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Mitogenicity of bacterial lipopolysaccharide on the T lymphocyte population bearing the T cell receptor

Department of Bacteriology, Ohu University School of Dentistry, Koriyama, Japan, Department of Microbiology, Jichi Medical School, Tochigi-ken, Japan

H. Imai

Department of Bacteriology, Ohu University School of Dentistry, Koriyama, Japan, Department of Microbiology, Jichi Medical School, Tochigi-ken, Japan

Y. Ogasawara

Department of Bacteriology, Ohu University School of Dentistry, Koriyama, Japan, Department of Microbiology, Jichi Medical School, Tochigi-ken, Japan

M. Nakano

In vitro [³H]-thymidine (TdR) uptake in T lymphocyte populations, taken and purified from proteose peptone-induced peritoneal exudate cells (PEC), spleens and thymuses of C3H/HeN mice, were investigated by stimulation with bacterial lipopolysaccharide (LPS). The T cells taken from PEC (PEC-T) were purified by passing them through a nylon fiber column (Nfc) and a G-10 column. They were then treated with anti-la^k, anti-Mac-1 and anti-LR-1 antibodies plus complement (C). The PEC-T cells showed an increased [ ³H]-TdR uptake in response to LPS, while the splenic T cells and thymic T cells that had been purified and treated by a similar procedure with minor modifications, poorly responded to LPS and did not respond to LPS, respectively. The response of PEC-T to LPS was abolished when the PEC-T were pretreated with anti-Thy-1 or anti- antibody plus C, but not β, T cell receptor (TCR) antibody plus C. The thymic T cells did not show any increase of [ H]-TdR uptake in response to LPS or anti-β or TCR antibody. However, obvious uptake did occur when the cells were stimulated with LPS and anti-TCR antibody, but not with anti-βTCR antibody. IL-1 did not substitute for LPS in the response. These results suggest that LPS has a mitogenic ability to respond to a T cell population bearing TCR in PEC, and to a TCR-stimulated cell population in thymic cells. The difference in response to LPS between PEC-T and thymic T cells was discussed.

Journal of Endotoxin Research, Vol. 1, No. 2, 101-107 (1994)
DOI: 10.1177/096805199400100204


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