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Recombinant Human Interleukin-10 Fails to Alter Proinflammatory Cytokine Production or Physiologic Changes Associated with the Jarisch-Herxheimer Reaction

Philip J. Cooper, Daniel Fekade, Daniel G. Remick, Paul Grint, Janice Wherry and George E. Griffin
The Journal of Infectious Diseases
Vol. 181, No. 1 (Jan., 2000), pp. 203-209
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30111291
Page Count: 7
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Recombinant Human Interleukin-10 Fails to Alter Proinflammatory Cytokine Production or Physiologic Changes Associated with the Jarisch-Herxheimer Reaction
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Abstract

Interleukin (IL)-10 may have a role in the treatment of cytokine-associated inflammatory syndromes. The Jarisch-Herxheimer reaction (J-HR), which follows antibiotic treatment of Borrelia recurrentis infection, is a useful model of acute systemic inflammation associated with a cytokine surge and characteristic pathophysiologic changes. In a double-blind, placebo-controlled study, 49 Ethiopian men with B. recurrentis infection were randomized to receive a single intravenous bolus of either 25 μg/kg of recombinant human (rh) IL-10 or vehicle control shortly before receiving intramuscular penicillin. Patients were monitored for physiologic changes, and plasma samples were taken repeatedly for 24 h after treatment. rhIL-10 had no impact on changes in any of the physiologic parameters of J-HR, plasma cytokine levels, or the rate of spirochete clearance. A single intravenous bolus of 25 μg/kg of rhIL-10 does not seem to have a useful role in the treatment of the J-HR associated with B. recurrentis infection.

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