Acetaminophen Intoxication Rapidly Induces Apoptosis of Intestinal Crypt Stem Cells and Enhances Intestinal Permeability
Open accessAbstract
Acetaminophen (APAP)‐induced liver injury is the most common cause of acute liver failure (ALF) in the Western world. APAP toxicity progresses to multiorgan dysfunction and thus has broader whole‐body implications. Importantly, greater 30‐day mortality has been observed in liver transplant recipients following ALF due to APAP‐related versus non‐APAP‐related causes. Reasons for this discrepancy have yet to be determined. Extrahepatic toxicities of APAP overdose may represent underappreciated and unaddressed comorbidities within this patient population. In the present study, rapid induction of apoptosis following APAP overdose was observed in the intestine, an organ that greatly influences the physiology of the liver. Strikingly, apoptotic cells appeared to be strictly restricted to the intestinal crypts. The use of leucine‐rich repeat‐containing G protein–coupled receptor 5 (LGR5) reporter mice confirmed that the LGR5‐positive (+) crypt base stem cells were disproportionately affected by APAP‐induced cell death. Although the apoptotic cells were cleared within 24 hours after APAP treatment, potentially long‐lived consequences on the intestine due to APAP exposure were indicated by prolonged deficits in gut barrier function. Moreover, small intestinal cell death was found to be independent of tumor necrosis factor receptor signaling and may represent a direct toxic insult to the intestine by exposure to high concentrations of APAP. Conclusion: APAP induces intestinal injury through a regulated process of apoptotic cell death that disproportionately affects LGR5+ stem cells. This work advances our understanding of the consequences of APAP toxicity in a novel organ that was not previously considered as a significant site of injury and thus presents potential new considerations for patient management.
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APAP-induced liver injury causes impairment of intestinal barrier integrity and increased bacterial translocation in mice.
“Recent studies in mice have demonstrated that APAP-induced liver injury causes impairment of intestinal barrier integrity and increased bacterial translocation29–31”
From Multimodal decoding of human liver regeneration (2024) · cites this paper as [29]
The Results section reports increased intestinal permeability in APAP-treated mice alongside liver injury. It does not establish that liver injury caused the barrier impairment, and the paper does not report increased bacterial translocation; it measured passage of FITC–dextran instead (Results and Materials and Methods, page unavailable). (LLM, conf=0.88)
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- Authors
- Chopyk, D. M., Stuart, J. D., Zimmerman, M. G., Wen, J., Gumber, S., Suthar, M. S., Thapa, M., Czaja, M. J., & Grakoui, A.
- Affiliations
- Emory University (US)
- Corresponding author
- Grakoui, Arash
- ORCID
- Venue
- Hepatology Communications
- Published
- 2019-07-15
- Volume
- 3
- Issue
- 11
- Pages
- 1435-1449
- ISSN
- 2471-254X (ISSN-L)
- PMC
- PMC6824060
- OpenAlex
- W2960902094
- Cited by
- 33
- References
- 39
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 8 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 1
- FWCI
- 3.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Hepatology Communications (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Emory University
- National Institutes of Health (P51OD011132)
- School of Medicine, Emory University
- Yerkes National Primate Research Center, Emory University (R01AI136533, R01AI124680, P51 OD011132, P51RR000165)
- National Institute on Alcohol Abuse and Alcoholism (F31AA024960)
- NIH Office of the Director (P51 OD 011132)
- National Institute of General Medical Sciences (T32GM008169, K12GM000680)
- National Institute of Allergy and Infectious Diseases (R01AI136533, R01AI124680, R01AI126890)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK109025, R01DK044234)
- National Center for Research Resources (P51RR000165)
- Topics
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Health Sciences › Medicine › Emergency Medicine › Poisoning and overdose treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- acetaminophen toxicity, acute liver failure, intestinal crypt stem cells, apoptosis, Lgr5, intestinal permeability, intestinal barrier, small bowel injury, tumor necrosis factor receptor signaling, liver transplant recipients
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