CISH controls bacterial burden early after infection with Mycobacterium tuberculosis in mice

Carow, Berit; Gao, Yu; Terán, Graciela; Yang, Xuexian O.; Dong, Chen; Yoshimura, Akihiko; Rottenberg, Martı́n E.

doi:10.1016/j.tube.2017.09.007

Cited by 9 publications

(11 citation statements)

References 32 publications

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“…14 In other quantitative RT-PCR (qRT-PCR) experiments, and in ELISA and immunoblotting experiments, BMDMs were instead generated using 20 ng/ml recombinant mouse macrophage colony-stimulating factor (M-CSF) (R&D Systems, Minneapolis, MN) in complete Dulbecco's modified Eagle's medium. For time-course experiments with PAM3CSK4 and Mycobacterium bovis Bacillus Calmette-Gu erin (BCG), we used complete Dulbecco's modified Eagle's medium supplemented with supernatant from L929 cell cultures as previously described.…”

Section: Cell Culturementioning

confidence: 99%

“…For time-course experiments with PAM3CSK4 and Mycobacterium bovis Bacillus Calmette-Gu erin (BCG), we used complete Dulbecco's modified Eagle's medium supplemented with supernatant from L929 cell cultures as previously described. 14 In other quantitative RT-PCR (qRT-PCR) experiments, and in ELISA and immunoblotting experiments, BMDMs were instead generated using 20 ng/ml recombinant mouse macrophage colony-stimulating factor (M-CSF) (R&D Systems, Minneapolis, MN) in complete Dulbecco's modified Eagle's medium. The study was approved by the Ethical Review Committee North, Stockholm County.…”

Section: Cell Culturementioning

confidence: 99%

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TRIM21 controls Toll‐like receptor 2 responses in bone‐marrow‐derived macrophages

et al. 2019

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TRIM21 is an interferon-stimulated E3 ligase that controls the activity of pattern-recognition signaling via ubiquitination of interferon regulatory factors and DDX41. Previous studies on the role of TRIM21 in innate immune responses have yielded contradictory results, suggesting that the role of TRIM21 is cell specific. Here, we report that bone-marrow-derived macrophages (BMDMs) generated from Trim21 À/À mice have reduced expression of mature macrophage markers. Reflecting their reduced differentiation in response to macrophage colony-stimulating factor (M-CSF), Trim21 À/À BMDMs had decreased expression of M-CSF signature genes. Although Trim21 À/À BMDMs responded normally to Toll-like receptor 9 (TLR9) activation, they produced lower levels of pro-inflammatory cytokines in response to the TLR2 agonist PAM3CSK4. In line with this, the response to infection with the Bacillus Calmette-Gu erin strain of Mycobacterium bovis was also diminished in Trim21 À/À BMDMs. Our results indicate that TRIM21 controls responses to TLR2 agonists.

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Section: Cell Culturementioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

TRIM21 controls Toll‐like receptor 2 responses in bone‐marrow‐derived macrophages

et al. 2019

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“…SOCS1, 4, and 5 are highly expressed in mice infected with hypervirulent Mtb (Manca et␣al , 2005). CISH, a founding member of the SOCS family, can mediate control of Mtb in mice shortly after infection (Carow et␣al , 2017). Meanwhile, SOCS6 expression is reportedly enhanced by exosomes from IL‐1β‐primed mesenchymal stem cells; this process is related to osteoarthritic signal regulation (Kim et␣al , 2021).…”

Section: Introductionmentioning

confidence: 99%

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

Lin

Tan

et al. 2021

EMBO Reports

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Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis (Mtb) that places a heavy strain on public health. Host susceptibility to Mtb is modulated by macrophages, which regulate the balance between cell apoptosis and necrosis. However, the role of molecular switches that modulate apoptosis and necrosis during Mtb infection remains unclear. Here, we show that Mtb‐susceptible mice and TB patients have relatively low miR‐342‐3p expression, while mice with miR‐342‐3p overexpression are more resistant to Mtb. We demonstrate that the miR‐342‐3p/SOCS6 axis regulates anti‐Mtb immunity by increasing the production of inflammatory cytokines and chemokines. Most importantly, the miR‐342‐3p/SOCS6 axis participates in the switching between Mtb‐induced apoptosis and necrosis through A20‐mediated K48‐linked ubiquitination and RIPK3 degradation. Our findings reveal several strategies by which the host innate immune system controls intracellular Mtb growth via the miRNA‐mRNA network and pave the way for host‐directed therapies targeting these pathways.

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“…Interestingly, the SNPs displaying the best p values were within the CISH-MAPKAPK3-DOCK3 locus. The CISH and MAPKAPK3 genes are known to modulate the immune response [ 21 , 22 , 23 , 24 , 25 , 26 ], whereas DOCK3 is mainly expressed in nervous system and involved in developmental disorders [ 27 , 28 , 29 ].…”

Section: Resultsmentioning

confidence: 99%

Genetic Predisposition to the Mortality in Septic Shock Patients: From GWAS to the Identification of a Regulatory Variant Modulating the Activity of a CISH Enhancer

Rosier

Dupuis

Baaklini

et al. 2021

IJMS

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The high mortality rate in septic shock patients is likely due to environmental and genetic factors, which influence the host response to infection. Two genome-wide association studies (GWAS) on 832 septic shock patients were performed. We used integrative bioinformatic approaches to annotate and prioritize the sepsis-associated single nucleotide polymorphisms (SNPs). An association of 139 SNPs with death based on a false discovery rate of 5% was detected. The most significant SNPs were within the CISH gene involved in cytokine regulation. Among the 139 SNPs associated with death and the 1311 SNPs in strong linkage disequilibrium with them, we investigated 1439 SNPs within non-coding regions to identify regulatory variants. The highest integrative weighted score (IW-score) was obtained for rs143356980, indicating that this SNP is a robust regulatory candidate. The rs143356980 region is located in a non-coding region close to the CISH gene. A CRISPR-Cas9-mediated deletion of this region and specific luciferase assays in K562 cells showed that rs143356980 modulates the enhancer activity in K562 cells. These analyses allowed us to identify several genes associated with death in patients with septic shock. They suggest that genetic variations in key genes, such as CISH, perturb relevant pathways, increasing the risk of death in sepsis patients.

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CISH controls bacterial burden early after infection with Mycobacterium tuberculosis in mice

Cited by 9 publications

References 32 publications

TRIM21 controls Toll‐like receptor 2 responses in bone‐marrow‐derived macrophages

TRIM21 controls Toll‐like receptor 2 responses in bone‐marrow‐derived macrophages

MiR‐342 controls Mycobacterium tuberculosis susceptibility by modulating inflammation and cell death

Genetic Predisposition to the Mortality in Septic Shock Patients: From GWAS to the Identification of a Regulatory Variant Modulating the Activity of a CISH Enhancer

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