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¹ Réanimation Médicale, Hôpital Central, 54035 Nancy Cedex, France
² Laboratoire de Physiologie Expérimentale, Faculté de Médecine, 54035 Nancy Cedex, France
³ Laboratoire d'Immunologie, Faculté de Médecine, 54035 Nancy Cedex, France
⁴ Laboratoire de Bactériologie, Hôpital Central, 54035 Nancy Cedex, France

Address correspondence to Sébastien Gibot, Hôpital Central, Service de Réanimation Médicale, 29 avenue du Maréchal de Lattre de Tassigny, 54035 Nancy Cedex, France. Phone: 33-3-83-85-29-70; Fax: 33-3-83-85-85-11; email: s.gibot{at}chu-nancy.fr

The triggering receptor expressed on myeloid cells (TREM)-1 is a recently discovered receptor expressed on the surface of neutrophils and a subset of monocytes. Engagement of TREM-1 has been reported to trigger the synthesis of proinflammatory cytokines in the presence of microbial products. Previously, we have identified a soluble form of TREM-1 (sTREM-1) and observed significant levels in serum samples from septic shock patients but not controls. Here, we investigated its putative role in the modulation of inflammation during sepsis. We observed that sTREM-1 was secreted by monocytes activated in vitro by LPS and in the serum of animals involved in an experimental model of septic shock. Both in vitro and in vivo, a synthetic peptide mimicking a short highly conserved domain of sTREM-1 appeared to attenuate cytokine production by human monocytes and protect septic animals from hyper-responsiveness and death. This peptide seemed to be efficient not only in preventing but also in down-modulating the deleterious effects of proinflammatory cytokines. These data suggest that in vivo modulation of TREM-1 by sTREM peptide might be a suitable therapeutic tool for the treatment of sepsis.

Key Words: triggering receptor expressed on myeloid cells-1 • inflammation • sepsis • proinflammatory cytokines • mouse model

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