Pediatric Rheumatology Online Journal → August 2003 → Lyme Disease → Abstract #157

CULTURED SYNOVIAL FIBROBLASTS FROM CHILDREN WITH ANTIBIOTIC RESISTANT LYME ARTHRITIS (ARLA) RELEASE ABNORMAL LEVELS OF IL-6

C. D. Rose, L. B. Fawcett, P. T. Fawcett

¹Pediatrics, Alfred I duPont Hospital for Children, Thomas Jefferson University, Wilmington, DE, United States

ARLA is defined as LA6 mos from Abx therapy. We reported a frequency of 39% in a study from the1998-2002 cohort. Postulated mechanisms include molecular mimicry and bacterial persistence. Synovial transformation has been less explored. For this study we harvested synovial fibroblasts (SFs) from 2 children with ARLA and compared them with a normal control (resting SF). Cells were grown in DMEM supplemented with 15% calf serum. Morphologic findings will be shown. Flow cytometry and molecular techniques for mRNA expression confirmed that after several passages all cells were of non-lymphoid affiliation and actively dividing. IL-6 levels in the supernatant was used as an endpoint to assess status of activation. Cells were also exposed to PMA, rOspA and heat-killed B burgdorferi for comparison with non-stimulated conditions.
RESULTS: IL-6 levels in pcg/ml for control (normal) cells were 2,124;
3,097; 10,467 and 1,830 for unstimulated and rOspA, PMA and sonicated B
burgodorferi stimulated respectively. For Lyme Arthritis #1 itwas 7, 744;
10,856; 25,911 and 11,411 and for Lyme Arthritis #2 14,689; 25,744; 39,681
and 14,189.
Non-stimulated ARLA SFs release amounts of IL-6 similar to PMA-stimulated normal SFs. rOspA but not killed B-burgdorferi is a strong stimulator of IL-6 release by ARLA SFs. This suggest a non-lymphoid dependent state of activation of SFs as well as an activating effect of rOspA. Pseudotransformation of SF could be the mechanism of ARLA