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Sophorolipid treatment decreases inflammatory cytokine expression in an in vitro model of experimental sepsis
Author(s) -
Mueller Cathy M,
Lin Yinyao,
Viterbo Domenico,
Pierre Joelle,
Murray Shirley A,
Shah Vishal,
Gross Richard,
Schulze Robert,
Zenilman Michael E,
Bluth Martin H
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a204-b
Subject(s) - sepsis , cytokine , in vitro , in vivo , tumor necrosis factor alpha , inflammation , pharmacology , immunology , medicine , chemistry , biology , biochemistry , microbiology and biotechnology
Sophorolipids are a class of membrane‐derived glycolipids that have wide ranging potential as treatment in clinical practice. Previous data from our laboratory show that in vivo sophorolipid therapy decreases sepsis related mortality in experimental models. In this study we investigated the effects of sophorolipid treatment on cytokine production in an in vitro model of experimental sepsis. LPS stimulated rat alveolar macrophage cells (NR8383) were cultured in the presence or absence of sophorolipids for 12, 24, 36, and 48 hr. RNA was harvested from each group and assayed for cytokine expression using multiplex PCR. Statistical analyses were performed comparing the LPS treated group (L) with the LPS + sophorolipid treated group (L+S). TNF‐a, a pro‐inflammatory cytokine known to play a pivotal role in septic shock was significantly decreased in the L+S group compared to the L group at 12–24 hr, but trended upward at 36–48hr. Pro‐inflammatory cytokines IL‐1a and IL‐1b followed the same pattern. IL‐1 receptor antagonist (RA), which provides a protective effect in experimental sepsis, also showed decreased expression in the L+S compared to L group at 12–24 hr and an upward trend at 36‐48hr. Similar expression pattern was found with IL‐10, which may affect Th1/Th2 type T cell responses. Sophorolipid treatment decreases expression of important pro‐inflammatory cytokines in an in vitro cellular sepsis model and this immunomodulation may be responsible, in part, for sophorolipid mediated decreases in sepsis related mortality. Sophorolipid treatment may delay or prevent sepsis progression by allowing host response immune mechanisms to exert their protective effects.