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Open AccessArticle

Microtubule-Mediated NLRP3 Inflammasome Activation Is Independent of Microtubule-Associated Innate Immune Factor GEF-H1 in Murine Macrophages

by 1,†, 1,†, 1,† and 1,2,*
1
Department of Life Science, National Taiwan University, Taipei 10617, Taiwan
2
Genome and Systems Biology Degree Program, National Taiwan University, Taipei 10617, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(4), 1302; https://doi.org/10.3390/ijms21041302
Received: 10 January 2020 / Revised: 8 February 2020 / Accepted: 12 February 2020 / Published: 14 February 2020
(This article belongs to the Special Issue Inflammasome)
Inflammasomes are intracellular multiple protein complexes that mount innate immune responses to tissue damage and invading pathogens. Their excessive activation is crucial in the development and pathogenesis of inflammatory disorders. Microtubules have been reported to provide the platform for mediating the assembly and activation of NLRP3 inflammasome. Recently, we have identified the microtubule-associated immune molecule guanine nucleotide exchange factor-H1 (GEF-H1) that is crucial in coupling microtubule dynamics to the initiation of microtubule-mediated immune responses. However, whether GEF-H1 also controls the activation of other immune receptors that require microtubules is still undefined. Here we employed GEF-H1-deficient mouse bone marrow-derived macrophages (BMDMs) to interrogate the impact of GEF-H1 on the activation of NLRP3 inflammasome. NLRP3 but not NLRC4 or AIM2 inflammasome-mediated IL-1β production was dependent on dynamic microtubule network in wild-type (WT) BMDMs. However, GEF-H1 deficiency did not affect NLRP3-driven IL-1β maturation and secretion in macrophages. Moreover, α-tubulin acetylation and mitochondria aggregations were comparable between WT and GEF-H1-deficient BMDMs in response to NLRP3 inducers. Further, GEF-H1 was not required for NLRP3-mediated immune defense against Salmonella typhimurium infection. Collectively, these findings suggest that the microtubule-associated immune modulator GEF-H1 is dispensable for microtubule-mediated NLRP3 activation and host defense in mouse macrophages. View Full-Text
Keywords: GEF-H1; microtubule; inflammasome; NLRP3; macrophage; inflammation GEF-H1; microtubule; inflammasome; NLRP3; macrophage; inflammation
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MDPI and ACS Style

Lai, H.-J.; Hsu, Y.-H.; Lee, G.-Y.; Chiang, H.-S. Microtubule-Mediated NLRP3 Inflammasome Activation Is Independent of Microtubule-Associated Innate Immune Factor GEF-H1 in Murine Macrophages. Int. J. Mol. Sci. 2020, 21, 1302. https://doi.org/10.3390/ijms21041302

AMA Style

Lai H-J, Hsu Y-H, Lee G-Y, Chiang H-S. Microtubule-Mediated NLRP3 Inflammasome Activation Is Independent of Microtubule-Associated Innate Immune Factor GEF-H1 in Murine Macrophages. International Journal of Molecular Sciences. 2020; 21(4):1302. https://doi.org/10.3390/ijms21041302

Chicago/Turabian Style

Lai, Hsuan-Ju; Hsu, Yi-Hsuan; Lee, Guan-Ying; Chiang, Hao-Sen. 2020. "Microtubule-Mediated NLRP3 Inflammasome Activation Is Independent of Microtubule-Associated Innate Immune Factor GEF-H1 in Murine Macrophages" Int. J. Mol. Sci. 21, no. 4: 1302. https://doi.org/10.3390/ijms21041302

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