Background/Purpose In Westernized nations, the incidence of autoimmune and inflammatory diseases has dramatically risen over the past few decades. Environmental influences and their interplay with genetic risk factors have been suggested as important contributors to the rapid epidemic progress. Among environmental influences, Western diet – high in fat, sugar and salt – has been postulated as important risk, while beneficial effects were described for dietary fibre and their bacterial fermentation products, short chain fatty acids (SCFA). In SLE, their impact remains largely unexplored and was addressed in this study.
Methods Lupus prone NZB/WF1 mice were fed a low– (LFD) versus high-fibre diet (HFD) from the age of 3 weeks and over the course of the whole experiment. Determined were development of clinical disease and associated changes in immune status, gut and energy homeostasis.
Results Animals fed a HFD showed lower autoantibody titres going along with an improved overall survival and a tendentiously lower infiltration of the kidney by leukocytes. Beneficial clinical effects were reflected in systemic immunologic changes, as the distribution and differentiation of main immune cell subsets in HFD animals more closely resembled that of yet healthy animals. We assume that most probably a complex interplay of different fiber-associated effects underlies these favorable effects. This may involve intestinal leakage and bacterial translocation that were increased in LFD animals. Further, LFD animals showed a significant increase in body weight and white adipose tissue expressing more leptin and inflammatory cytokines. We are currently testing, if the observed beneficial effects may also be attributed to an increased fermentation of dietary fibre into SCFA. SCFA intersect in various ways and at different sites with the immune system and mostly have anti-inflammatory effects.
Conclusion Altogether, we think that intake of dietary fiber affects immune status, gut and energy homeostasis. These may be interlinked and affect each other, inflicting more or less systemic chronic inflammation promoting lupus pathology.
Acknowledgment This work was supported by the B. Braun Stiftung, the Forschungskommission Freiburg and the Ministry of Science, Research, and Arts Baden-Wurttemberg (Margarete von Wrangell Programm).
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