Robert Lochhead, PhD
Assistant Professor; Secondary Faculty in Medicine (Rheumatology)
- Arthritis, Rheumatoid
- Borrelia burgdorferi
- Disease Models, Animal
- Endothelial Cells
- Gene Expression Regulation
- Host-Pathogen Interactions
- Lyme Disease
MCW Program / Core Facilities
- Center for Infectious Disease Research
Lyme disease, caused by infection with the tick-borne pathogen Borrelia burgdorferi, is the most common vector-borne disease in the U.S., and is reaching epidemic levels in many regions, including the Upper Midwest. Lyme disease is an infection-induced multisystem disorder affecting skin (erythema migrans), heart (carditis), joints (arthritis) or neurologic tissue (neuroborreliosis) (Fig. 1). Although most patients are effectively treated with antibiotics, 10-20% of treated patients develop post-treatment Lyme disease syndromes, potentially resulting in months or years of disability. Identifying immune factors that contribute to variability in disease severity and treatment outcome is critically important for public health in Lyme-endemic communities such as Wisconsin.
Our basic research project focuses on elucidating cellular mechanisms of murine Lyme arthritis and Lyme carditis pathogenesis. Whereas some strains of mice appropriately regulate this inflammatory response to B. burgdorferi and develop mild disease, others fail to appropriately regulate immune responses and develop severe Lyme arthritis or Lyme carditis. We use this animal system as a model of infection-induced immune dysregulation by comparing strains of mice with different disease outcomes to effectively elucidate mechanisms Lyme disease pathogenesis in ways not possible in human patients.
Our translational research project involves working with clinicians to collect and analyze samples from patients with Lyme disease and other related inflammatory diseases here in Wisconsin. Many autoimmune and clinical features of post-infectious Lyme arthritis, the most common post-treatment syndrome, are similar to that seen in rheumatoid arthritis (Fig. 2), an autoimmune joint disease that may be triggered by oral or gut microbial infections. By using Lyme disease as a model of infection-induced autoimmunity, we may gain valuable insight into mechanisms of how infections may contribute to development of other autoimmune joint diseases.
Dr. Robert Lochhead and members of the Lochhead Lab at the Medical College of Wisconsin fully endorse the new guidelines for Prevention, Diagnosis, and Treatment of Lyme disease, proposed by the Infectious Diseases Society of America (IDSA), the American College of Rheumatology (ACR), and the American Academy of Neurology (AAN). The guidelines are well-grounded in decades of basic, translational, and clinical research from various perspectives, with a focus on improving patient health. They also highlight existing challenges in the field of Lyme disease and other tick-borne disease research and clinical care. In particular, we were very pleased by the updated treatment guidelines, discussion of co-infections, inclusion of modified two-tiered antibody test, and addressing controversial issues surrounding Lyme disease in an evidence-based manner. We believe these guidelines will help the biomedical community generate new, clinically relevant research that will fill existing gaps in our understanding of, and treatment of, Lyme disease and other tickborne diseases. We appreciate the work of the authors and strongly encourage all healthcare providers and patient advocacy groups to adhere to and support these guidelines.
(Jutras BL, Lochhead RB, Kloos ZA, Biboy J, Strle K, Booth CJ, Govers SK, Gray J, Schumann P, Vollmer W, Bockenstedt LK, Steere AC, Jacobs-Wagner C.) Proc Natl Acad Sci U S A. 2019 07 02;116(27):13498-13507 PMID: 31209025 PMCID: PMC6613144 SCOPUS ID: 2-s2.0-85068263050 06/19/2019
(Lochhead RB, Ordoñez D, Arvikar SL, Aversa JM, Oh LS, Heyworth B, Sadreyev R, Steere AC, Strle K.) Cell Microbiol. 2019 02;21(2):e12992 PMID: 30550623 PMCID: PMC6336510 SCOPUS ID: 2-s2.0-85059527799 12/15/2018
(Lochhead RB, Arvikar SL, Aversa JM, Sadreyev RI, Strle K, Steere AC.) Cell Microbiol. 2019 02;21(2):e12954 PMID: 30218476 PMCID: PMC6724218 SCOPUS ID: 2-s2.0-85055262062 09/16/2018
(Sulka KB, Strle K, Crowley JT, Lochhead RB, Anthony R, Steere AC.) Arthritis Rheumatol. 2018 11;70(11):1835-1846 PMID: 29790305 PMCID: PMC6203610 SCOPUS ID: 2-s2.0-85053733387 05/24/2018
(Lochhead RB, Strle K, Kim ND, Kohler MJ, Arvikar SL, Aversa JM, Steere AC.) Arthritis Rheumatol. 2017 05;69(5):1100-1110 PMID: 28076897 PMCID: PMC5406251 SCOPUS ID: 2-s2.0-85018719753 01/12/2017
(Lochhead RB, Zachary JF, Dalla Rosa L, Ma Y, Weis JH, O'Connell RM, Weis JJ.) PLoS One. 2015;10(8):e0135142 PMID: 26252010 PMCID: PMC4529177 SCOPUS ID: 2-s2.0-84941978921 08/08/2015
(Ma Y, Bramwell KK, Lochhead RB, Paquette JK, Zachary JF, Weis JH, Teuscher C, Weis JJ.) J Immunol. 2014 Dec 15;193(12):6050-60 PMID: 25378596 PMCID: PMC4258437 SCOPUS ID: 2-s2.0-84916898548 11/08/2014
(Lochhead RB, Ma Y, Zachary JF, Baltimore D, Zhao JL, Weis JH, O'Connell RM, Weis JJ.) PLoS Pathog. 2014 Jun;10(6):e1004212 PMID: 24967703 PMCID: PMC4072785 SCOPUS ID: 2-s2.0-84903484100 06/27/2014
(Lochhead RB, Sonderegger FL, Ma Y, Brewster JE, Cornwall D, Maylor-Hagen H, Miller JC, Zachary JF, Weis JH, Weis JJ.) J Immunol. 2012 Sep 01;189(5):2488-501 PMID: 22851707 PMCID: PMC3424307 SCOPUS ID: 2-s2.0-84865441928 08/02/2012
(Pontes MH, Babst M, Lochhead R, Oakeson K, Smith K, Dale C.) PLoS One. 2008;3(10):e3541 PMID: 18958153 PMCID: PMC2568817 SCOPUS ID: 2-s2.0-56149106746 10/30/2008