Abstract
Mammalian tachykinins such as substance P (SP) and neurokinin A (NKA) play a significant role in inflammatory and immune diseases by interacting with different cell populations 1-3. Mononuclear phagocytes, either circulating blood monocytes or tissue macrophages, largely participate in host defense responses: we previously demonstrated that human and guinea-pig alveolar macrophages possess NK2 and NK1 receptors and that in vitro stimulation by SP, NKA and NK2 selective agonists results in superoxide anion (O2 ) production 4,5. Lotz et al 6 reported that low concentrations of SP or NKA (the former less active) induce the release of inflammatory cytokines (e.g., TNF-α, IL-1 and IL-6) from human monocytes, whereas Kavelaars et al 7 observed IL-6 release only after high micromolar concentrations of SP and described “a non-neurokinin substance P receptor” on human monocytes. Different experimental approaches suggest a role for mammalian tachykinins in the onset and development of rheumatoid arthritis (RA): SP contributes to the severity of experimental arthritis, induces PGE2 and collagenase release from human synoviocytes and has been demonstrated to be significantly enhanced in joint fluids from rheumatoid patients 8-10. Therefore, we decided to evaluate whether or not mammalian tachykinins and synthetic selective agonists could exert a stimulatory effect on monocytes obtained from healthy donors or rheumatoid patients.
Published Version
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