Abstract
ABSTRACT Non-communicable diseases, such as the metabolic syndrome and inflammatory bowel disease, constitute serious public health threats in developed countries. Besides environmental factors, genetic predispositions contribute to the onset and progression of the disease. State-of-the-art mouse models recently highlight the involvement of Toll-like receptor 5 (TLR5)–driven microbiota composition in the development of metabolic disorders. Here, we discuss the causes and consequences of an altered enteric microbiota and provide information on a similar mechanism in another species, the pig. We show for the first time that a single nucleotide polymorphism in the porcine TLR5 gene conferring impaired functionality is associated with changes in the intestinal microbiota in adult sows and neonatal piglets. Changes in the developing adaptive cellular immune response support the concept of TLR5-driven changes of the microbe-host interplay also in the pig. Together, these findings suggest that pigs with impaired TLR-functionality might represent a model for TLR5-driven diseases in humans.
Highlights
The propagation of vaccination by Edward Jenner in 1796 and the discovery of penicillin by Sir Alexander Fleming in 1928 dramatically changed the prospects of medicine
Alterations in the micro biota composition have been associated with a wide spectrum of metabolic, inflammatory and immunemediated disorders and appear to contribute to the etiology or progression of at least some highly prevalent diseases.[5,6]
Western-type diet and gestational age have previously been linked to markers for metabolic syndrome in pig models.[34,35]
Summary
The propagation of vaccination by Edward Jenner in 1796 and the discovery of penicillin by Sir Alexander Fleming in 1928 dramatically changed the prospects of medicine. Microbiota of patients suffering from MetS consti tute a lower bacterial richness compared to nonobese individuals.[11] Recent data suggest that the observed compositional changes of the microbiota may play a functional role in the disease pathogenesis.[12,13,14,15] In addition, genetic factors were identified to contribute significantly.[16,17,18] The clinical symptoms of IBD, MetS and type-2 diabetes mellitus are reminiscent of the phenotype of mice deficient for the innate immune receptor Toll-like receptor 5 (TLR5), the receptor for bacterial flagel lin.
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