ArticleAmerican journal of physiology. Lung cellular and molecular physiology2026
TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.
Anastasia Malyshkina, Mack Solar, Natarajan Balasubramaniyan, Lijun Zheng, David J McCulley, Musah Morro, Cadence Seymour, Eniko Sajti, David J Orlicky, Alexander Sosa and 2 more
Abstract read
In one paragraphArticle in American journal of physiology. Lung cellular and molecular physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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What it found
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2 · The registryThe trial behind it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
12 authors.
Anastasia MalyshkinaSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.ORCID 0009-0005-4043-8730 Mack SolarSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.
Natarajan BalasubramaniyanSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.
Lijun ZhengSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.
David J McCulleyDivision of Neonatology, Department of Pediatrics, University of California, San Diego, California, United States.
Musah MorroSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.
Cadence SeymourDivision of Neonatology, Department of Pediatrics, University of California, San Diego, California, United States.
Eniko SajtiDivision of Neonatology, Department of Pediatrics, University of California, San Diego, California, United States.ORCID 0000-0002-0531-7715 David J OrlickyDepartment of Pathology, University of Colorado Anschutz School of Medicine, Aurora, Colorado, United States.ORCID 0000-0002-0417-1400 Alexander SosaDepartment of Biomedical Engineering, University of Colorado Denver, Anschutz Campus, Aurora, Colorado, United States.
Bradford J SmithDepartment of Biomedical Engineering, University of Colorado Denver, Anschutz Campus, Aurora, Colorado, United States.ORCID 0000-0002-1583-6762 Clyde J WrightSection of Neonatology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, United States.ORCID 0000-0002-8449-5631 Funding
Research Supplement to Promote Diversity in Health Related Research: Pulmonary implications ofperinatal acetaminophen exposureR01HD107700 · NICHD · UNIVERSITY OF COLORADO DENVER · PI Clyde Jason Wright · 2022 to 2026
$2.2MHHS | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) R01HD107700NICHD NIH HHS R01 HD107700
6 · The paper itselfAbstract
Acetaminophen (APAP) exposures during human development are common. Emerging epidemiological and experimental evidence links these exposures to subsequent pulmonary morbidity; however, the underlying mechanisms remain incompletely defined. Cell-type-specific expression of the xenobiotic enzyme CYP2E1 is a critical determinant of susceptibility to APAP toxicity. CYP2E1-mediated formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) induces mitochondrial injury, which can trigger sterile inflammation through Toll-like receptor 9 (TLR9)-dependent innate immune signaling. The developing mouse lung is particularly vulnerable to APAP exposure at
Indexed as
AcetaminophenAcute Lung InjuryImmunity, InnateLungSignal TransductionToll-Like Receptor 9AnimalsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutAcetaminophenTlr9 protein, mouseToll-Like Receptor 9acetaminophen/paracetamolCYP2E1lung injurysterile inflammationTLR9
Identifiers
PMID42155595
PMCPMC13273618
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