Interleukin 1 alpha (IL-1α) restricts Brucella abortus 544 survival through promoting lysosomal-mediated killing and NO production in macrophages

Hop, Huynh Tan; Reyes, Alisha Wehdnesday Bernardo; Arayan, Lauren Togonon; Huy, Tran Xuan Ngoc; Vu, Son Hai; Min, Wongi; Lee, Hu Jang; Kang, Chang Keun; Rhee, Man Hee; Kim, Suk

doi:10.1016/j.vetmic.2019.04.019

Cited by 9 publications

(2 citation statements)

References 42 publications

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“…3, C and D). Consistently, previous reports have shown that knockdown or activation of IL1A positively correlates with C/EBPβ expression (Hop et al, 2019;Montes et al, 2015;Yang et al, 2015). Similar to what others have shown, our data suggest that changes in C/EBPβ and IL6, IL1B, and CXCL8 expression are downstream of IL1A (Orjalo et al, 2009) and not simply a consequence of decreased C/EBPβ due to DOT1L knockdown.…”

Section: Dot1l Expression Is Necessary For Sasp Gene Expressionsupporting

confidence: 93%

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

Leon

Buj

Lesko

et al. 2021

Journal of Cell Biology

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Oncogene-induced senescence (OIS) is a stable cell cycle arrest that occurs in normal cells upon oncogene activation. Cells undergoing OIS express a wide variety of secreted factors that affect the senescent microenvironment termed the senescence-associated secretory phenotype (SASP), which is beneficial or detrimental in a context-dependent manner. OIS cells are also characterized by marked epigenetic changes. We globally assessed histone modifications of OIS cells and discovered an increase in the active histone marks H3K79me2/3. The H3K79 methyltransferase disruptor of telomeric silencing 1-like (DOT1L) was necessary and sufficient for increased H3K79me2/3 occupancy at the IL1A gene locus, but not other SASP genes, and was downstream of STING. Modulating DOT1L expression did not affect the cell cycle arrest. Together, our studies establish DOT1L as an epigenetic regulator of the SASP, whose expression is uncoupled from the senescence-associated cell cycle arrest, providing a potential strategy to inhibit the negative side effects of senescence while maintaining the beneficial inhibition of proliferation.

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Section: Dot1l Expression Is Necessary For Sasp Gene Expressionsupporting

confidence: 93%

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

Leon

Buj

Lesko

et al. 2021

Journal of Cell Biology

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“…Our results show that both type I IFN and IL-1 signaling cooperate to induce production of NO in an additive manner. While type I IFN signaling has been more closely linked with NO production through the inducible nitric oxide synthase ( Nos2 ) [ 43 , 64 ], it is possible that IL-1 could also drive NO production as in the case of Brucella infection [ 65 ]. Collectively, the data suggest that the dispensability of either signaling pathway during in vivo rpoB -H445Y Mtb infection is tied to compensatory NO production that is sufficient for protection.…”

Section: Discussionmentioning

confidence: 99%

A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y

Bobba,

Chauhan,

Akter

et al. 2024

PLoS Pathog

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Interleukin-1 (IL-1) signaling is essential for controlling virulent Mycobacterium tuberculosis (Mtb) infection since antagonism of this pathway leads to exacerbated pathology and increased susceptibility. In contrast, the triggering of type I interferon (IFN) signaling is associated with the progression of tuberculosis (TB) disease and linked with negative regulation of IL-1 signaling. However, mice lacking IL-1 signaling can control Mtb infection if infected with an Mtb strain carrying the rifampin-resistance conferring mutation H445Y in its RNA polymerase β subunit (rpoB-H445Y Mtb). The mechanisms that govern protection in the absence of IL-1 signaling during rpoB-H445Y Mtb infection are unknown. In this study, we show that in the absence of IL-1 signaling, type I IFN signaling controls rpoB-H445Y Mtb replication, lung pathology, and excessive myeloid cell infiltration. Additionally, type I IFN is produced predominantly by monocytes and recruited macrophages and acts on LysM-expressing cells to drive protection through nitric oxide (NO) production to restrict intracellular rpoB-H445Y Mtb. These findings reveal an unexpected protective role for type I IFN signaling in compensating for deficiencies in IL-1 pathways during rpoB-H445Y Mtb infection.

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Omp16, a conserved peptidoglycan-associated lipoprotein, is involved in Brucella virulence in vitro

Zhi

Zhou

et al. 2020

J Microbiol.

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Interleukin 1 alpha (IL-1α) restricts Brucella abortus 544 survival through promoting lysosomal-mediated killing and NO production in macrophages

Cited by 9 publications

References 42 publications

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y

Omp16, a conserved peptidoglycan-associated lipoprotein, is involved in Brucella virulence in vitro

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