scholarly journals Innate immune signaling by Toll-like receptor-4 (TLR4) shapes the inflammatory microenvironment in colitis-associated tumors

2009 ◽  
Vol 15 (7) ◽  
pp. 997-1006 ◽  
Author(s):  
Masayuki Fukata ◽  
Yasmin Hernandez ◽  
Daisy Conduah ◽  
Jason Cohen ◽  
Anli Chen ◽  
...  
Keyword(s):  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Immune Signaling ◽  
Inflammatory Microenvironment ◽  
Innate Immune Signaling ◽  
Associated Tumors

scholarly journals Hexa-Acylated Lipid A Is Required for Host Inflammatory Response to Neisseria gonorrhoeae in Experimental Gonorrhea

2013 ◽  
Vol 82 (1) ◽  
pp. 184-192 ◽  
Author(s):  
Xiyou Zhou ◽  
Xi Gao ◽  
Peter M. Broglie ◽  
Chahnaz Kebaier ◽  
James E. Anderson ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Lipid A ◽  
Innate Immune ◽  
Immune Recognition ◽  
Toll Like Receptor ◽  
Inflammatory Signaling ◽  
Toll Like Receptor 4 ◽  
Immune Signaling ◽  
Content Type ◽  
Innate Immune Signaling

ABSTRACTNeisseria gonorrhoeaecauses gonorrhea, a sexually transmitted infection characterized by inflammation of the cervix or urethra. However, a significant subset of patients withN. gonorrhoeaeremain asymptomatic, without evidence of localized inflammation. Inflammatory responses toN. gonorrhoeaeare generated by host innate immune recognition ofN. gonorrhoeaeby several innate immune signaling pathways, including lipooligosaccharide (LOS) and other pathogen-derived molecules through activation of innate immune signaling systems, including toll-like receptor 4 (TLR4) and the interleukin-1β (IL-1β) processing complex known as the inflammasome. The lipooligosaccharide ofN. gonorrhoeaehas a hexa-acylated lipid A.N. gonorrhoeaestrains that carry an inactivatedmsbB(also known aslpxL1) gene produce a penta-acylated lipid A and exhibit reduced biofilm formation, survival in epithelial cells, and induction of epithelial cell inflammatory signaling. We now show thatmsbB-deficientN. gonorrhoeaeinduces less inflammatory signaling in human monocytic cell lines and murine macrophages than the parent organism. The penta-acylated LOS exhibits reduced toll-like receptor 4 signaling but does not affectN. gonorrhoeae-mediated activation of the inflammasome. We demonstrate thatN. gonorrhoeaemsbBis dispensable for initiating and maintaining infection in a murine model of gonorrhea. Interestingly, infection withmsbB-deficientN. gonorrhoeaeis associated with less localized inflammation. Combined, these data suggest that TLR4-mediated recognition ofN. gonorrhoeaeLOS plays an important role in the pathogenesis of symptomatic gonorrhea infection and that alterations in lipid A biosynthesis may play a role in determining symptomatic and asymptomatic infections.

Interactions between Viperin, IRAK1 andTRAF6 couple innate immune signaling to antiviral ribonucleotide synthesis

2018 ◽  
Author(s):  
Arti B. Dumbrepatil ◽  
Soumi Ghosh ◽  
Ayesha M. Patel ◽  
Kelcie A. Zegalia ◽  
Paige A. Malec ◽  
...  
Keyword(s):  
Structural Changes ◽  
Interleukin 1 ◽  
Innate Immune ◽  
Tnf Receptor ◽  
Toll Like Receptor ◽  
Immune Signaling ◽  
Innate Immune Signaling ◽  
Synergistic Activation ◽  
Catalytically Active ◽  
Cellular Antiviral Response

SummaryViperin is a radical S-adenosylmethionine (SAM) enzyme that plays a multifaceted role in the cellular antiviral response. Viperin was recently shown to catalyze the SAM-dependent formation of 3′-deoxy-3′,4′-didehydro-CTP (ddhCTP), which inhibits some viral RNA polymerases. Viperin is also implicated in regulating K63-linked poly-ubiquitination of interleukin-1 receptor-associated kinase-1 (IRAK1) by the E3 ubiquitin ligase TNF Receptor-Associated Factor 6 (TRAF6) as part of the Toll-like receptor-7 and 9 (TLR7/9) innate immune signaling pathways. We show that IRAK1 and TRAF6 activate viperin to efficiently catalyze the radical-mediated dehydration of CTP to ddhCTP. Furthermore, poly-ubiquitination of IRAK1 requires the association of viperin with IRAK1 and TRAF6. Poly-ubiquitination appears dependent on structural changes induced by SAM binding to viperin but does not require catalytically active viperin. The synergistic activation of viperin and IRAK1 provides a mechanism that couples innate immune signaling with the production of the antiviral nucleotide ddhCTP.

scholarly journals Viral Double-Strand RNA-Binding Proteins Can Enhance Innate Immune Signaling by Toll-Like Receptor 3

PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e25837 ◽  
Author(s):  
Yvonne Lai ◽  
Guanghui Yi ◽  
Alice Chen ◽  
Kanchan Bhardwaj ◽  
Brady J. Tragesser ◽  
...  
Keyword(s):  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Immune Signaling ◽  
Innate Immune Signaling

scholarly journals Structural elucidation of innate immune signaling

2014 ◽  
Vol 70 (a1) ◽  
pp. C298-C298
Author(s):  
Hao Wu
Keyword(s):  
Signal Transduction ◽  
Interleukin 1 ◽  
Structural Elucidation ◽  
Innate Immune ◽  
Structural Studies ◽  
Toll Like Receptor ◽  
Immune Signaling ◽  
Kinase Activation ◽  
Innate Immune Signaling

Signal transduction in the Toll-like receptor and interleukin-1 receptor pathways requires both kinase activation and ubiquitination. Here, we will present our recent structural studies on critical mediators of the pathways.

scholarly journals Toll-like Receptor-Deficient Mice Reveal How Innate Immune Signaling Influences Salmonella Virulence Strategies

2014 ◽  
Vol 15 (2) ◽  
pp. 203-213 ◽  
Author(s):  
Kelsey E. Sivick ◽  
Nicholas Arpaia ◽  
Gabrielle L. Reiner ◽  
Bettina L. Lee ◽  
Bethany R. Russell ◽  
...  
Keyword(s):  
Innate Immune ◽  
Toll Like Receptor ◽  
Immune Signaling ◽  
Innate Immune Signaling ◽  
Salmonella Virulence ◽  
Deficient Mice
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