IRGB10 Liberates Bacterial Ligands for Sensing by the AIM2 and Caspase-11-NLRP3 Inflammasomes

Man, Si Ming; Karki, Rajendra; Sasai, Miwa; Place, David E.; Kesavardhana, Sannula; Temirov, Jamshid; Frase, Sharon; Zhu, Qifan; Malireddi, R. K. Subbarao; Kuriakose, Teneema; Peters, Jennifer L.; Neale, Geoffrey; Brown, Scott A.; Yamamoto, Masahiro; Kanneganti, Thirumala‐Devi

doi:10.1016/j.cell.2016.09.012

Cited by 255 publications

(317 citation statements)

References 56 publications

Supporting

Mentioning

302

Contrasting

Unclassified

Order By: Relevance

“…GBPs also participate in directly activating the NLRP3 inflammasome in response to both Salmonella and Chlamydia 55, 56 . Further, GBPs recruit the interferon-inducible protein IRGB10 to intracellular bacteria, which then mediates the release of bacterial ligands for detection by inflammasome sensors 57 .…”

Section: Ifn-γ and Control Of Salmonella In The Phagocyte Scvmentioning

confidence: 99%

Interferon-γ in Salmonella pathogenesis: New tricks for an old dog

2017

View full text Add to dashboard Cite

Salmonella enterica is a facultative intracellular bacterium that is the leading cause of food borne illnesses in humans. The cytokine IFN-γ has well-established antibacterial properties against Salmonella and other intracellular microbes, for example its capacity to activate macrophages, promote phagocytosis, and destroy phagocytosed microbes by free radical-driven toxification of phagosomes. But IFN-γ induces the expression of hundreds of uncharacterized genes, suggesting that this cytokine deploys additional antimicrobial strategies that await discovery. Recently, one such mechanism, mediated by a family of IFN-inducible small GTPases called Guanylate Binding Proteins (GBPs) has been uncovered. GBPs were shown to facilitate the pyroptotic clearance of Salmonella from infected macrophages by rupturing the protective intracellular vacuole this microbe forms around itself. Once this protective vacuole is lost, exposed Salmonella activates pyroptosis, which destroys the infected cell. In this review, we summarize such emerging roles for IFN-γ in restricting Salmonella pathogenesis.

show abstract

Section: Ifn-γ and Control Of Salmonella In The Phagocyte Scvmentioning

confidence: 99%

Interferon-γ in Salmonella pathogenesis: New tricks for an old dog

2017

View full text Add to dashboard Cite

show abstract

“…This requires NF-κB and Stat1 binding to the caspase-11 promoter [125] . There is also emerging literature suggesting that additional IFN-induced genes, guanylate-binding proteins (GBPs) and IRGB10, are required for LPS release from bacteria into the cytoplasm [126] .…”

Section: Priming Of the Non-canonical Inflammasomementioning

confidence: 99%

Inflammasome Priming in Sterile Inflammatory Disease

Patel

Carroll

Galván-Peña

et al. 2017

Trends in Molecular Medicine

211

167

View full text Add to dashboard Cite

“…IRGs and GBPs facilitate cell-intrinsic immunity in vitro and host resistance in vivo to a broad spectrum of intracellular pathogens (16). In infected cells, IRGs and GBPs colocalize with intracellular bacterial pathogens residing in the host cell cytosol or within PVs (16,18), and several studies have suggested functional interactions between members of the IRG and GBP families (18)(19)(20)(21)(22)(23). Although IRGs and GBPs can combat intracellular infections cooperatively, mounting evidence suggests that these two protein families also execute unique cellular functions independent of one another (16).…”

Section: Significancementioning

confidence: 99%

Galectin-3 directs antimicrobial guanylate binding proteins to vacuoles furnished with bacterial secretion systems

Feeley

Pilla-Moffett

Zwack

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

127

155

View full text Add to dashboard Cite

Many invasive bacteria establish pathogen-containing vacuoles (PVs) as intracellular niches for microbial growth. Immunity to these infections is dependent on the ability of host cells to recognize PVs as targets for host defense. The delivery of several host defense proteins to PVs is controlled by IFN-inducible guanylate binding proteins (GBPs), which themselves dock to PVs through poorly characterized mechanisms. Here, we demonstrate that GBPs detect the presence of bacterial protein secretion systems as “patterns of pathogenesis” associated with PVs. We report that the delivery of GBP2 to Legionella-containing vacuoles is dependent on the bacterial Dot/Icm secretion system, whereas the delivery of GBP2 to Yersinia-containing vacuoles (YCVs) requires hypersecretion of Yersinia translocon proteins. We show that the presence of bacterial secretion systems directs cytosolic carbohydrate-binding protein Galectin-3 to PVs and that the delivery of GBP1 and GBP2 to Legionella-containing vacuoles or YCVs is substantially diminished in Galectin-3–deficient cells. Our results illustrate that insertion of bacterial secretion systems into PV membranes stimulates Galectin-3–dependent recruitment of antimicrobial GBPs to PVs as part of a coordinated host defense program.

show abstract

IRGB10 Liberates Bacterial Ligands for Sensing by the AIM2 and Caspase-11-NLRP3 Inflammasomes

Cited by 255 publications

References 56 publications

Interferon-γ in Salmonella pathogenesis: New tricks for an old dog

Interferon-γ in Salmonella pathogenesis: New tricks for an old dog

Inflammasome Priming in Sterile Inflammatory Disease

Galectin-3 directs antimicrobial guanylate binding proteins to vacuoles furnished with bacterial secretion systems

Contact Info

Product

Resources

About