
Holly M. Algood, Ph.D.
- Assistant Professor of Medicine (Infectious Diseases)
- Assistant Professor Pathology, Microbiology and Immunology
- Research Microbiologist
Phone
Nashville, TN 37232
Holly M. Algood, Ph.D.
- Assistant Professor of Medicine (Infectious Diseases)
- Assistant Professor Pathology, Microbiology and Immunology
- Research Microbiologist
615-343-9242
holly.m.algood@vanderbilt.edu
Nashville, TN 37232
Research Program
Departments/Affiliations
Profile
H. pylori is the most common pathogen colonizing humans today. Colonization with H. pylori can lead to detrimental outcomes including gastric adenocarcinoma, MALT lymphoma, peptic ulcer disease and atrophic gastritis. H. pylori is the only bacteria classified by the World Health Organization as a carcinogen. Yet, H. pylori’s classification as a bone fide pathogen has been questioned due to an inverse correlation between H. pylori colonization and immune-mediated diseases, such as allergic airway disease and inflammatory bowel disease. These divergent outcomes can be attributed to a number of factors including host, environment and pathogen.
My laboratory has made noteworthy contributions to understanding which host factors drive gastritis during chronic H. pylori infection. Specifically, our research has described how cytokines produced by proinflammatory T cells influence control of H. pylori colonization and gastritis. A major role of these T cells and the cytokines they produce is to recruit innate immune cells which lead to increased inflammation. Some stresses of the immune response include sequestration of nutrient metals (nutritional immunity), oxidative stress and metabolic stress. Despite the chronic immune response, H. pylori persists for the life of the host. A fundamental gap in our knowledge is how H. pylori responds to and flourishes under the pressures of the host’s immune response and how diet modifications might alter those host responses.
Education
- Mount Union College (Alliance, OH), Bachelors of Science, May 1998
- University of Pittsburgh:(Pittsburgh, PA), Doctor of Philosophy, (Molecular Virology and Microbiology Program in the School of Medicine), December 2003
- Vanderbilt University (Nashville, TN), Post-doctoral Fellow, June 2004- March 2008
Research Emphasis
Helicobacter pylori, inflammation, T lymphocytes, cytokines, bacterial pathogenesis, Th17, bacterial response, oxidative stress, host-pathogen interactions, macrophages, cancer
Research Description
Projects in Dr. Algood's lab focus on pathogen - host interactions in chronic infections and during chronic inflammation. Her main model system is Helicobacter pylori infection. Helicobacter pylori is a Gram-negative pathogen which can chronically colonize the human stomach and lead to adverse disease outcomes such as peptic ulcers or gastric cancer. Her projects investigate how T cell cytokines influence gastric epithelial cells responding to infection but also even more broadly how T cell cytokines activate other cells to protect the epithelial cells and the mucosal barrier they maintain. Dr. Algood's research utilizes H. pylori as a model mucosal pathogen, but her long-term research interests lie in understanding the balance between the mucosal immune responses, pathogens, and normal flora. While immune responses may be necessary to control bacterial colonization at the mucosal surfaces, the immune response must also be well controlled to maintain epithelial cell integrity and to control infiltration of other potentially damaging immune cells. Th17-driven immune responses have been implicated in pro-inflammatory activity and induction of chronic inflammation; she would like to better understand how the Th17 response is balanced. Moreover, since the inflammatory/immune response is not sufficient to clear the infection, Dr. Algood's laboratory is beginning studies to investigate how the bacteria persist while combated with the stresses of the immune response.
Publications
- Dale BL, Pandey AK, Chen Y, Smart CD, Laroumanie F, Ao M, Xiao L, Dikalova AE, Dikalov SI, Elijovich F, Foss JD, Barbaro NR, Van Beusecum JP, Deger SM, Alsouqi A, Itani HA, Norlander AE, Alexander MR, Zhao S, Ikizler TA, Algood HMS, Madhur MS. Critical role of Interleukin 21 and T follicular helper cells in hypertension and vascular dysfunction. JCI Insight. 2019 Apr 4/23/2019; 5: PMID: 31013256, PMCID: PMC6629096, PII: 129278, DOI: 10.1172/jci.insight.129278, ISSN: 2379-3708.
- Sutton JA, Rogers LM, Dixon BREA, Kirk L, Doster R, Algood HM, Gaddy JA, Flaherty R, Manning SD, Aronoff DM. Protein kinase D mediates inflammatory responses of human placental macrophages to Group B Streptococcus. Am. J. Reprod. Immunol [print-electronic]. 2019 Mar; 81(3): e13075. PMID: 30582878, PMCID: PMC6459189, DOI: 10.1111/aji.13075, ISSN: 1600-0897.
- Piazuelo MB, Riechelmann RP, Wilson KT, Algood HMS. Resolution of Gastric Cancer-Promoting Inflammation: A Novel Strategy for Anti-cancer Therapy. Curr. Top. Microbiol. Immunol. 2019; 421: 319-59. PMID: 31123895, PMCID: PMC6602908, DOI: 10.1007/978-3-030-15138-6_13, ISSN: 0070-217X.
- Beckett AC, Loh JT, Chopra A, Leary S, Lin AS, McDonnell WJ, Dixon BREA, Noto JM, Israel DA, Peek RM, Mallal S, Algood HMS, Cover TL. Helicobacter pylori genetic diversification in the Mongolian gerbil model. PeerJ. 2018; 6: e4803. PMID: 29796347, PMCID: PMC5961626, PII: 4803, DOI: 10.7717/peerj.4803, ISSN: 2167-8359.
- Guckes KR, Breland EJ, Zhang EW, Hanks SC, Gill NK, Algood HM, Schmitz JE, Stratton CW, Hadjifrangiskou M. Signaling by two-component system noncognate partners promotes intrinsic tolerance to polymyxin B in uropathogenic Escherichia coli. Sci Signal. 2017 Jan 1/10/2017; 10(461): PMID: 28074004, PII: 10/461/eaag1775, DOI: 10.1126/scisignal.aag1775, ISSN: 1937-9145.
- Shaffer CL, Zhang EW, Dudley AG, Dixon BR, Guckes KR, Breland EJ, Floyd KA, Casella DP, Algood HM, Clayton DB, Hadjifrangiskou M. Purine Biosynthesis Metabolically Constrains Intracellular Survival of Uropathogenic Escherichia coli. Infect. Immun [electronic-print]. 2017 Jan; 85(1): PMID: 27795353, PMCID: PMC5203662, PII: IAI.00471-16, DOI: 10.1128/IAI.00471-16, ISSN: 1098-5522.
- Varga MG, Piazuelo MB, Romero-Gallo J, Delgado AG, Suarez G, Whitaker ME, Krishna US, Patel RV, Skaar EP, Wilson KT, Algood HM, Peek RM. TLR9 activation suppresses inflammation in response to Helicobacter pylori infection. Am. J. Physiol. Gastrointest. Liver Physiol [print-electronic]. 2016 Nov 11/1/2016; 311(5): G852-G858. PMID: 27758771, PMCID: PMC5130555, PII: ajpgi.00175.2016, DOI: 10.1152/ajpgi.00175.2016, ISSN: 1522-1547.
- Beckett AC, Piazuelo MB, Noto JM, Peek RM, Washington MK, Algood HM, Cover TL. Dietary composition influences incidence of Helicobacter pylori-induced iron deficiency anemia and gastric ulceration. Infect. Immun [print-electronic]. 2016 Sep 9/12/2016; PMID: 27620719, PII: IAI.00479-16, DOI: 10.1128/IAI.00479-16, ISSN: 1098-5522.
- Beceiro S, Radin JN, Chatuvedi R, Piazuelo MB, Horvarth DJ, Cortado H, Gu Y, Dixon B, Gu C, Lange I, Koomoa DL, Wilson KT, Algood HM, Partida-Sánchez S. TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection. Mucosal Immunol [print-electronic]. 2016 Jul 7/20/2016; PMID: 27435104, PII: mi201660, DOI: 10.1038/mi.2016.60, ISSN: 1935-3456.
- Dixon BR, Radin JN, Piazuelo MB, Contreras DC, Algood HM. IL-17a and IL-22 Induce Expression of Antimicrobials in Gastrointestinal Epithelial Cells and May Contribute to Epithelial Cell Defense against Helicobacter pylori. PLoS ONE. 2016; 11(2): e0148514. PMID: 26867135, PMCID: PMC4750979, PII: PONE-D-15-33690, DOI: 10.1371/journal.pone.0148514, ISSN: 1932-6203.