Vitamin E supplementation increases T helper 1 cytokine production in old mice infected with influenza virus

Abstract

SUMMARYCompared with young mice, old mice infected with in¯uenza virus have signi®cantly higher pulmonary viral titres, although these can be reduced signi®cantly with dietary vitamin E supplementation. T helper 1 (Th1) cytokines, especially interferon-c (IFN-c), play an important role in defending against in¯uenza infection. However, there is an age-associated loss of Th1 cytokine production. Prostaglandin E 2 (PGE 2 ) production, which increases with age, can modulate the T helper cell function by suppressing Th1 cytokine production. To investigate the mechanism of vitamin E supplementation on reduction of in¯uenza severity in old mice, we studied the cytokine production by splenocytes, and PGE 2 production by macrophages (Mw), in young and old C57BL mice fed semipuri®ed diets containing 30 (control) or 500 parts per million (ppm) (supplemented) vitamin E for 8 weeks, and then infected with in¯uenza A/PC/1/73 (H3N2). Old mice fed the control diet had signi®cantly higher viral titres than young mice; old mice fed the vitamin E-supplemented diet had signi®cantly lower pulmonary viral titres than those fed the control diet (P=0 . 02 and 0 . 001 for overall age and diet effect, respectively). Following in¯uenza infection, interleukin (IL)-2 and IFN-c production was signi®cantly lower in old mice than in young mice. Vitamin E supplementation increased production of IL-2 and IFN-c in old mice; higher IFN-c production was associated with lower pulmonary viral titre. Old mice fed the control diet showed signi®cantly higher lipopolysaccharide (LPS)-stimulated Mw PGE 2 production than old mice fed the vitamin E diet or young mice fed either diet. There was no signi®cant age difference in IL-6, IL-1b, or tumour necrosis factor-a (TNF-a) production by splenocytes. Young mice fed the vitamin E-supplemented diet had signi®cantly lower IL-1b (day 7) and TNF-a production (day 5) compared with those fed the control diet. Old mice fed the vitamin E-supplemented diet had signi®cantly lower TNF-a production (day 2) than those fed the control diet. Our results indicate that the vitamin E-induced decrease in in¯uenza viral titre is mediated through enhancement of Th1 cytokines, which may be the result of reduced PGE 2 production caused by vitamin E.

The prevalence and risk factors for age-related macular degeneration in rural–urban India, Sankara Nethralaya Rural–Urban Age-related Macular degeneration study, Report No. 1

“…Old mice fed 30 ppm of vitamin E had higher viral titres than young mice fed the same way. Influenza lung viral titres were lower in old mice fed 500 ppm vitamin E compared with the age-matched mice fed 30 ppm vitamin E. In a subsequent study, Han et al (126) showed that the preventive effect of vitamin E was not observed following supplementation with other antioxidant compounds such as glutathione, melatonin or strawberry extract. Furthermore, vitamin E prevented the weight loss associated with influenza infection, while other dietary antioxidant treatments had no effect on weight loss.…”

“…Vitamin E supplementation (125,126) has also been shown to reduce lung viral titres following influenza infection. The evidence thus far suggests that improved immune response following nutrient intervention might have clinical significance for this age group.…”

Physiological regulatory networks: ecological roles and evolutionary constraints

“…For example, faced with a drop in the abundance of a preferred resource, a species might shift to an alternative resource that happens to have a different vitamin E content. Vitamin E has multiple physiological roles, including as an antioxidant and regulator of the immune system [23]. Hypothetically, a shift in vitamin E intake might affect regulation of oxidative balance as well as response to a parasite.…”

?-Tocopherol and Ketorolac on Pain in Long Evans Rats

“…No similar study was found to support this observation. It has been suggested that, αTmight reduce inflammatory pain by decreasing plasma NO (Nitric oxide), TNF-α (Tumor necrosis factor -alpha), PGE 2 (Prostaglandin E type 2) [41][42][43][44] . In addition, KT also reduces inflammatory mediators by inhibiting the prostaglandin synthesis by competitively blocking cyclooxygenase (COX) 40,45 .…”