ArticleiScience2021
Pulmonary infection induces persistent, pathogen-specific lipidomic changes influencing trained immunity.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Non-hematopoietic tryptophan metabolism is a driver of ineffective T cell responses during secondary pulmonary bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Single-cell lipidomics: protocol development for reliable cellular profiling using capillary sampling.The Analyst · 2025Article
- Preservation of scRNA-Seq Libraries Using Existing Inactivation Protocols.Pathogens (Basel, Switzerland) · 2024Article
- Understanding virus-host interactions in tissues.Nature microbiology · 2023Review
- Relevance of PUFA-derived metabolites in seminal plasma to male infertility.Frontiers in endocrinology · 2023Article
- Insights into the Antibacterial Activity of Prolactin-Inducible Protein against the Standard and Environmental MDR Bacterial Strains.Microorganisms · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resolution of infection results in development of trained innate immunity which is typically beneficial for defense against unrelated secondary infection. Epigenetic changes including modification of histones via binding of various polar metabolites underlie the establishment of trained innate immunity. Therefore, host metabolism and this response are intimately linked. However, little is known regarding the influence of lipids on the development and function of trained immunity. Utilizing two models of pulmonary bacterial infection combined with multi-omic approaches, we identified persistent, pathogen-specific changes to the lung lipidome that correlated with differences in the trained immune response against a third unrelated pathogen. Further, we establish the specific cellular populations in the lung that contribute to this altered lipidome. Together these results expand our understanding of the pulmonary trained innate immune response and the contributions of host lipids in informing that response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.