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Interferon (IFN)-? is present in lesions of patients with
Lyme disease and positively correlates with the severity of manifestations. To investigate the role of IFN? in the development of
Lyme carditis, wild-type and IFN?-deficient C57BL/6 mice were infected with the causative bacterium, Borrelia burgdorferi. Histological analysis revealed no change in the severity of carditis between wild-type and IFN?-deficient mice at 14, 21, 25, and 28 days after infection. However, a distinct shift in the types of leukocytes within the hearts of IFN?-deficient mice was observed at 25 days. In the absence of IFN?, the number of neutrophils in the heart was increased, whereas the number of T lymphocytes was decreased. Bacterial loads within hearts were the same as in wild-type mice. Macrophages secrete chemokines that recruit immune cells, which could contribute to the accumulation of leukocytes in murine
Lyme carditis. The ability of IFN? and B. burgdorferi to activate murine macrophages was examined, and the two stimuli synergistically induced chemoattractants for mononuclear cells (ie, CXCL9, CXCL10, CXCL11, CXCL16, and CCL12) and decreased those for neutrophils (ie, CXCL1, CXCL2, and CXCL3). IFN? and B. burgdorferi also synergistically enhanced secretion of CXCL9 and CXCL10 by murine cardiac endothelial cells. These results indicate that IFN? influences the composition of inflammatory infiltrates in
Lyme carditis by promoting the accumulation of leukocytes associated with chronic inflammation and suppressing that of cells that typify acute inflammation.
Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.