Ian Marriott

ACADEMIC DEGREES

• D., Physiology, (1996). Tulane University School of Medicine
• S., Physiology, (1994). Tulane University School of Medicine
• Sc. Honors, Biological Sciences (Physiology), (1989). University of Birmingham, UK.

COURSES TAUGHT

• Biology 4251/5251: Immunology
• Biology 6103/8103: Immunology of Infection

POSITIONS AND HONORS

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 University

1998: Leah Seidman Schaffer Award for Excellence in Postdoctoral Research, Tulane University

1998: Chancellor’s Award for Excellence in Research by a Postdoctoral Fellow, Tulane University

1998-2000: Research Assistant Professor, Department of Biology, UNC Charlotte

1999-present: Regular Member, American Association of Immunologists

2000-2004: Assistant Professor, Department of Biology, UNC Charlotte

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

2002-2006: Editorial Board Member, Journal of Immunology

2003: American Association of Immunologists Junior Faculty Travel Award.

2004-2008: Associate Professor, Department of Biology, Univ. North Carolina at Charlotte, NC

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

2011-present: Editor-in-Chief, Frontiers in Microbial Immunology

2012-2013: Chair, College Faculty Development Awards Committee, UNCC

2013: Chair, Departmental Chair Comprehensive Review Committee, UNCC

2013-2014: Chair, Biology Departmental Review Committee, UNCC

2013-2014: Vice-Chair, College Review Committee, UNCC

2016-present: Chartered Member, NIH CSR Brain Disorders and Clinical Neuroscience (CNBT) study section

2016-present: Vice Chair for Research, Department of Biological Sciences

2017: UNCC College of Liberal Arts and Sciences Award for the Integration of Undergraduate Teaching and Research

2017-present: Writing Coach, “Catalyst” College Professional Development and Mentoring Program

RESEARCH PROJECTS

The role of the neuropeptide substance P in microbe-induced CNS inflammation

Substance P, mediates a variety of biological effects via high affinity receptors for this neuropeptide (termed neurokinin-1 receptors: NK-1R). As such, NK-1R antagonists have been subjected to extensive research for use in the treatment of a variety of disease conditions, and several of these agents have recently been introduced clinically to prevent nausea and vomiting. Importantly, our laboratory has assembled a compelling body of evidence indicating that substance P/NK-1R interactions exacerbate inflammation at mucosal sites and within the CNS. In addition to its effects on leukocytes, we have demonstrated that substance P exacerbates the inflammatory responses of resident brain cells including microglia and astrocytes to clinically relevant bacterial pathogens. Furthermore, we have also shown that endogenous substance P/NK-1R interactions are required for maximal inflammation and CNS damage in murine models of meningitis. Interestingly, our data indicate that prophylactic or therapeutic systemic administration of an NK-1R antagonist can markedly attenuate bacterially-induced neuroinflammation in animal models. As such, these data suggest that the NK-1R may represent an important new target in the treatment of potentially lethal CNS inflammation.

Recent Publications:

• Johnson, M.B., Young, A.D., and Marriott, I. (2017).  The therapeutic potential of targeting substance P/NK-1R interactions in inflammatory CNS disorders. Cell. Neurosci.  10: 296.
• Martinez, A.N., Burmeister, A.R., Ramesh, G., Doyle-Meyers, L., Marriott, I., and Philipp, M.T. (2017).   Aprepitant limits in vivo neuroinflammatory responses in a rhesus model of Lyme neuroborreliosis.  Neuroinflamm. 14: 37.
• Burmeister, A.R., Johnson, M.B., Chauhan, V.S., Moerdyk-Schauwecker, M., Young, A.D., Cooley, I.D., Martinez, A.N., Ramesh, G., Philipp, M.T., and Marriott, I. (2017).  Human microglia and astrocytes constitutively express the neurokinin-1 receptor and functionally respond to substance P.  Neuroinflamm. 14: 245.

Glia utilize cell surface and cytosolic innate immune receptors to recognize microbial and viral pathogens

Glial cells such as microglia and astrocytes are increasingly recognized to play a critical role in the initiation, progression, and/or maintenance of inflammatory host responses to CNS pathogens. Our laboratory has been at the forefront in the study of the mechanisms by which these cells perceive viral and bacterial pathogens.  The innate immune system recognizes a wide spectrum of pathogens without the need for prior exposure and the identification of highly conserved families of proteins that serve as microbial pattern recognition receptors including the Toll-like (TLR), nucleotide-binding oligomerization domain-like (NLR), and retinoic acid inducible gene-I-like (RLR) receptors has shed light on the mechanisms by which this is accomplished. These microbial sensors precipitate the production of inflammatory cytokines and antiviral type I interferons. Hence, activation of cells in this manner can initiate the repertoire of defense mechanisms used by the innate immune system.  We have shown that microglia and astrocytes express cell surface TLRs and use cytosolic sensors for the detection of intracellular pathogens that include NOD2, an intracellular receptor for bacterial peptidoglycans, and two members of the RLR family, RIG-I and MDA5, that serve as cytosolic sensors for replicative RNA viruses.  Furthermore, we have subsequently described the expression of two cytosolic sensors for double-stranded DNA by glia, DNA-dependent activator of interferon-regulatory factors (DAI) and cyclic GMP-AMP synthase (cGAS), suggesting that these novel sensors might play a critical role in the detection of replicative DNA viruses by CNS cells.

Current Project Support:

1R03 NS097840  PI: Marriott, 03/01/17-02/28/20 “Role of DAI in viral CNS infection: A pilot study”

Recent Publications:

• Crill, E.K., Furr-Rogers, S.R., and Marriott, I. (2015). RIG-I is required for VSV-induced cytokine production by murine glia and acts in combination with DAI to initiate responses to HSV-1. Glia.63: 2168-2180.
• Jeffries, A.M., and Marriott, I. (2017).  Human microglia and astrocytes express cGAS-STING viral sensing components.  Neurosci Lett. 658: 53-56.
• Park, J., Wetzel, I., Marriott, I., Dréau, D., Luisa, Q., Kim, D.Y., Tanzi, R.E., Cho, H. (2018).  Neuron-glia interactions recapitulated in a 3D organotypic human Alzheimer’s disease brain model.  Nature Neurosci. 21: 941-951.

CURRENT LAB MEMBERS

Brittany Johnson, Ph.D.

Austin Jeffries, Ph.D. Candidate

Alexander Suptela, Graduate Student