In summary, employing human organoids and established human colon-derived epithelial cell lines, the mitochondrial fragmentation caused by infection with the AIEC E. coli-LF82 was reduced in severity by co-treatment with butyrate, acting in part via FFAR3 (the possibilities of butyrate-evoked changes in metabolism or action as a HDAC inhibitor should not be dismissed). The gene discussed is FFAR3; the disease is infection.