Abstract
Immune system alteration has been implicated in the pathogenesis of chronic pain conditions, epilepsy and generalized anxiety disorder. Targeting cytokines has recently been proposed for the management of such conditions. Pregabalin (PGB) is an antiepileptic agent used for the management of these conditions. However, little is known about its immunomodulatory effects on cytokine secretion in vivo and in vitro. Hence, a mitogen (Lipopolysaccharide [LPS] or Concanavalin A [ConA])-induced murine model of inflammation was used to investigate the effect of PGB on in vivo and in vitro IL-1β, IL-6, TNF-α and IL-2 cytokine secretion using ELISA. In addition, PGB effect on spleen histology, as a lymphoid organ, was examined. Our results revealed that PGB significantly inhibited the secretion of ConA-induced IL-6 secretion, basal and ConA-induced TNF-α and IL-2 secretion in splenocytes in vitro. In vivo, PGB inhibited basal and LPS/ConA-induced IL-6 and TNF-α secretion in addition to LPS-induced IL-1β and ConA-induced IL-2 secretion. Moreover, PGB attenuated mitogen-induced inflammatory changes in the spleen. These findings provide an evidence of the anti-inflammatory properties of PGB on cytokine secretion and lymphoid organ inflammation. This might give insights into the role of PGB in the management of the inflammatory state in PGB-indicated conditions.
Highlights
Several antiepileptic drugs have documented immunomodulatory effects, in particular, the old generation agents[1,2,3,4,5]
As peripheral inflammation and elevated systemic cytokines levels were demonstrated in the above-mentioned PGB-indicated conditions, we investigated in this study the effect of PGB on murine models of peripheral inflammation
We used for the first time, LPS and ConA-induced murine models of inflammation to examine the effect of PGB on peripheral proinflammatory cytokine secretion (IL-6, TNF-α, IL-1β and IL-2) in vitro and in vivo in BALB/c mice
Summary
Several antiepileptic drugs have documented immunomodulatory effects, in particular, the old generation agents[1,2,3,4,5]. It acts through binding to a specific subunit in the voltage-dependent calcium channels in the brain[6] It is indicated for the treatment of several neuropathic pain conditions, fibromyalgia, and generalized anxiety disorder, and it is indicated as an adjunctive therapy for the management partial onset seizure[6]. We used for the first time, LPS and ConA-induced murine models of inflammation to examine the effect of PGB on peripheral proinflammatory cytokine secretion (IL-6, TNF-α, IL-1β and IL-2) in vitro and in vivo in BALB/c mice. The lack of reports that examined the effect of PGB on the secretion of cytokines in immune cells prompted us to investigate such effects of PGB on basal and mitogen-induced proinflammatory cytokines secretion in splenocytes and peritoneal macrophages (PMs)
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