{"id":5,"date":"2012-03-26T16:37:03","date_gmt":"2012-03-26T16:37:03","guid":{"rendered":"http:\/\/pages.charlotte.edu\/ian-marriott\/?page_id=5"},"modified":"2025-08-11T18:44:36","modified_gmt":"2025-08-11T18:44:36","slug":"home","status":"publish","type":"page","link":"https:\/\/pages.charlotte.edu\/ian-marriott\/","title":{"rendered":"Home"},"content":{"rendered":"

\"\"<\/a><\/p>\n

CONTACT ME<\/strong><\/p>\n

Phone: 704-503-1402<\/p>\n

Office: 202 Klein Hall<\/p>\n

Email: imarriot@charlotte.edu<\/p>\n

\u00a0<\/strong><\/p>\n

ACADEMIC DEGREES<\/strong><\/p>\n

Ph.D., Physiology, (1996). Tulane University School of Medicine<\/p>\n

M.S., Physiology, (1994). Tulane University School of Medicine<\/p>\n

B.Sc. Honors, Biological Sciences (Physiology), (1989). University of Birmingham, UK.<\/p>\n

\u00a0<\/strong><\/p>\n

COURSES TAUGHT<\/strong><\/p>\n

Biology 4251\/5251: Immunology<\/p>\n

Biology 6103\/8103: Immunology of Infection<\/p>\n

 <\/p>\n

POSITIONS AND HONORS<\/strong><\/p>\n

1996-1998: Research Associate, Department of Microbiology and Immunology, Tulane University School of Medicine<\/p>\n

1998: Leah Seidman Schaffer Award for Excellence in Postdoctoral Research, Tulane University School of Medicine<\/p>\n

1998: Chancellor\u2019s Award for Excellence in Research by a Postdoctoral Fellow, Tulane University School of Medicine<\/p>\n

1998-2000: Research Assistant Professor, Department of Biology, UNC Charlotte<\/p>\n

1999-present: Regular Member, American Association of Immunologists<\/p>\n

2000-2004: Assistant Professor, Department of Biology, UNC Charlotte<\/p>\n

2002-2006: Editorial Board Member, Journal of Immunology<\/p>\n

2004-2008: Associate Professor, Department of Biology, UNC Charlotte<\/p>\n

2008-present: Professor, Department of Biological Sciences, UNC Charlotte<\/p>\n

2011-present: Editor-in-Chief, Frontiers in Microbial Immunology<\/p>\n

2016-2020: Chartered Member, NIH CSR Brain Disorders and Clinical Neuroscience (CNBT) study section<\/p>\n

2016-2022: Associate Chair for Research, Department of Biological Sciences, UNC Charlotte<\/p>\n

2017: UNCC College of Liberal Arts and Sciences Award for the Integration of Undergraduate Teaching and Research<\/p>\n

2017-2021: Writing Coach, \u201cCatalyst\u201d College Professional Development and Mentoring Program<\/p>\n

2023-present: Member and Co-Focused Area Team Leader (Biomedicine) for The Center for Innovation, Translational Research, and Applications of Nanostructured Systems (CITRANS)<\/p>\n

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RESEARCH PROJECTS<\/strong><\/p>\n

    \n
  1. The role of the neuropeptide substance P in microbe-induced inflammation<\/strong><\/li>\n<\/ol>\n

    The tachykinin, substance P, mediates a variety of biological effects via high affinity receptors for this neuropeptide (termed neurokinin-1 receptors: NK-1R).\u00a0 As such, NK-1R antagonists have been subjected to extensive research for use in the treatment of a variety of disease conditions.\u00a0 Our laboratory has assembled a compelling body of evidence that substance P\/NK-1R interactions exacerbate classical inflammation at mucosal sites and within the CNS.\u00a0 We have demonstrated that macrophages and dendritic cells express NK-1R and showed that ligation of this receptor initiates the activation of the key inflammatory regulator NF-kB while inhibiting the production of the immunosuppressive cytokine TGF-beta1.\u00a0 Consistent with these effects on leukocytes, we demonstrated that substance P exacerbates the inflammatory responses of isolated brain cells, such as microglia and astrocytes, to clinically relevant bacterial pathogens including B. burgdorferi<\/em>, N. meningitidis,<\/em> and S. pneumoniae<\/em> via NK-1R.\u00a0 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.\u00a0 The translational potential of these studies is underscored by our demonstration that prophylactic or therapeutic treatment of mice with a systemically delivered NK-1R antagonist attenuates the development of bacterially induced inflammatory CNS damage, and by our collaborative work showing that such antagonists can attenuate inflammatory responses in a non-human primate model of Lyme neuroborreliosis.\u00a0 Recently, we have found that substance P can similarly exacerbate the inflammatory responses of resident bone cells to S. aureus<\/em>, the principal causative agent of osteomyelitis.\u00a0 Together, these studies suggest that NK-1R represents an important new target in the treatment of microbe-induced inflammatory damage at sites as disparate as brain and bone tissue.<\/p>\n

     <\/p>\n

    Current Project Support:<\/strong><\/p>\n

      \n
    • NIH: 1R01 AI170012 \u201cSubstance P exacerbation of staphylococcal bone damage\u201d<\/li>\n<\/ul>\n

       <\/p>\n

      Recent Publications:<\/strong><\/p>\n

        \n
      • Sipprell, S.E., Krueger, Q.A., Mills, E.L., Marriott, I., and Johnson, M.B. (2025).\u00a0 Substance P augments chemokine production by Staphylococcus aureus infected murine osteoclasts.\u00a0 Inflammation<\/em>.\u00a0 In Press.\u00a0 PMID: 40056352.<\/li>\n
      • Sipprell, S.E., and Marriott, I. (2024).\u00a0 Substance P in inflammation.\u00a0 In: Substance P: From pain to cancer (Vink, R. Ed). Elsevier. Amsterdam, Netherlands.<\/li>\n
      • Johnson, M.B., Suptela, S.R., Sipprell, S.E., and Marriott, I. (2023).\u00a0 Substance P exacerbates the inflammatory and pro-osteoclastogenic responses of murine osteoclasts and osteoblasts to Staphylococcus aureus.\u00a0 Inflammation<\/em>.\u00a0 46: 256-269.\u00a0 PMID: 36040535.<\/li>\n<\/ul>\n

         <\/p>\n

          \n
        1. The role of bone-forming osteoblasts in bacterially-induced inflammatory bone diseases<\/strong><\/li>\n<\/ol>\n

          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.\u00a0 The Gram-positive organism, Staphylococcus aureus,<\/em> is the most common causative agent of OM.\u00a0 Despite improvements in prophylaxis and diagnosis, this condition is often refractory to current treatment strategies and is recurrent.\u00a0 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).\u00a0 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.\u00a0 The activation of these sensors precipitates the production of inflammatory cytokines and chemokines, and antigen presenting and co-stimulatory molecules.\u00a0 Consistent with these observations, our in vitro and in vivo studies show that S. aureus<\/em> 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. \u00a0Such production could significantly contribute to the damaging inflammation associated with OM.\u00a0 However, our recent studies indicate that resident bone cells may also produce type I interferons, mediators that can serve to restrict bacterial survival following internalization, suggesting that certain bone cell immune responses can serve a protective function during infections.<\/p>\n

          \u00a0<\/strong><\/p>\n

          Current Project Support:<\/strong><\/p>\n

            \n
          • NIH: 1R01 AI170012 \u201cSubstance P exacerbation of staphylococcal bone damage\u201d<\/li>\n
          • NIH: 1R03 AI176300 \u201cType I interferon responses of bone cells to Staphylococcus aureus<\/em>: A pilot study\u201d<\/li>\n<\/ul>\n

            \u00a0<\/strong><\/p>\n

            Recent Publications:<\/strong><\/p>\n

              \n
            • Mills, E.L., Suptela, S.R., Key, M-K., Marriott, I., and Johnson, M.B. (2025).\u00a0 RIG-I and cGAS mediate antimicrobial and inflammatory responses of primary osteoblasts and osteoclasts to Staphylococcus aureus<\/em>.\u00a0 mBio<\/em>. 16: e0397124.\u00a0 PMID: 40135931.<\/li>\n
            • Mills, E.L., Avila, Y.I., Beasock, D., Radwan, Y., Suptela, S.R., Marriott, I., Afonin, K.A., and Johnson, M.B. (2024).\u00a0 Immunostimulatory nucleic acid nanoparticles (NANPs) augment protective osteoblast and osteoclast type I interferon responses to Staphylococcus aureus<\/em>.\u00a0 Nanomedicine<\/em>.\u00a0 60: 102762. PMID: 38866196<\/li>\n
            • Sipprell, S.E., Johnson, M.B., Leach, W., Suptela, S.R., and Marriott, I. (2023).\u00a0 Staphylococcus aureus infection induces the production of the neutrophil chemoattractants CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by murine Osteoblasts.\u00a0 Infect Immun<\/em>. 91: e0001423. PMID: 36880752.<\/li>\n
            • Johnson, M.B., Furr, K.H., Suptela, S.R., Leach, W., and Marriott, I. (2022). Induction of protective interferon-beta responses in murine osteoblasts following Staphylococcus aureus infection.\u00a0 Microbiol. Immunol<\/em>.\u00a0 13: 1066237. PMID: 36532419.<\/li>\n<\/ul>\n

               <\/p>\n

                \n
              1. Resident cells of the brain use cell surface and cytosolic pattern recognition receptors to recognize bacterial and viral pathogens<\/strong><\/li>\n<\/ol>\n

                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 the innate immune system recognizes a wide array of pathogens.\u00a0 Studies from our group were among the first to demonstrate that resident brain cells (glia) express cell surface and endosomal TLRs that recognize bacterial and viral motifs.\u00a0 In addition, we determined that glial cells functionally express cytosolic sensors for bacterial and viral motifs, such as NOD2, RIG-I, and MDA5, that may be more relevant for the detection of intracellular pathogens.\u00a0 We subsequently showed that RIG-I plays a critical role in the inflammatory responses of human astrocytes to neurotropic RNA viruses and showed that this sensor can also mediate the detection of bacterial nucleic acids in human microglia.\u00a0 Furthermore, we described the expression of several cytosolic sensors for DNA in human and murine glia, including cGAS, IFI16, and ZBP1. \u00a0We showed that cGAS mediates, in part, human microglial responses to exogenous cytosolic DNA, while ZBP1 expression is critical for maximal inflammatory mouse glial responses to HSV-1 infection, suggesting that these novel cytosolic dsDNA sensors might play a critical role in the detection of replicative DNA viruses by glia. \u00a0More recently, we identified a broader role for such intracellular nucleic acid sensors in glial cells, with the demonstration that cGAS can mediate glial responses to the abnormal presence of self-DNA in the cytosol following damage resulting from oxidative stress or radiation.<\/p>\n

                \u00a0<\/strong><\/p>\n

                Current Project Support:<\/strong><\/p>\n

                  \n
                • NIH: 1R21 AI193539 \u201cTherapeutic potential of targeting glia as an inflammatory mediator source and bacterial reservoir\u201d<\/li>\n<\/ul>\n

                  \u00a0<\/strong><\/p>\n

                  Recent Publications:<\/strong><\/p>\n

                    \n
                  • Suptela, A.J., Radwan, Y., Richardson, C., Yan, S., Afonin, K.A., and Marriott, I. (2024).\u00a0 cGAS mediates the\u00a0inflammatory\u00a0responses of human microglial cells to genotoxic DNA damage.\u00a0 Inflammation<\/em>.\u00a0 47:<\/strong> 822-836.\u00a0 PMID: 38148453.<\/li>\n
                  • Suptela, A.J., and Marriott, I. (2023).\u00a0 Cytosolic DNA sensors and glial responses to endogenous DNA.\u00a0 Immunol<\/em>. 14:<\/strong>1130172. PMID: 36999037.<\/li>\n
                  • Jeffries, A.M., Suptela, A.J., and Marriott, I. (2022).\u00a0 Z-DNA binding protein 1 mediates necroptotic and apoptotic cell death pathways in murine astrocytes following herpes simplex virus-1 infection. Neuroinflamm. <\/em>19:<\/strong>109. PMID: 35549723.<\/li>\n<\/ul>\n

                     <\/p>\n

                    CURRENT LAB MEMBERS<\/strong><\/p>\n

                    Dr. Quinton Krueger, Postdoctoral Fellow<\/p>\n

                    Andrew Dunphy, PhD Candidate<\/p>\n

                    Elizabeth Hall, Graduate Student<\/p>\n

                    Ayanna Blake, Honors Student<\/p>\n

                    Temmy Ogunsakin, Honors Student<\/p>\n

                     <\/p>\n","protected":false},"excerpt":{"rendered":"

                    CONTACT ME Phone: 704-503-1402 Office: 202 Klein Hall Email: imarriot@charlotte.edu \u00a0 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. \u00a0 COURSES TAUGHT Biology 4251\/5251: Immunology Biology 6103\/8103: Immunology of Infection   POSITIONS AND HONORS 1996-1998: […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"open","ping_status":"open","template":"","meta":{"jetpack_post_was_ever_published":false,"footnotes":""},"class_list":["post-5","page","type-page","status-publish","hentry"],"jetpack_shortlink":"https:\/\/wp.me\/P2le8v-5","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/pages\/5","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/comments?post=5"}],"version-history":[{"count":13,"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/pages\/5\/revisions"}],"predecessor-version":[{"id":51,"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/pages\/5\/revisions\/51"}],"wp:attachment":[{"href":"https:\/\/pages.charlotte.edu\/ian-marriott\/wp-json\/wp\/v2\/media?parent=5"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}