Table 2.

The ATG16L1 gene mutation and its impact on the microbiota in IBD.

	Genes Studied	Conclusions of the Study
Animal studies	ATG16L1 gene	There were changes in the composition of the fecal microbiota of knock-in mice expressing the variant ATG16L1 (T300A) compared to wild-type (WT) mice. An increase in the number of Bacteroides (Bacteroides ovatus) was demonstrated. During dextran sulfate sodium (DSS)-induced colitis, knock-in mice show an altered fecal microbial composition associated with a decrease in Firmicutes and an increase in Bacteroidetes, Proteobacteria, and Cyanobacteria compared to WT mice. Changes occurred before the onset of the disease, suggesting that ATG16L1 T300A contributes to dysbiosis before the onset of IBD symptoms [28]. Mice with ATG16L1 (T300A) mutations show reduced antimicrobial autophagy and abnormal lysozyme distribution in Paneth cells [53]. ATG16L1 mice show morphological abnormalities in Paneth and cup cells, but do not develop intestinal autophagy or inflammatory bowel disease [54]. ATG16L1 T300A/T300A mice showed a significant increase in the abundance of Tyzzerella, Mucispirillum, Ruminococcaceae and Cyanobacteria in both feces and intestinal mucosa, while Akkermansia, a mucin-associated bacterium, was significantly reduced in ATG16L1 T300A/T300A mice. Dysbiosis in ATG16L1 T300A mice may be an important factor that contributes to increased susceptibility to IBD [55].
Research involving humans	ATG16L1 gene	The inflamed ileum of patients homozygous for the ATG16L1 allele (ATG16L1-T300A) contained an increased number of Fusobacteriaceae, while the inflamed ileal tissue of patients homozygous for the protective allele of ATG16L1 (ATG16L1-300) showed a decreased number of Bacteroidaceae and Enterobacteriaceae and an increase in Lachnospiraceae. [56].