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Follistatin-like protein 1 is a critical mediator of experimental Lyme arthritis and the humoral response to Borrelia burgdorferi infection.
Microb Pathog. 2014 Aug; 73:70-9.MP

Abstract

Follistatin-like protein 1 (FSTL-1) has recently been described as a critical mediator of CIA and a marker of disease activity. Lyme arthritis, caused by Borrelia burgdorferi, shares similarities with autoimmune arthritis and the experimental murine model collagen-induced arthritis (CIA). Because FSTL-1 is important in CIA and autoimmune arthritides, and Lyme arthritis shares similarities with CIA, we hypothesized that FSTL-1 may be an important mediator of Lyme arthritis. We demonstrate for the first time that FSTL-1 is induced by B. burgdorferi infection and is required for the development of Lyme arthritis in a murine model, utilizing a gene insertion to generate FSTL-1 hypomorphic mice. Using qPCR and qRT-PCR, we found that despite similar early infectious burden, FSTL-1 hypomorphic mice have improved spirochetal clearance in the face of attenuated arthritis and inflammatory cytokine production. Further, FSTL-1 mediates pathogen-specific antibody production and antigen recognition when assessed by ELISA and one- and two-dimensional immunoblotting. This study is the first to describe a role for FSTL-1 in the development of Lyme arthritis and anti-Borrelia response, and the first to demonstrate a role for FSTL-1 in response to infection, highlighting the potential for FSTL-1 as a target in the treatment of B. burgdorferi infection.

Authors+Show Affiliations

Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pathology, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.Department of Pediatrics, University of Pittsburgh School of Medicine, 4401 Penn Avenue, Pittsburgh, PA 15224, USA. Electronic address: nowaaj@chp.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24768929

Citation

Campfield, Brian T., et al. "Follistatin-like Protein 1 Is a Critical Mediator of Experimental Lyme Arthritis and the Humoral Response to Borrelia Burgdorferi Infection." Microbial Pathogenesis, vol. 73, 2014, pp. 70-9.
Campfield BT, Nolder CL, Marinov A, et al. Follistatin-like protein 1 is a critical mediator of experimental Lyme arthritis and the humoral response to Borrelia burgdorferi infection. Microb Pathog. 2014;73:70-9.
Campfield, B. T., Nolder, C. L., Marinov, A., Bushnell, D., Davis, A., Spychala, C., Hirsch, R., & Nowalk, A. J. (2014). Follistatin-like protein 1 is a critical mediator of experimental Lyme arthritis and the humoral response to Borrelia burgdorferi infection. Microbial Pathogenesis, 73, 70-9. https://doi.org/10.1016/j.micpath.2014.04.005
Campfield BT, et al. Follistatin-like Protein 1 Is a Critical Mediator of Experimental Lyme Arthritis and the Humoral Response to Borrelia Burgdorferi Infection. Microb Pathog. 2014;73:70-9. PubMed PMID: 24768929.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Follistatin-like protein 1 is a critical mediator of experimental Lyme arthritis and the humoral response to Borrelia burgdorferi infection. AU - Campfield,Brian T, AU - Nolder,Christi L, AU - Marinov,Anthony, AU - Bushnell,Daniel, AU - Davis,Amy, AU - Spychala,Caressa, AU - Hirsch,Raphael, AU - Nowalk,Andrew J, Y1 - 2014/04/24/ PY - 2013/11/11/received PY - 2014/04/10/revised PY - 2014/04/15/accepted PY - 2014/4/29/entrez PY - 2014/4/29/pubmed PY - 2015/3/31/medline KW - Arthritis KW - Borrelia burgdorferi KW - FSTL-1 KW - Lyme disease KW - Mouse model KW - humoral immunity SP - 70 EP - 9 JF - Microbial pathogenesis JO - Microb. Pathog. VL - 73 N2 - Follistatin-like protein 1 (FSTL-1) has recently been described as a critical mediator of CIA and a marker of disease activity. Lyme arthritis, caused by Borrelia burgdorferi, shares similarities with autoimmune arthritis and the experimental murine model collagen-induced arthritis (CIA). Because FSTL-1 is important in CIA and autoimmune arthritides, and Lyme arthritis shares similarities with CIA, we hypothesized that FSTL-1 may be an important mediator of Lyme arthritis. We demonstrate for the first time that FSTL-1 is induced by B. burgdorferi infection and is required for the development of Lyme arthritis in a murine model, utilizing a gene insertion to generate FSTL-1 hypomorphic mice. Using qPCR and qRT-PCR, we found that despite similar early infectious burden, FSTL-1 hypomorphic mice have improved spirochetal clearance in the face of attenuated arthritis and inflammatory cytokine production. Further, FSTL-1 mediates pathogen-specific antibody production and antigen recognition when assessed by ELISA and one- and two-dimensional immunoblotting. This study is the first to describe a role for FSTL-1 in the development of Lyme arthritis and anti-Borrelia response, and the first to demonstrate a role for FSTL-1 in response to infection, highlighting the potential for FSTL-1 as a target in the treatment of B. burgdorferi infection. SN - 1096-1208 UR - https://www.unboundmedicine.com/medline/citation/24768929/Follistatin_like_protein_1_is_a_critical_mediator_of_experimental_Lyme_arthritis_and_the_humoral_response_to_Borrelia_burgdorferi_infection_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0882-4010(14)00056-4 DB - PRIME DP - Unbound Medicine ER -