Hybrid liposomes are nanosized liposomal particles and can be prepared by sonication of vesicular and micellar molecules in a buffer solution. In this study, we obtained the first successful experiment resulting in a good correlation between inhibitory effects of hybrid liposomes on the growth of various tumor cells and the membrane fluidity of tumor cells (plasma membranes). The results indicated that hybrid liposomes could provide the possibility of novel membrane-targeted nanotherapy for intractable cancers.

Clustering of lipid rafts in plasma membranes by hybrid liposomes (HL-23) composed of l-α-dimyristoylphosphatidylcholine (DMPC) and polyoxyethylene(23) dodecyl ether (C12(EO)23) for human leukemia HL-60 cells was observed for the first time. It was suggested that the induction of apoptosis by HL-23 could be related to an increase of membrane fluidity and the formation of lipid rafts in the plasma membranes of HL-60 cells.

The effects of ultraviolet (UV) irradiation on cell-mediated cytolysis were examined in order to clarify the inhibitory mechanisms of allosensitization by UV irradiation. UV-B-irradiated target cells (Sa; an Epstein-Barr virus-transformed B cell line) exhibited more resistance against alloreactive cytotoxic T lymphocytes (CTL) than mitomycin C (MMC)-treated target cells. In the conjugate formation assay, UV-B-irradiated target cells showed a considerably lower binding to alloreactive CTL than MMC-treated target cells. UV-B irradiation induced a reduction of HLA-class I, -DR, CD54 (ICAM-1) and CD58 (LFA-3) expression on target cells. However, it does not seem to contribute to the inhibition of cell adhesion induced by UV-B irradiation because a similar reduction of cell surface antigens was observed in MMC-treated target cells. Number of cells capped with anti-HLA-class I, -DR, CD54 or CD58 monoclonal antibody were markedly reduced by UV-B irradiation compared to that by MMC treatment. These findings suggest the possibility that the inhibition of cell adhesion between UV-B-irradiated Sa target cells and alloreactive CTL is due to the impaired mobility of cell surface antigens which will affect the early process of cell-mediated cytolysis.

Bone marrow (BM)-resident hematopoietic stem and progenitor cells (HSPCs) are often activated following bacterial insults to replenish the host hemato-immune system, but how they integrate the associated tissue damage signals to initiate distal tissue repair is largely unknown. Here, we show that acute gut inflammation expands HSPCs in the BM and directs them to inflamed mesenteric lymph nodes through GM-CSFR activation for further expansion and potential differentiation into Ly6C + /G + myeloid cells specialized in gut tissue repair. We identified this process to be mediated by Bacteroides, a commensal gram-negative bacteria that activates innate immune signaling. These findings establish cross-organ communication between the BM and distant inflamed sites, whereby a certain subset of multipotent progenitors is specified to respond to imminent hematopoietic demands and to alleviate inflammatory symptoms.

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