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Low dietary intake of n-3 polyunsaturated fatty acids (PUFAs) has been associated with an increased propensity for the development of inflammatory conditions. Recent evidence indicates that this occurs through alterations of several innate immune cells, but the direct effects of dietary PUFAs on adaptive immunity are less clear. To address this, we analyzed the in vitro ability of splenocytes from rodents fed a PUFA-deficient diet to respond to murine and human T cell stimuli. Splenocytes from PUFA-deficient mice produced higher levels of interleukin (IL)-17A, IL-17F, and IL-23, while the production of IL-4 was reduced. In addition, we observed an increase in IL-17A-producing splenocytes from PUFA-deficient mice that express enhanced levels of retinoid-related orphan receptor gamma t (RORgamma t). PUFA-deficient splenocytes also showed an enhanced ability to undergo differentiation into T helper 17 (Th17) cells. In contrast, the ability of splenocytes from PUFA-deficient mice to mount Th1 and Th2 responses was unaffected. These changes were accompanied by a reduction in the expression of PUFA-conjugated n-3 PUFA-derived mediators (eicosanoids and neuroprotectins) and an increase in their lipoxin A4 (LXA4) analog (15-epiLXA4) and 15-epi15-epi-LXA4. Conversely, the precursor (17(S)-hydroxy-DHA) to LXA4 was elevated. These data indicate that PUFA deficiency alters the ability of splenocytes to respond to T cell stimuli and suggest that differences in systemic PUFA levels may play a role in inflammatory conditions.Q:
Will a recursive table be slower than a flat, but count-based one?
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ID | PARENTID
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