{'fraction_non_alphanumeric': 0.020935960591133004, 'fraction_numerical': 0.017241379310344827, 'mean_word_length': 5.7190082644628095, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Articles of Significant Interest Selected from This Issue by the Editors

MyD88-dependent signaling plays a key role in innate host defense against enteric bacterial infections, helping promote host survival. However, the intestinal cell types in which protective MyD88 signaling occurs are undefined. Bhinder et al. (p. 3753–3763) report that mice with intestinal epithelial cell (IEC)-specific MyD88 deficiency suffer accelerated tissue damage upon Citrobacter rodentium or Salmonella enterica serovar Typhimurium infection due to impaired goblet cell and antimicrobial responses. These defects allow pathogens to rapidly and closely associate with the intestinal mucosal surface, triggering accelerated tissue damage. These findings thus highlight a novel protective role for innate signaling in IECs in vivo.