

• Ad Hoc Reviewer: Dept. of Veterans Affairs merit review, USDA extramural grant program, Wellcome Trust, Los Alamos National Laboratory directed research internal funding, Medical Research Council UK, Am. J. Physiology, Am. J. Pathology, Biotechnology and Applied Biochemistry, BMC Infectious Diseases, Bone, Brain Research, Cellular Physiology and Biochemistry, Current Opinion in Investigational Drugs, Glia, Infection and Immunity, Int. J. Infectious Diseases, International Immunopharmacology, Journal of Bone and Mineral Research, Journal of Cellular Physiology, Journal of Immunology, Journal of Neurochemistry, Journal of Neuroimmunology, J. Neuroscience Research, Microbes and Infection, Molecular and Cellular Biochemistry.

• Membership in Professional Societies:  American Association of Immunologists; International Society for Neurochemistry; Society for Neuroscience

• NIH Study Section Assignments:  NCCAM Special Emphasis Panel, ZAT1 DB-17, "Botanicals Centers", (2004). NCCAM Special Emphasis Panels, ZAT1 DB-18, DB-19, DB-21, DB-22, DB-26, DB-27, DB-28, DB-29, PK-01  "Basic Science", (2005-2008). NIDCR Special Grants Review Committee, (2005).  NIAMS Specialized Centers (P50s), ZAR1 MLB-G M1 1 "Centers of Research Translation", NIAMS Special Emphasis Panel, ZRG1 MOSS-L (05), "Orthopaedic Device-associated Immunology" (2008).

RESEARCH PROJECTS

1. The role of the neuropeptide substance P in microbially induced CNS inflammation

Microglia are the principle immune cells of the central nervous system (CNS) and play a key role in host defense against invading pathogens. However, much like macrophages to which these cells are related, microglia may play a far more sinister role by amplifying the effects of inflammation leading to damage in the CNS. Deleterious inflammatory reactions mediated by microglia include such chronic conditions as cerebral malaria, HIV infection of the nervous system, and multiple sclerosis. Much study has been devoted to the study of microglial involvement in these conditions, but despite this work the nature of the stimuli that initiate and exacerbate the inflammatory activities of microglia remains a mystery. The neuropeptide, substance P, is the most abundant neurokinin within the CNS. Importantly, substance P has been implicated in a wide variety of inflammatory events where it is recognized to augment immune responses. While it is well known that substance P plays a significant role in the development of inflammatory responses, the ability of substance P to influence the function of resident immune cells of the brain remains obscure. Our central hypothesis is that substance P released by peripheral CNS cells augments the initiation of microglia and astrocyte-mediated immune responses against pathogens or immunogens by increasing pro-inflammatory monokine production, decreasing anti-inflammatory cytokine production, increasing expression of co-stimulatory molecules and increasing class II MHC expression.

Current Project Support:

NIH R01 NS050325 "Substance P exacerbation of CNS inflammation", Ian Marriott, PI, 08/01/06-07/31/10.

Recent Publications:

Chauhan, V.S., Sterka, D.G. Jr., Gray, D.L., Bost, K.L., and Marriott, I.  (2008). Neurogenic exacerbation of microglial and astrocyte responses to Neisseria meningitidis and Borrelia burgdorferi. J. Immunol. 180: 8241-9.

2. Resident CNS cells use NLR and RLR proteins to recognize intracellular pathogens

Astrocytes and microglia, resident glial cells of the CNS, can respond to bacterial pathogens by the rapid production of an array of inflammatory mediators.  Previous work from our laboratory has shed light on the possible mechanisms that underlie glial activation with the demonstration that these cells express members of the Toll-like family of receptors (TLR) that can recognize extracellular microbial motifs.  However, these cell surface receptors are not the only means by which innate immune cells can perceive pathogens and the mechanisms by which resident cells of the CNS perceive intracellular microbes have not been defined.  Members of the nucleotide-binding oligomerization domain-like receptor (NLR) and retinoic acid-inducible gene I-like receptor (RLR) families of proteins have recently been described and are reported to act as intracellular specific pattern recognition receptors for bacterial and viral motifs, respectively. Our central hypothesis is that NLR and RLR molecules represent important mechanisms underlying the initiation and/or maintenance of immune responses during bacterial CNS challenge or neurotropic viral infection.

Current Project Support:

NIH R03 NS057434 ""Novel intracellular pattern recognition receptor expression by resident CNS cells", Ian Marriott, PI, 06/01/07-05/31/09.

Recent Publications:

Chauhan^, V.S., Sterka, D.G., Jr., Furr^, S.R., Young, A.B., and Marriott^, I.  NOD2 plays an important role in the inflammatory responses of microglia and astrocytes to bacterial CNS pathogens.  Glia.  In Press.

Furr, S.R., Chauhan, V.S., Sterka, D.G. Jr., Grdzelishvili, V., and Marriott, I.  Characterization of retinoic acid-inducible gene-I expression in primary murine glia following exposure to VSV.  J. Neurovirol.  In Press.

3. The role of gender and reproductive status in innate immune responses to microbial pathogens

Gender has long been known to be a contributory factor in the incidence and progression of disorders associated with immune system dysregulation. More recently, evidence has accumulated that gender may also play an important role in infectious disease susceptibility. In general, females generate more robust and potentially protective humoral and cell-mediated immune responses following antigenic challenge than their male counterparts. In contrast, males have frequently been observed to mount more aggressive and damaging inflammatory immune responses to microbial stimuli. In collaboration with Dr. Yvette Huet-Hudson, we have recently begun to investigate the molecular mechanisms underlying gender-based differences observed in conditions such as bacterial sepsis. We have shown that male and female-derived macrophages differ significantly in their level of expression of critical host pattern recognition receptors for gram-negative bacteria derived LPS.  Furthermore, we have described the ability of the male reproductive hormone, testosterone, to directly influence expression of the LPS receptor TLR4 on macrophages both in vivo and in vitro.  Studies to assess the in vivo and in vitro effect of estrogen on microbial pattern receptor expression and function are currently ongoing in our laboratory.

Recent Publications:

Rettew, J.A., Huet-Hudson, Y.M., and Marriott, I.  (2008).  Testosterone reduces macrophage expression of Toll-like receptor 4, a trigger for inflammation and innate immunity.  Biol. Reprod. 78: 432-437.

4. The role of bone-forming osteoblasts in bacterially-induced inflammatory bone diseases

The initiation of immune responses in bone infections, such as osteomyelitis, is not well understood even though such infections are difficult to treat and recurrent infections often occur. In collaboration with Dr. Michael Hudson, we have investigated the ability of osteoblasts to initiate an immune response following infection with Staphylococcus aureus. Results of these studies suggest an unappreciated ability of osteoblasts to contribute to an inflammatory response following such infection. Such responses could be protective and limit infection, however we are also exploring the possibility that activated osteoblasts may contribute to the inflammation and bone destruction associated with Staphylococcus infections.

Recent Publications:

Marriott, I., Miller, J.R., and Sahraei, M.  (2007).  Therapeutic strategies against the inflammation and bone loss associated with osteomyelitis.  Curr. Opin. Investig. Drugs.  8: 887-899.

McCall, S.H, Sahraei, M., Young, A.B., Worley, C.S., Duncan, J.A., Ting, J.P. and Marriott, I.  (2008).  Osteoblasts express NLRP3, a nucleotide-binding domain and leucine-rich repeat region containing receptor implicated in bacterially induced cell death.  J. Bone. Min. Res.  23: 30-40.

CURRENT LAB MEMBERS

• Vinita Singh Chauhan, Ph.D.

• Amy Young, M.S.

• Jennifer Rettew, M.S.

• Mahnaz Sahraei ManuouchehrAbadi, M.S.

• David Sterka