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Journal of Endotoxin Research
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Rhodobacter sphaeroides diphosphoryl lipid A inhibits interleukin-6 production in CD14-negative murine marrow stromal ST2 cells stimulated with lipopolysaccharide or paclitaxel (taxol)

T. Kirikae

Department of Microbiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken, Japan

F. Kirikae

Department of Microbiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken, Japan

K. Tominaga

Department of Microbiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken, Japan

N. Qureshi

Mycobacteriology Research Laboratory, William S. Middleton Memorial Veteran's Hospital, Department of Bacteriology, College of Agricultural and Life Sciences, University of Wisconsin, Madison, Wisconsin, USA

S. YamaMoto

Department of Pathology, Oita Medical University, Oita, Japan

M. Nakano

Department of Microbiology, Jichi Medical School, Minamikawachi-machi, Tochigi-ken, Japan

Paclitaxel (taxol), a microtubule stabilizer with anticancer activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages in vitro. Recent studies have shown that the Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA) inhibits both LPS- and paclitaxel-induced activation of murine macrophages, and have suggested that LPS, RsDPLA, and paclitaxel share the same receptor site on murine macrophages. To analyze this receptor site, the present study focused on the interactions between LPS, RsDPLA and paclitaxel in the activation of ST2 cells derived from murine bone marrow stroma. The ST2 cells did not express CD14 mRNA. The cells produced IL-6 molecules and expressed IL-6 mRNA in response to LPS, but did not produce TNF and nitric oxide. Paclitaxel induced IL-6 mRNA expression in ST2 cells. RsDPLA inhibited both LPS- and paclitaxel-induced IL-6 mRNA expression in a dose-dependent manner. These results suggest that LPS, RsDPLA, and paclitaxel are recognized by the same receptor complex on ST2 cells, and that the receptor functions without membrane CD14.

Journal of Endotoxin Research, Vol. 4, No. 2, 115-122 (1997)
DOI: 10.1177/096805199700400205
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