ArticleThe Journal of clinical investigation2008
Host-derived oxidized phospholipids and HDL regulate innate immunity in human leprosy.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Silence on the plate: revisiting the enigma ofFrontiers in microbiology · 2025Pooled it
- miRNome Expression Analysis Reveals New Players on Leprosy Immune Physiopathology.Frontiers in immunology · 2018Trial
- Oral Apolipoprotein A-I Mimetic D-4F Lowers HDL-Inflammatory Index in High-Risk Patients: A First-in-Human Multiple-Dose, Randomized Controlled Trial.Clinical and translational science · 2017Trial
- Oxidized phospholipid damage signals as modulators of immunity.Open biology · 2025Review
- Article
- IFN-γ induced the formation of foamy macrophages via CD40 signal to controlFrontiers in immunology · 2025Article
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- Cisplatin-induced oxPAPC release enhances MDSCs infiltration into LL2 tumour tissues through MCP-1/CCL2 and LTB4/LTB4R pathways.Cell proliferation · 2024Article
- Identification of gene signatures and molecular mechanisms underlying the mutual exclusion between psoriasis and leprosy.Scientific reports · 2024Article
- Review
- CD1-mediated immune responses in mucosal tissues: molecular mechanisms underlying lipid antigen presentation system.Experimental & molecular medicine · 2023Review
- Macrophage Biology in Human Granulomatous Skin Inflammation.International journal of molecular sciences · 2023Review
- Gene expression patterns associated with multidrug therapy in multibacillary leprosy.Frontiers in cellular and infection microbiology · 2022Article
- Modulation of the Response toFrontiers in microbiology · 2022Review
- In search of biomarkers for leprosy by unraveling the host immune response to Mycobacterium leprae.Immunological reviews · 2021Review
- Increased oxidative stress in elderly leprosy patients is related to age but not to bacillary load.PLoS neglected tropical diseases · 2021Article
- Article
- Plasma Phospholipids: A Promising Simple Biochemical Parameter to Evaluate COVID-19 Infection Severity.Bioinformatics and biology insights · 2021Article
- Host-Related Laboratory Parameters for Leprosy Reactions.Frontiers in medicine · 2021Review
- Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities.Frontiers in immunology · 2021Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Intracellular pathogens survive by evading the host immune system and accessing host metabolic pathways to obtain nutrients for their growth. Mycobacterium leprae, the causative agent of leprosy, is thought to be the mycobacterium most dependent on host metabolic pathways, including host-derived lipids. Although fatty acids and phospholipids accumulate in the lesions of individuals with the lepromatous (also known as disseminated) form of human leprosy (L-lep), the origin and significance of these lipids remains unclear. Here we show that in human L-lep lesions, there was preferential expression of host lipid metabolism genes, including a group of phospholipases, and that these genes were virtually absent from the mycobacterial genome. Host-derived oxidized phospholipids were detected in macrophages within L-lep lesions, and 1 specific oxidized phospholipid, 1-palmitoyl-2-(5,6-epoxyisoprostane E2)-sn-glycero-3-phosphorylcholine (PEIPC), accumulated in macrophages infected with live mycobacteria. Mycobacterial infection and host-derived oxidized phospholipids both inhibited innate immune responses, and this inhibition was reversed by the addition of normal HDL, a scavenger of oxidized phospholipids, but not by HDL from patients with L-lep. The accumulation of host-derived oxidized phospholipids in L-lep lesions is strikingly similar to observations in atherosclerosis, which suggests that the link between host lipid metabolism and innate immunity contributes to the pathogenesis of both microbial infection and metabolic disease.
Indexed as
Identifiers
What OpenQuestion holds
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.