• 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.



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



  • 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: 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
  • 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: American Association of Immunologists Junior Faculty Travel Award.
  • 2006-2008: Coordinator, M.S. Program in Biology, UNC Charlotte.
  • 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
  • 2011-2013: College Faculty Development Awards Committee, UNCC
  • 2012-2014: College Review Committee, UNCC
  • 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
  • 2015-present: Department of Biological Sciences Diversity Liaison
  • Chief Editor: Frontiers in Microbial Immunology (2011-present).
  • Editorial board memberships: Journal of Immunology (2002-2006), Current Immunology Reviews (2004-present), Immunopharmacology and Immunotoxicology (2007-present)
  • Membership in Professional Societies: American Association of Immunologists
  • NIH Study Section Assignments: NCCAM Special Emphasis Panel, ZAT1 DB-17, “Botanicals Centers”, (2004). NCCAM Special Emphasis Panels, ZAT1 DB-18, 19, 21, 22, 26, 27, 28, and 29, PK-01, 02, 03, 05, 07, 09, and 11 “Basic and Preclinical Science”, (2005-2010). NIDCR Special Grants Review Committee, (2005). NIAMS Specialized Centers (P50s), ZAR1 MLB-G M1 1 “Centers of Research Translation”, NIAMS Special Emphasis Panels, ZRG1 MOSS-
    (05) “Orthopaedic Device-associated Immunology” (2008) and ZRG1 MOSS-A (03) (2009). NIAID Broad Agency Announcement, ZAI1-PA-I-C1, “Innate Immune Receptors and Adjuvant Discovery” (2009). NIAID Immune Mechanisms of Virus Control program “opportunity pool” (2010). NCCAM Special Emphasis Panel, ZAT1 PK-14, “Education Panel” (2010). NIH CSR Skeletal Biology Structure and Regeneration Study Section (2010,2012,2013,2014). NIH CSR Oral, Dental, Craniofacial Sciences (2012). NIAID Broad Agency Announcement, ZAI1-QV-1-C1, “Adjuvant Discovery Program” (2014). NIH CSR Brain Disorders and Clinical Neuroscience (2013,2014,2015). NIR CSR Skeletal Biology Special Emphasis Panel, ZRG1 MOSS-U(90) (2015).



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

The tachykinin, 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 postoperative and chemotherapy-induced nausea and vomiting. Importantly, our laboratory has assembled a compelling body of evidence indicating that substance P/NK-1R interactions exacerbate classical inflammation at mucosal sites and within the CNS. As such, the therapeutic targeting of the actions of SP could potentially limit neurogenic or classical inflammation. 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 including B. burgdorferi, N. meningitidis, and S. pneumoniae via the NK-1R. 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 our mouse models. As such
, these data suggest that the NK-1R may represent an important new target in the treatment of potentially lethal CNS inflammation. In collaboration with Dr. Mario Philipp at Tulane University Primate Center, we are currently performing a comprehensive preclinical evaluation of the ability of substance P to augment classical inflammation in isolated primary human CNS cells and a non-human primate model of bacterial meningitis. These studies represent an essential preclinical translational step to evaluate the therapeutic potential of NK-1R antagonists in the treatment of classical CNS inflammation.

Current Project Support:

NIH 2R01NS050325 “Substance P exacerbation of CNS inflammation”, Ian Marriott, PI, 09/30/12-05/31/17.

Recent Publications:

  • Chauhan, V.S., Kluttz, J.M., Bost, K.L., and Marriott, I. (2011). Prophylactic and therapeutic targeting of the neurokinin-1 receptor limits neuroinflammation in a murine model of pneumococcal meningitis. Immunol. 186: 7255-7263.


  1. Resident cells of the brain use cell surface and cytosolic pattern recognition receptors to recognize bacterial and viral pathogens.

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 glial 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. Microglia and astrocytes can express cell surface and endosomal TLRs. In addition, we have determined that glial cells also express cytosolic sensors for microbial motifs that may be more relevant for the detection of intracellular pathogens. For example, we described the expression by microgl
ia and astrocytes of NOD2, an intracellular receptor for bacterial peptidoglycans, and we demonstrated the essential role played by this molecule in the inflammatory responses of glia to an array of clinically relevant bacterial CNS pathogens. More recently, we discovered that glia also express two members of the RLR family, RIG-I and MDA5, that function as cytosolic sensors for replicative RNA viruses. Furthermore, we subsequently showed that RIG-I plays a critical role in the inflammatory immune responses of primary human astrocytes to a model neurotropic RNA virus. Finally, we described the expression of a cytosolic sensor for double-stranded DNA, DNA-dependent activator of interferon-regulatory factors (DAI), by murine glia. This molecule has been shown to mediate innate immune responses in murine cell lines following the intracellular administration of viral DNA and we showed that DAI expression was critical for maximal inflammatory glial responses to HSV-1 infection, suggesting that this novel cytosolic dsDNA sensor might play a critical role in the detection of replicative DNA viruses by glia.

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.
  • Cooley, I.D., Chauhan, V.S., Donneyz, M.A. and Marriott, I. (2014). Astrocytes produce IL-19 in response to bacterial challenge and are sensitive to the immunosuppressive effects of this IL-10 family member. Glia. 62: 818-828.
  • Furr, S.F. and Marriott, I. (2012). Viral CNS infections: Role of glial pattern recognition receptors in neuroinflammation. Microb. 3: 201.
  • Furr, S.R., Chauhan, V.S., Moerdyk-Schauwecker, M., and Marriott, I. (2011). ­A role for DNA-dependent activator of interferon regulatory factor in the recognition of herpes simplex virus type 1 by glial cells. Neuroinflammation. 8: 99.


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

Osteomyelitis (OM) is a severe infection of bone tissue that is associated with significant morbidity and often leads to
bone resorption, dysfunction, and progressive inflammatory destruction. The Gram-positive organism, Staphylococcus aureus, is the most common causative agent of OM. Despite improvements in prophylaxis and diagnosis this condition is often refractory to current treatment strategies and is recurrent. An explanation for these phenomena may lie in the ability of the causative agents of OM to invade and persist within resident bone cells including osteoblasts (OB). Importantly, our laboratory has demonstrated that isolated OBs utilize members of the TLR and NLR families of innate immune receptors to detect the presence of microbial products. The activation of these sensors precipitates the production of inflammatory cytokines and chemokines, and antigen presenting and co-stimulatory molecules. Consistent with this observation, our in vitro and in vivo studies show that S. aureus provides a potent stimulus for the production of soluble and cell surface molecules by isolated OBs that could play key roles in the initiation and/or progression of inflammatory immune responses, and enhance the activity of bone-resorbing osteoclasts. As such, the production of these mediators by bacterially challenged OBs may significantly contribute to involucrum and sequestrum formation during OM, and the development of damaging inflammatory host responses following infection.

Recent Publications:

  • Marriott, I. (2013). Apoptosis-associated uncoupling of bone formation and resorption in osteomyelitis. Cell. Infect. Microbiol. 3:101.
  • Young, A.B., Cooley, I.D., Chauhan, V.S., and Marriott, I. (2011). Causative agents of osteomyelitis induce death domain-containing TNF-related apoptosis-inducing ligand receptor expression on osteoblasts. Bone 48: 857-863.



Angelica N. Martins, Ph.D.

Brittany Johnson, Ph.D.

Amanda Burmeister

Austin Jeffries



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