ArticleScientific reports2016
Mycobacterium leprae-induced Insulin-like Growth Factor I attenuates antimicrobial mechanisms, promoting bacterial survival in macrophages.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 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
- Dual-Action Regenerative Therapies: Regeneration and Antimicrobial Effects of Platelet- and Marrow-Derived Biologics.Biomedicines · 2025Review
- IFN-γ-Driven macrophage responses in the immunity toFrontiers in cellular and infection microbiology · 2025Review
- MicroRNA biomarkers in leprosy: insights from the Northern Brazilian Amazon population and their implications in disease immune-physiopathology.Frontiers in genetics · 2024Article
- Review
- GRP78 facilitates M2 macrophage polarization and tumour progression.Cellular and molecular life sciences : CMLS · 2021Article
- In search of biomarkers for leprosy by unraveling the host immune response to Mycobacterium leprae.Immunological reviews · 2021Review
- Silver(I) and Copper(II) Complexes of 1,10-Phenanthroline-5,6-Dione AgainstFrontiers in microbiology · 2021Article
- Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities.Frontiers in immunology · 2021Review
- Reanalysis and integration of public microarray datasets reveals novel host genes modulated in leprosy.Molecular genetics and genomics : MGG · 2020Article
- Macrophages From Subjects With Isolated GH/IGF-I Deficiency Due to a GHRH Receptor Gene Mutation Are Less Prone to Infection byFrontiers in cellular and infection microbiology · 2019Article
- Type I Interferons, Autophagy and Host Metabolism in Leprosy.Frontiers in immunology · 2018Review
- Host Lipid Mediators in Leprosy: The Hypothesized Contributions to Pathogenesis.Frontiers in immunology · 2018Review
- ELISA-based assay of immunoglobulin G antibodies against mammalian cell entry 1A (Mce1A) protein: a novel diagnostic approach for leprosy.Memorias do Instituto Oswaldo Cruz · 2017Article
- New Genome-Wide Algorithm Identifies Novel In-Vivo Expressed Mycobacterium Tuberculosis Antigens Inducing Human T-Cell Responses with Classical and Unconventional Cytokine Profiles.Scientific reports · 2016Article
- Identifying the levels of pro-fibrotic cytokines in pulmonary tuberculosis.Lung India : official organ of Indian Chest SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium leprae (ML), the etiologic agent of leprosy, can subvert macrophage antimicrobial activity by mechanisms that remain only partially understood. In the present study, the participation of hormone insulin-like growth factor I (IGF-I) in this phenomenum was investigated. Macrophages from the dermal lesions of the disseminated multibacillary lepromatous form (LL) of leprosy expressed higher levels of IGF-I than those from the self-limited paucibacillary tuberculoid form (BT). Higher levels of IGF-I secretion by ML-infected macrophages were confirmed in ex vivo and in vitro studies. Of note, the dampening of IGF-I signaling reverted the capacity of ML-infected human and murine macrophages to produce antimicrobial molecules and promoted bacterial killing. Moreover, IGF-I was shown to inhibit the JAK/STAT1-dependent signaling pathways triggered by both mycobacteria and IFN-γ most probably through its capacity to induce the suppressor of cytokine signaling-3 (SOCS3). Finally, these in vitro findings were corroborated by in vivo observations in which higher SOCS3 expression and lower phosphorylation of STAT1 levels were found in LL versus BT dermal lesions. Altogether, our data strongly suggest that IGF-I contributes to the maintenance of a functional program in infected macrophages that suits ML persistence in the host, reinforcing a key role for IGF-I in leprosy pathogenesis.
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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.