Vitamin E supplementation exhibits anti-inflammatory properties. In the lung, the beneficial effects of
vitamin E supplementation on
inflammation and
infections are well documented, but potential consequences of alimentary
vitamin E deficiency to the immunological status of lung cells are not known. It is unclear if temporary
vitamin E deficiency exhibits deleterious consequences or can be compensated for by other cellular
antioxidants. To address this question, the alimentary
vitamin E supply to rats was modified. We then investigated the effects on major histocompatibility molecule (MHC) class II,
cell adhesion molecules,
interleukin (IL)10,
tumor necrosis factor (
TNF)alpha in various lung cells. The constitutive expression of MHC class II,
intercellular adhesion molecule (ICAM)-1,
L-selectin, alpha5-integrin, and CD 166, was demonstrated by flow cytometry on type II pneumocytes, alveolar macrophages, and on co-isolated lymphocytes.
Vitamin E depletion increased
ICAM-1 and CD166 on type II cells and macrophages, whereas the expression of
L-selectin increased only on macrophages. Furthermore, the
vitamin E depletion increased the cellular content and secretion of
IL10 in type II cells, but decreased the content and secretion of
TNFalpha.
Vitamin E depletion decreased the cellular
vitamin E content, but did not change the activity of
antioxidant enzymes (
catalase,
superoxide dismutase) and the glutathion (GSH)/oxidized glutathion (
GSSG) ratio in alveolar type II cells. The shift of
protein kinase C (PKC) from the cytosol to membranes indicates that a PKC-dependent signaling pathway may be involved in the change of the immunological status of type II cells. All these effects were reversed by
vitamin E repletion. In summary, these results are clearly compatible with the view that a temporary
vitamin E deficiency induces a reversible immunological dysregulation in alveolar type II cells and lung macrophages. This deficiency might predispose the lung to develop acute or chronic
inflammation.