||The Li laboratory utilizes molecular and cellular tools and animal models to study bacterial pathogenesis. A current focus of the laboratory is on Borrelia burgdorferi, a bacterium that causes Lyme disease, the most common vector-borne illness in the northern hemisphere. The laboratory’s main objectives in this research area are (i) to dissect the molecular mechanisms employed by the spirochete to persist in nature in an infectious cycle that involves a tick vector and a vertebrate host, and (ii) to identify both bacterial and host factors that contribute to the pathogenesis of Lyme disease, particularly to the development of Lyme arthritis. Findings from this research project can lead to the discovery of new venues for better prevention and treatment of the Lyme disease.
Work in the Li laboratory is currently supported by an R01 grant from NIAID.
|Training + Education
University of Maryland School of Medicine; Yale University School of Medicine
||View Accepted Insurances at Tufts MC + Floating Hospital
Wang P, Glowacki MN, Hoet AE, Needham GR, Smith KA, Gary RE, Li X. Emergence of Ixodes scapularis and Borrelia burgdorferi, the Lyme disease vector and agent, in Ohio. Frontiers in Cellular and Infection Microbiology 2014; 4:70. doi: 10.3389/fcimb.2014.00070. PMCID: PMC4044495
Wang P, Cheng Z, Zianni MR, Dadhwal P, Rikihisa Y, Liang FT, Li X. Borrelia burgdorferi oxidative stress regulator BosR directly represses lipoproteins primarily expressed in the tick during mammalian infection. Molecular Microbiology 2013; 89:1140-1153. PMCID: PMC3772987
Li X, Strle K, Wang P, Acosta DI, McHugh GA, Sikand N, Strle F, Steere AC. Tick-specific Borrelial antigens appear to be up-regulated in American but not European patients with Lyme arthritis, a late manifestation of Lyme borreliosis. Journal of Infectious Diseases. 2013; 208:934-941. PMCID: PMC3749008
Petnicki-Ocwieja T, Chung E, Acosta DI, Ramos LT, Shin OS, Ghosh S, Kobzik, Li X, Hu LT. TRIF mediates Toll-like receptor 2-dependent inflammatory responses to Borrelia burgdorferi. Infection and Immunity 2013; 81:402-410. PMCID: PMC3553797
Wang P, Lutton A, Olesik J, Vali H, Li X. A novel iron- and copper-binding protein in the Lyme disease spirochete. Molecular Microbiology 2012; 86:1441-1451.
Miura K, Matsuo J, Rahman MA, Kumagai Y, Li X, Rikihisa Y. Ehrlichia chaffeensis induces monocyte inflammatory responses through MyD88, ERK, and NF-B but not through TRIF, interleukin-1 receptor 1 (IL-1R1)/IL-18R1, or toll-like receptors. Infection and Immunity 2011; 79:4947-4956. PMCID: PMC3232640
Li X, McHugh G, Damle N, Sikand VK, Glickstein L, Steere AC. Burden and viability of Borrelia burgdorferi in skin and joints of patients with erythema migrans or Lyme arthritis. Arthritis and Rheumatism 2011; 63:2238-2247.
Strle K, Jones K, Drouin EE, Li X, Steere AC. Borrelia burgdorferi RST1 (OspC Type A) genotype is associated with greater inflammation and more severe Lyme disease. The American Journal of Pathology 2011; 178:2726-2739. PMCID: PMC3123987
Shen S, Shin JJ, Strle K, McHugh G, Li X, Glickstein LJ, Drouin EE, Steere AC. Treg cell numbers and function in patients with antibiotic-refractory or antibiotic-responsive Lyme arthritis. Arthritis and Rheumatism 2010; 62:2127-37. PMCID: PMC2913315
Pal U, Dai J, Li X, Neelakanta G, Luo P, Kumar M, Wang P, Yang X, Anderson JF, Fikrig E. A differential role for BB0365 in the persistence of Borrelia burgdorferi in mice and ticks. Journal of Infectious Diseases. 2008; 197:148-55
Li X*, Neelakanta G*, Liu X*, Beck DS, Kantor FS, Fish D, Anderson JF, Fikrig E. Role of outer surface protein D in the Borrelia burgdorferi life cycle. Infection and Immunity 2007; 75:4237-4244. PMCID: PMC1951184 (*equal contribution)
Neelakanta G*, Li X*, Pal U, Liu X, Beck DS, DePonte K, Fish D, Kantor FS, Fikrig E. Outer surface protein B is critical for Borrelia burgdorferi adherence and survival within Ixodes ticks. PLoS Pathogens 2007; 3:e33. PMCID: PMC1817655 (*equal contribution)
Li X, Pal U, Ramamoorthi N, Liu X, Desrosiers DC, Eggers CH, Anderson JF, Radolf JD, Fikrig E. The Lyme disease agent Borrelia burgdorferi requires BB0690, a Dps homologue, to persist within ticks. Molecular Microbiology 2007; 63:694-710
Hovius JW, Li X, Ramamoorthi N, van Dam AP, Barthold SW, van der Poll T, Speelman P, Fikrig E. Coinfection with Borrelia burgdorferi sensu stricto and Borrelia garinii alters the course of murine Lyme borreliosis. FEMS Immunology and Medical Microbiology 2007; 49:224-234.
Li X, Liu X, Beck DS, Kantor FS, Fikrig E. Borrelia burgdorferi lacking BBK32, a fibronectin-binding protein, retains full pathogenicity. Infection and Immunity 2006; 74:3305-3313. PMCID: PMC1479267
Xin Li is an Assistant Professor of Medicine at Tufts Medical Center. Dr. Li received her B.S. in Microbiology from Fudan University in China and her PhD in Molecular and Cell Biology from the University of Maryland School of Medicine where she completed her PhD dissertation under the guidance of Dr. Harry Mobley. It is during her postdoctoral training in the laboratory of Dr. Erol Fikrig at Yale University School of Medicine when Dr. Li entered the field of Lyme Disease research, which has remained an investigative focus of her current laboratory. Prior to joining Tufts Medical Center, Dr. Li was an Instructor in Medicine at Harvard Medical School and then an Assistant Professor at the Ohio State University.
Email: Xin Li