Research Areas

The Lochhead Lab focuses on mechanisms of arthritis pathogenesis, using animal models of Lyme arthritis and clinical samples collected from patients with various types of arthritis. Much of our research focuses on Lyme disease, caused by infection with the tick-borne pathogen Borrelia burgdorferi (Bb). Lyme disease 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 multi-system disorder affecting skin (erythema migrans), heart (carditis), joints (arthritis) or neurologic tissue (neuro-borreliosis). Lyme arthritis (LA) is the most common late-stage manifestation of Lyme disease. Although most patients are effectively treated with antibiotics, 10-20% of treated patients develop post-infectious Lyme arthritis, 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. By studying LA, we hope to gain important insights into how infection may trigger immune dysregulation, leading to tissue damage, arthritis, and autoimmunity,

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Current Members

Rebecca Danner

Research Technologist III

rdanner@mcw.edu

Kristen Hansen

Research Technologist I

krhansen@mcw.edu

Amanda Wahhab

Research Technologist II

awahhab@mcw.edu

Joseph Rouse

Graduate Student

jorouse@mcw.edu

Lyme arthritis: linking infection, inflammation and autoimmunity.

(Lochhead RB, Strle K, Arvikar SL, Weis JJ, Steere AC.) Nat Rev Rheumatol. 2021 Aug;17(8):449-461 PMID: 34226730 PMCID: PMC9488587 SCOPUS ID: 2-s2.0-85109836229 07/07/2021
Lyme arthritis: linking infection, inflammation and autoimmunity

(Lochhead RB, Strle K, Arvikar SL, Weis JJ, Steere AC.) Nature Reviews Rheumatology. August 2021;17(8):449-461 SCOPUS ID: 2-s2.0-85109836229 08/01/2021
Report of the Pathogenesis and Pathophysiology of Lyme Disease Subcommittee of the HHS Tick Borne Disease Working Group.

(Donta ST, States LJ, Adams WA, Bankhead T, Baumgarth N, Embers ME, Lochhead RB, Stevenson B.) Front Med (Lausanne). 2021;8:643235 PMID: 34164410 PMCID: PMC8215209 06/25/2021
Borrelia burgdorferi peptidoglycan is a persistent antigen in patients with Lyme arthritis.

(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 Jul 02;116(27):13498-13507 PMID: 31209025 PMCID: PMC6613144 SCOPUS ID: 2-s2.0-85068263050 06/19/2019
Interferon-gamma production in Lyme arthritis synovial tissue promotes differentiation of fibroblast-like synoviocytes into immune effector cells.

(Lochhead RB, Ordoñez D, Arvikar SL, Aversa JM, Oh LS, Heyworth B, Sadreyev R, Steere AC, Strle K.) Cell Microbiol. 2019 Feb;21(2):e12992 PMID: 30550623 PMCID: PMC6336510 SCOPUS ID: 2-s2.0-85059527799 12/15/2018
Robust interferon signature and suppressed tissue repair gene expression in synovial tissue from patients with postinfectious, Borrelia burgdorferi-induced Lyme arthritis.

(Lochhead RB, Arvikar SL, Aversa JM, Sadreyev RI, Strle K, Steere AC.) Cell Microbiol. 2019 Feb;21(2):e12954 PMID: 30218476 PMCID: PMC6724218 SCOPUS ID: 2-s2.0-85055262062 09/16/2018
Correlation of Lyme Disease-Associated IgG4 Autoantibodies With Synovial Pathology in Antibiotic-Refractory Lyme Arthritis.

(Sulka KB, Strle K, Crowley JT, Lochhead RB, Anthony R, Steere AC.) Arthritis Rheumatol. 2018 Nov;70(11):1835-1846 PMID: 29790305 PMCID: PMC6203610 SCOPUS ID: 2-s2.0-85053733387 05/24/2018
MicroRNA Expression Shows Inflammatory Dysregulation and Tumor-Like Proliferative Responses in Joints of Patients With Postinfectious Lyme Arthritis.

(Lochhead RB, Strle K, Kim ND, Kohler MJ, Arvikar SL, Aversa JM, Steere AC.) Arthritis Rheumatol. 2017 May;69(5):1100-1110 PMID: 28076897 PMCID: PMC5406251 SCOPUS ID: 2-s2.0-85018719753 01/12/2017
Antagonistic Interplay between MicroRNA-155 and IL-10 during Lyme Carditis and Arthritis.

(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
Borrelia burgdorferi arthritis-associated locus Bbaa1 regulates Lyme arthritis and K/B×N serum transfer arthritis through intrinsic control of type I IFN production.

(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
MicroRNA-146a provides feedback regulation of lyme arthritis but not carditis during infection with Borrelia burgdorferi.

(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
Endothelial cells and fibroblasts amplify the arthritogenic type I IFN response in murine Lyme disease and are major sources of chemokines in Borrelia burgdorferi-infected joint tissue.

(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

Lochhead Laboratory