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ATG16L1 and pathogenesis of urinary tract infections

Caihong Wang1, Jane W Symington, Indira U Mysorekar

  • 1Department of Obstetrics and Gynecology, Washington University School of Medicine St. Louis, St. Louis, MO, USA.

Autophagy
|August 10, 2012
PubMed

Insights

ATG16L1 deficiency protects against urinary tract infections (UTIs) by enhancing bacterial clearance and reducing pathogen reservoirs. This finding reveals a novel host-protective role for ATG16L1 in combating uropathogenic E. coli (UPEC).

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Autophagy is generally considered antipathogenic, but the role of the autophagy gene ATG16L1 in host defense against bacterial infections is complex.
  • Mutations in ATG16L1 are linked to Crohn disease (CD), and mice with reduced ATG16L1 function (ATG16L1(HM)) model CD features.
  • Intriguingly, ATG16L1(HM) mice, susceptible to intestinal inflammation, show protection against urinary tract infections (UTIs).

Purpose of the Study:

  • To investigate the role of ATG16L1 deficiency in host protection against acute urinary tract infections (UTIs) and uropathogenic E. coli (UPEC) persistence.
  • To elucidate the mechanisms by which ATG16L1 deficiency impacts UPEC colonization, innate immune response, and the formation of quiescent intracellular reservoirs (QIRs).

Main Methods:

  • Utilized ATG16L1 hypomorphic (ATG16L1(HM)) mice to study UPEC infection models.
  • Assessed bacterial loads, innate immune cell recruitment, and urothelial cell morphology in infected mice.
  • Quantified the formation of quiescent intracellular reservoirs (QIRs) within the bladder epithelium.

Main Results:

  • ATG16L1(HM) mice demonstrated accelerated and more complete clearance of UPEC from the urinary tract.
  • ATG16L1 deficiency in innate immune components contributed to enhanced bacterial clearance.
  • Urothelial cells in ATG16L1(HM) mice exhibited architectural aberrations, leading to a significant reduction in UPEC QIR formation.

Conclusions:

  • ATG16L1 deficiency confers protection against acute UTI and UPEC latency.
  • The protective effect is mediated by both enhanced innate immune responses and altered urothelial cell architecture.
  • This study reveals a novel host-protective role for ATG16L1 deficiency against common bacterial pathogens like UPEC.
Keywords:
Atg16L1Atg5Crohn diseaseautophagybladderurinary tract infectionsuropathogenic E. coli

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