Non-specific Local Defense of Inner Ears of Guinea Pigs

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To clarify the non-specific defense mechanism (first defense mechanism) of the inner ear against pathogens, we injected K562 myelogenous leukemia cells into guinea pigs' perilymphatic space through the round window membrane and observed the reaction in the inner ear on day 1 to day 9. K562 cells injected into the perilymphatic space could survive and multiply for a couple of days. At 67 hours, however, some macrophages entered the perilymphatic space, and at 86 hours some K562 cells had degenerated a little, but most of them seemed to be intact. NK (natural killer) cells which were positive for anti-asialo GM1 appeared in the perilymphatic space on day 7 when most K562 cells were still intact. On day 9 there were many K562 cells with adherent phlogocytes in the perilymphatic space, and most of them had degenerated. K562 cells were attacked by NK cells coming from the surrounding venules. The source of NK cells in the perilymphatic space may be vessels around the modiolus and the cochlear bony wall. Also, NK cells derived from white blood cells of guinea pig whole blood could attach to, recognize, and attack K562 cells, and their attack showed an ordinary pattern of NK cell-induced cytolysis. The emergence of NK cells was much later in the perilymphatic space than in the skin after the injection of K562 cells. It is possible that this delay can lead to an irreversible change in the cochlea due to pathogens before the mobilization of NK cells. In addition, humoral factors in the inner ear fluid are not so powerful in suppressing viral infection, and the endolymphatic sac does not seem to play an important role to rescue the cochlea from viral infection. Thus the inner ear seems to be an environment in which it is relatively difficult for immunocompetent cells to function.
日本めまい平衡医学会の論文

Non-specific Local Defense of Inner Ears of Guinea Pigs

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