ArticlePloS one2013
The scavenger protein apoptosis inhibitor of macrophages (AIM) potentiates the antimicrobial response against Mycobacterium tuberculosis by enhancing autophagy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- CD5L is a potential negative regulator of chondrocyte apoptosis in osteoarthritis.Osteoarthritis and cartilage open · 2026Article
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- [CD5L is elevated in the serum of patients with candidemia and promotes disease progression in mouse models].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Characterization and Proteomic Analysis of Plasma EVs Recovered from Healthy and Diseased Dogs with Canine Leishmaniosis.International journal of molecular sciences · 2023Article
- Measurement of Autophagy Activity Reveals Time-Dependent, Bacteria-Specific Turnover duringPathogens (Basel, Switzerland) · 2022Article
- Article
- Nontuberculous Mycobacteria, Macrophages, and Host Innate Immune Response.Infection and immunity · 2021Review
- Multifaceted Roles of CD5L in Infectious and Sterile Inflammation.International journal of molecular sciences · 2021Review
- MIR337-3p Enhances Mycobacterial Pathogenicity Involving TLR4/MYD88 and STAT3 Signals, Impairing VDR Antimicrobial Response and Fast-Acting Immunity.Frontiers in immunology · 2021Article
- Administration of GDF3 Into Septic Mice Improves SurvivalFrontiers in immunology · 2021Article
- CD5L is a pleiotropic player in liver fibrosis controlling damage, fibrosis and immune cell content.EBioMedicine · 2019Article
- Mycobacterium tuberculosis and macrophage nuclear receptors: What we do and don't know.Tuberculosis (Edinburgh, Scotland) · 2019Review
- IL-36/LXR axis modulates cholesterol metabolism and immune defense to Mycobacterium tuberculosis.Scientific reports · 2018Article
- CD5L Promotes M2 Macrophage Polarization through Autophagy-Mediated Upregulation of ID3.Frontiers in immunology · 2018Article
- A Beneficial Effect of Low-Dose Aspirin in a Murine Model of Active Tuberculosis.Frontiers in immunology · 2018Article
- TLR4-NOX2 axis regulates the phagocytosis and killing of Mycobacterium tuberculosis by macrophages.BMC pulmonary medicine · 2017Article
- Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy.Scientific reports · 2017Article
- Mycobacterium tuberculosis PE_PGRS41 Enhances the Intracellular Survival of M. smegmatis within Macrophages Via Blocking Innate Immunity and Inhibition of Host Defense.Scientific reports · 2017Article
- Inflammatory protein response in CDKL5-Rett syndrome: evidence of a subclinical smouldering inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis inhibitor of macrophages (AIM), a scavenger protein secreted by tissue macrophages, is transcriptionally regulated by the nuclear receptor Liver X Receptor (LXR) and Retinoid X Receptor (RXR) heterodimer. Given that LXR exerts a protective immune response against M. tuberculosis, here we analyzed whether AIM is involved in this response. In an experimental murine model of tuberculosis, AIM serum levels peaked dramatically early after infection with M. tuberculosis, providing an in vivo biological link to the disease. We therefore studied the participation of AIM in macrophage response to M. tuberculosis in vitro. For this purpose, we used the H37Rv strain to infect THP-1 macrophages transfected to stably express AIM, thereby increasing infected macrophage survival. Furthermore, the expression of this protein enlarged foam cell formation by enhancing intracellular lipid content. Phagocytosis assays with FITC-labeled M. tuberculosis bacilli indicated that this protein was not involved in bacterial uptake; however, AIM expression decreased the number of intracellular cfus by up to 70% in bacterial killing assays, suggesting that AIM enhances macrophage mycobactericidal activity. Accordingly, M. tuberculosis-infected AIM-expressing cells upregulated the production of reactive oxygen species. Moreover, real-time PCR analysis showed increased mRNA levels of the antimicrobial peptides cathelicidin and defensin 4B. These increases were concomitant with greater cellular concentrations of the autophagy-related molecules Beclin 1 and LC3II, as well as enhanced acidification of mycobacterial phagosomes and LC3 co-localization. In summary, our data support the notion that AIM contributes to key macrophage responses to M. tuberculosis.
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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.