Author/Editor		Shin, Junghee J; Strle, Klemen; Glickstein, Lisa J; Luster, Andrew D; Steere, Allen C
Title		Borrelia burgdorferi stimulation of chemokine secretion by cells of monocyte lineage in patients with Lyme arthritis
Type		članek
Source		Arthritis Res Ther
Vol. and No.		Letnik 12, št. 5
Publication year		2010
Volume		str. R168
Language		eng
Abstract		Introduction: Joint fluid in patients with Lyme arthritis often contains high levels of CCL4 and CCL2, which are chemoattractants for monocytes and some T cells, and CXCL9 and CXCL10, which are chemoattractants for CD4+ and CD8+ T effector cells. These chemokines are produced primarily by cells of monocyte lineage in TH1-type immune responses. Our goal was to begin to learn how infection with Borrelia burgdorferi leads to the secretion of these chemokines, using patient cell samples. We hypothesized that B. burgdorferi stimulates chemokine secretion from monocytes/macrophages in multiple ways, thereby linking innate and adaptive immune responses. Methods: Peripheral blood mononuclear cells (PBMC) from 24 Lyme arthritis patients were stimulated with B. burgdorferi, interferon (IFN)-gamma, or both, and the levels of CCL4, CCL2, CXCL9 and CXCL10 were measured in culture supernatants. CD14+ monocytes/macrophages from PBMC and synovial fluid mononuclear cells (SFMC) were stimulated in the same way, using available samples. CXCR3, the receptor for CXCL9 and CXCL10, and CCR5, the receptor for CCL4, were assessed on T cells from PBMC and SFMC. Results: In patients with Lyme arthritis, B. burgdorferi but not IFN-gamma induced PBMC to secrete CCL4 and CCL2, and B. burgdorferi and IFN-gamma each stimulated the production of CXCL9 and CXCL10. However, with the CD14+ cell fraction, B. burgdorferi alone stimulated the secretion of CCL4; B. burgdorferi and IFN-gamma together induced CCL2 secretion, and IFN-gamma alone stimulated the secretion of CXCL9 and CXCL10. The percentage of T cells expressing CXCR3 or CCR5 was significantly greater in SFMC than PBMC, confirming that TH1 effector cells were recruited to inflamed joints. However, when stimulated with B. burgdorferi or IFN-gamma, SFMC and PBMC responded similarly. (Abstract truncated at 2000 characters)
Descriptors		CELL LINEAGE LYME DISEASE BORRELIA BURGDORFERI ARTHRITIS, INFECTIOUS CHEMOKINES ANTIGENS, CD14 CELL SEPARATION FLOW CYTOMETRY MACROPHAGE ACTIVATION MACROPHAGES LEUKOCYTES, MONONUCLEAR ERYTHEMA CHRONICUM MIGRANS SYNOVIAL FLUID POLYMERASE CHAIN REACTION