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Rheumatology Advance Access published online on June 16, 2003
Rheumatology, doi:10.1093/rheumatology/keg372
Rheumatology © British Society for Rheumatology 2003; all rights reserved
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© 2003 Rheumatology 42 © British Society for Rheumatology 2003; all rights reserved

Original Papers

Ciprofloxacin reduces the stimulation of prostaglandin E2 output by interleukin-1{beta} in human tendon-derived cells

A. N. Corps 1*, V. A. Curry 1, R. L. Harrall 1, D. Dutt 1, B. L. Hazleman 1, and G. P. Riley 1

1 Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK

Received 20 January 2003 ; accepted 25 March 2003

Abstract

Objective. Fluoroquinolone antibiotics such as ciprofloxacin can induce tendon pathology and have various effects on tendon-derived cells in culture. We are investigating whether ciprofloxacin modifies signalling responses in tendon cells.

Methods. Human Achilles tendon-derived cells were preincubated with or without ciprofloxacin (50 µg/ml) and were then challenged with interleukin-1{beta} (IL-1{beta}, 1 ng/ml) for up to 48 h. Prostaglandin E2 (PGE2) output was assayed by ELISA. The expression of cyclooxygenase-2 (COX-2) was examined by Western blotting.

Results. IL-1{beta} stimulated a substantial and prolonged increase in the output of PGE2. Preincubation with ciprofloxacin reduced IL-1{beta}-induced PGE2 output at all times tested; the reduction at 48 h was 69% (99% confidence interval 59-79%; 15 experiments). Norfloxacin and ofloxacin also reduced PGE2 output. However, ciprofloxacin did not affect the induction of COX-2 by IL-1{beta}, measured at 4 or 48 h.

Conclusions. Ciprofloxacin reduces IL-1{beta}-induced PGE2 output in tendon-derived cells. The reduction in PGE2 output could modulate various cellular activities of IL-1{beta}, and may be implicated in fluoroquinolone-induced tendinopathy.

Key words: Tendon, Fluoroquinolone, Prostaglandin, Interleukin, Cyclooxygenase-2.
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A. N. Corps, R. L. Harrall, V. A. Curry, B. L. Hazleman, and G. P. Riley
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