ArticleBMC microbiology2017
IRAK-M alters the polarity of macrophages to facilitate the survival of Mycobacterium tuberculosis.
Article in BMC microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 33 citations in OpenAlex.
- IRAK-M Knockout Exacerbates Inflammation in Mice Infected withMicroorganisms · 2026Article
- IRAK-M attenuates pain hypersensitivity and anxiety-like behaviors in a nitroglycerin-induced chronic migraine mouse model with concomitant reductions in microglial activation and neuroinflammation.The journal of headache and pain · 2026Article
- The role and mechanisms of multiple immunoregulatory cells in pulmonary tuberculosis.Frontiers in immunology · 2026Review
- Research progress in PANoptosis mechanisms and their interplay with tuberculosis.Frontiers in cellular and infection microbiology · 2026Review
- Delineation of signaling routes that underlie differences in macrophage phenotypic states.NAR molecular medicine · 2025Article
- Masterful macrophages: understanding and targeting activation dysfunction in diabetic wounds.Burns & trauma · 2025Review
- Macrophages, Metabolism, Mitochondria, Circadian Rhythmicity and the Pathogen: The Multidimensional Nature of Tuberculosis.Results and problems in cell differentiation · 2024Review
- Mutations in the Vicinity of the IRAK3 Guanylate Cyclase Center Impact Its Subcellular Localization and Ability to Modulate Inflammatory Signaling in Immortalized Cell Lines.International journal of molecular sciences · 2023Article
- Macrophages in aseptic loosening: Characteristics, functions, and mechanisms.Frontiers in immunology · 2023Review
- Human M1 macrophages express unique innate immune response genes after mycobacterial infection to defend against tuberculosis.Communications biology · 2022Article
- E3 Ligase FBXW7 FacilitatesFrontiers in cellular and infection microbiology · 2022Article
- Arginase 1 is involved in lacrimal hyposecretion in male NOD mice, a model of Sjögren's syndrome, regardless of dacryoadenitis status.The Journal of physiology · 2020Article
- HIV and the tuberculosis "set point": how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease.Retrovirology · 2020Review
- Hacking the host: exploitation of macrophage polarization by intracellular bacterial pathogens.Pathogens and disease · 2020Review
- Mycobacterial Trehalose 6,6'-Dimycolate-Induced M1-Type Inflammation.The American journal of pathology · 2020Article
- In vitro and in vivo immunomodulatory properties of octyl-β-D-galactofuranoside during Leishmania donovani infection.Parasites & vectors · 2019Article
- Long non-coding RNA deep sequencing reveals the role of macrophage in liver disorders.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracellular bacterium, Mycobacterium tuberculosis (M. tb), infects specifically macrophages as host cells. IRAK-M, a member of IRAK family, is a negative regulator in TLR signaling and specifically expresses in monocytes and macrophages. The role of IRAK-M in intracellular growth of M. tb and macrophage polarization was explored, for deeply understanding the pathogenesis of M. tb, the significance of IRAK-M to innate immunity and pathogen-host interaction.
methodsIRAK-M expression was detected in M. tb infected macrophages and in human lung tissue of pulmonary tuberculosis with immunofluorescence staining, Western blot and immunohistochemistry. IRAK-M knock-down and over-expressing cell strains were constructed and intracellular survival of M. tb was investigated by acid-fast staining and colony forming units. Molecular markers of M1-type (pSTAT1 and iNOS) and M2-type (pSTAT6 and Arg-1) macrophages were detected using Western blot in IRAK-M knockdown U937 cells infected with M. tb H37Rv. U937 cells were stimulated with immunostimulant CpG7909 into M1 status and then infected with M. tb H37Rv. Expression of IRAK-M, IRAK-4 and iNOS was detected with immunofluorescence staining and Western blot, to evaluate the effect of IRAK-M to CpG directed M1-type polarization of macrophages during M. tb infection. Molecules related with macrophage's bactericidal ability such as Hif-1 and phosphorylated ERK1/2 were detected with immunohistochemistry and Western blot.
resultsIRAK-M increased in M. tb infected macrophage cells and also in human lung tissue of pulmonary tuberculosis. IRAK-M over-expression resulted in higher bacterial load, while IRAK-M interference resulted in lower bacterial load in M. tb infected cells. During M. tb infection, IRAK-M knockdown induced M1-type, while inhibited M2-type polarization of macrophage. M1-type polarization of U937 cells induced by CpG7909 was inhibited by M. tb infection, which was reversed by IRAK-M knockdown in U937 cells. IRAK-M affected Hif-1 and MAPK signaling cascade during M. tb infection.
conclusionsConclusively, IRAK-M might alter the polarity of macrophages, to facilitate intracellular survival of M. tb and affect Th1-type immunity of the host, which is helpful to understanding the pathogenesis of M. tb.
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.