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dc.contributor.authorHorst, Sarah A
dc.contributor.authorLinnér, Anna
dc.contributor.authorBeineke, Andreas
dc.contributor.authorLehne, Sabine
dc.contributor.authorHöltje, Claudia
dc.contributor.authorHecht, Alexander
dc.contributor.authorNorrby-Teglund, Anna
dc.contributor.authorMedina, Eva
dc.date.accessioned2014-01-10T10:33:53Zen
dc.date.available2014-01-10T10:33:53Zen
dc.date.issued2013en
dc.identifier.citationPrognostic value and therapeutic potential of TREM-1 in Streptococcus pyogenes- induced sepsis. 2013, 5 (6):581-90 J Innate Immunen
dc.identifier.issn1662-8128en
dc.identifier.pmid23571837en
dc.identifier.doi10.1159/000348283en
dc.identifier.urihttp://hdl.handle.net/10033/311202en
dc.description.abstractTREM-1 (triggering receptor expressed on myeloid cells) is a surface molecule expressed on neutrophils and macrophages which has been implicated in the amplification of inflammatory responses triggered during infection. In the present study, we have investigated the clinical significance of TREM-1 in Streptococcus pyogenes-induced severe sepsis in both experimentally infected mice as well as in patients with streptococcal toxic shock. We found that S. pyogenes induced a dose-dependent upregulation of TREM-1 in in vitro cultured phagocytic cells and in the organs of S. pyogenes-infected mice. Furthermore, we reported a positive correlation between serum levels of soluble TREM-1 (sTREM-1) and disease severity in infected patients as well as in experimentally infected mice. Hence, sTREM-1 may represent a useful surrogate marker for streptococcal sepsis. We found that modulation of TREM-1 by administration of the TREM-1 decoy receptor rTREM-1/Fc substantially attenuated the synthesis of inflammatory cytokines. More importantly, treatment of S. pyogenes-infected septic mice with rTREM-1/Fc or the synthetically produced conserved extracellular domain LP17 significantly improved disease outcome. In summary, our data suggest that TREM-1 may not only represent a valuable marker for S. pyogenes infection severity but it may also be an attractive target for the treatment of streptococcal sepsis.
dc.language.isoenen
dc.rightsArchived with thanks to Journal of innate immunityen
dc.titlePrognostic value and therapeutic potential of TREM-1 in Streptococcus pyogenes- induced sepsis.en
dc.typeArticleen
dc.contributor.departmentDep. of infection immunology, Helmholtz Centre for infection research, Braunschweig, Germanyen
dc.identifier.journalJournal of innate immunityen
refterms.dateFOA2018-06-12T23:31:17Z
html.description.abstractTREM-1 (triggering receptor expressed on myeloid cells) is a surface molecule expressed on neutrophils and macrophages which has been implicated in the amplification of inflammatory responses triggered during infection. In the present study, we have investigated the clinical significance of TREM-1 in Streptococcus pyogenes-induced severe sepsis in both experimentally infected mice as well as in patients with streptococcal toxic shock. We found that S. pyogenes induced a dose-dependent upregulation of TREM-1 in in vitro cultured phagocytic cells and in the organs of S. pyogenes-infected mice. Furthermore, we reported a positive correlation between serum levels of soluble TREM-1 (sTREM-1) and disease severity in infected patients as well as in experimentally infected mice. Hence, sTREM-1 may represent a useful surrogate marker for streptococcal sepsis. We found that modulation of TREM-1 by administration of the TREM-1 decoy receptor rTREM-1/Fc substantially attenuated the synthesis of inflammatory cytokines. More importantly, treatment of S. pyogenes-infected septic mice with rTREM-1/Fc or the synthetically produced conserved extracellular domain LP17 significantly improved disease outcome. In summary, our data suggest that TREM-1 may not only represent a valuable marker for S. pyogenes infection severity but it may also be an attractive target for the treatment of streptococcal sepsis.


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