cytokines – F.I.G.H.T for your health!

Reduced immune response to Lyme

Linda — Wed, 23 Nov 2011 06:21:38 +0000

Linda’s comment: We previously observed that γδ T cells in vitro are activated by Borrelia burgdorferi in a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cells in vitro to produce cytokines and chemokines that are important for the adaptive immune response.

This paralleled greater Borreli a burden in
γδ-deficient mice as well as more cardiac inflammation. These findings
are consistent with a model of γδ T cells functioning to promote the
adaptive immune response during infection.

Borrelia burgdorferi Stimulates Macrophages to Secrete Higher Levels of Cytokines

Linda — Wed, 25 Nov 2009 21:35:42 +0000

To delineate the inflammatory potential of the 3 pathogenic species of Borrelia burgdorferi sensu lato, we stimulated monocyte-derived macrophages from healthy human donors with 10 isolates each of B. burgdorferi, Borrelia afzelii, or Borrelia garinii recovered from erythema migrans skin lesions of patients with Lyme borreliosis from the United States or Slovenia. B. burgdorferi isolates from the United States induced macrophages to secrete significantly higher levels of interleukin (IL)-8, CCL3, CCL4, IL-6, IL-10, and tumor necrosis factor than B. garinii or B. afzelii isolates. Consistent with this response in cultured macrophages, chemokine and cytokine levels in serum samples of patients from whom the isolates were obtained were significantly greater in B. burgdorferi-infected patients than in B. afzelii- or B. garinii-infected patients. These results demonstrate in vitro and in vivo that B. burgdorferi has greater inflammatory potential than B. afzelii and B. garinii, which may account in part for variations in the clinical manifestations of Lyme borreliosis.

J Infect Dis. 2009 Dec 15;200(12):1936-1943.
Borrelia burgdorferi Stimulates Macrophages to Secrete Higher Levels of Cytokines and Chemokines than Borrelia afzelii or Borrelia garinii.
Strle K, Drouin EE, Shen S, Khoury JE, McHugh G, Ruzic-Sabljic E, Strle F, Steere AC.
Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, 2Infectious Diseases Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and 3Institute of Microbiology and Immunology, University of Ljubljana, 4Department of Infectious Diseases, University Medical Center Ljubljana, Ljubljana, Slovenia.

Borrelia burgdorferi & Macrophages

Linda — Mon, 16 Nov 2009 08:10:57 +0000

Klemen Strle,1
Elise E. Drouin,1
Shiqian Shen,1
Joseph El Khoury,1,2
Gail McHugh,1
Eva Ruzic‐Sabljic,3
Franc Strle,4 and
Allen C. Steere1

Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, 2Infectious Diseases Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and 3Institute of Microbiology and Immunology, University of Ljubljana, 4Department of Infectious Diseases, University Medical Center Ljubljana, Ljubljana, Slovenia

To delineate the inflammatory potential of the 3 pathogenic species of Borrelia burgdorferi sensu lato, we stimulated monocyte‐derived macrophages from healthy human donors with 10 isolates each of B. burgdorferi, Borrelia afzelii, or Borrelia garinii recovered from erythema migrans skin lesions of patients with Lyme borreliosis from the United States or Slovenia. B. burgdorferi isolates from the United States induced macrophages to secrete significantly higher levels of interleukin (IL)‐8, CCL3, CCL4, IL‐6, IL‐10, and tumor necrosis factor than B. garinii or B. afzelii isolates. Consistent with this response in cultured macrophages, chemokine and cytokine levels in serum samples of patients from whom the isolates were obtained were significantly greater in B. burgdorferi–infected patients than in B. afzelii– or B. garinii–infected patients.

These results demonstrate in vitro and in vivo that B. burgdorferi has greater inflammatory potential than B. afzelii and B. garinii, which may account in part for variations in the clinical manifestations of Lyme borreliosis.

Received 28 April 2009; accepted 6 July 2009; electronically published 12 November 2009.

Reprints or correspondence: Klemen Strle, Massachusetts General Hospital, 55 Fruit St, CNY149/8301, Boston, MA 02114 (kstrle@partners.org).

http://www.journals.uchicago.edu/doi/abs/10.1086/648091