Paternal chronic colitis causes epigenetic inheritance of susceptibility to colitis

Markus Tschurtschenthaler, Priyadarshini Kachroo, Femke Anouska Heinsen, Timon Erik Adolph, Malte Christoph Rühlemann, Johanna Klughammer, Felix Albert Offner, Ole Ammerpohl, Felix Krueger, Sébastien Smallwood, Silke Szymczak, Arthur Kaser*, Andre Franke

*Corresponding author for this work
6 Citations (Scopus)


Inflammatory bowel disease (IBD) arises by unknown environmental triggers in genetically susceptible individuals. Epigenetic regulation of gene expression may integrate internal and external influences and may thereby modulate disease susceptibility. Epigenetic modification may also affect the germ-line and in certain contexts can be inherited to offspring. This study investigates epigenetic alterations consequent to experimental murine colitis induced by dextran sodium sulphate (DSS), and their paternal transmission to offspring. Genome-wide methylome-and transcriptome-profiling of intestinal epithelial cells (IECs) and sperm cells of males of the F 0 generation, which received either DSS and consequently developed colitis (F 0 DSS), or non-supplemented tap water (F 0 Ctrl) and hence remained healthy, and of their F 1 offspring was performed using reduced representation bisulfite sequencing (RRBS) and RNA-sequencing (RNA-Seq), respectively. Offspring of F 0 DSS males exhibited aberrant methylation and expression patterns of multiple genes, including Igf1r and Nr4a2, which are involved in energy metabolism. Importantly, DSS colitis in F 0 DSS mice was associated with decreased body weight at baseline of their F 1 offspring, and these F 1 mice exhibited increased susceptibility to DSS-induced colitis compared to offspring from F 0 Ctrl males. This study hence demonstrates epigenetic transmissibility of metabolic and inflammatory traits resulting from experimental colitis.

Original languageEnglish
Article number31640
JournalScientific Reports
Publication statusPublished - 19.08.2016


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