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https://www.readbyqxmd.com/read/29629899/ask1-2-signaling-promotes-inflammation-in-a-mouse-model-of-neutrophilic-dermatosis
#1
Sarang Tartey, Prajwal Gurung, Tejasvi Krishna Dasari, Amanda Burton, Thirumala-Devi Kanneganti
Mice homozygous for the Tyr208Asn amino acid substitution in the carboxy terminus of Src homology region 2 (SH2) domain-containing phosphatase 1 (SHP-1) (referred to as Ptpn6spin mice) spontaneously develop a severe inflammatory disease resembling neutrophilic dermatosis in humans. Disease in Ptpn6spin mice is characterized by persistent footpad swelling and suppurative inflammation. Recently, in addition to IL-1α and IL-1R signaling, we demonstrated a pivotal role for several kinases such as SYK, RIPK1, and TAK1 in promoting inflammatory disease in Ptpn6spin mice...
April 9, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29576451/irf8-regulates-transcription-of-naips-for-nlrc4-inflammasome-activation
#2
Rajendra Karki, Ein Lee, David Place, Parimal Samir, Jayadev Mavuluri, Bhesh Raj Sharma, Arjun Balakrishnan, R K Subbarao Malireddi, Rechel Geiger, Qifan Zhu, Geoffrey Neale, Thirumala-Devi Kanneganti
Inflammasome activation is critical for host defenses against various microbial infections. Activation of the NLRC4 inflammasome requires detection of flagellin or type III secretion system (T3SS) components by NLR family apoptosis inhibitory proteins (NAIPs); yet how this pathway is regulated is unknown. Here, we found that interferon regulatory factor 8 (IRF8) is required for optimal activation of the NLRC4 inflammasome in bone-marrow-derived macrophages infected with Salmonella Typhimurium, Burkholderia thailandensis, or Pseudomonas aeruginosa but is dispensable for activation of the canonical and non-canonical NLRP3, AIM2, and Pyrin inflammasomes...
March 16, 2018: Cell
https://www.readbyqxmd.com/read/29562174/detrimental-type-i-interferon-signaling-dominates-protective-aim2-inflammasome-responses-during-francisella-novicida-infection
#3
Qifan Zhu, Si Ming Man, Rajendra Karki, R K Subbarao Malireddi, Thirumala-Devi Kanneganti
Interferons (IFNs) and inflammasomes are essential mediators of anti-microbial immunity. Type I IFN signaling drives activation of the AIM2 inflammasome in macrophages; however, the relative contribution of IFNs and inflammasome responses in host defense is less understood. We report intact AIM2 inflammasome responses in mice lacking type I IFN signaling during infection with F. novicida. Lack of type I IFN signaling conferred protection to F. novicida infection in contrast to the increased susceptibility in AIM2-deficient mice...
March 20, 2018: Cell Reports
https://www.readbyqxmd.com/read/29514058/food-for-training-western-diet-and-inflammatory-memory
#4
Parimal Samir, R K Subbarao Malireddi, Thirumala-Devi Kanneganti
In recent years, trained immunity has emerged as an attractive concept to explain cross-protection against pathogens mediated by the innate immune system. Using a diet-based sterile inflammation model, Christ et al. (2018) have shown in a recent issue of Cell that trained immunity may also play a critical role in responding to diet and endogenous sterile triggers.
March 6, 2018: Cell Metabolism
https://www.readbyqxmd.com/read/29500178/tak1-restricts-spontaneous-nlrp3-activation-and-cell-death-to-control-myeloid-proliferation
#5
R K Subbarao Malireddi, Prajwal Gurung, Jayadev Mavuluri, Tejasvi Krishna Dasari, Jeffery M Klco, Hongbo Chi, Thirumala-Devi Kanneganti
The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis...
April 2, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29353059/ask-family-kinases-are-required-for-optimal-nlrp3-inflammasome-priming
#6
David E Place, Parimal Samir, Rajendra Karki, Benoit Briard, Peter Vogel, Thirumala-Devi Kanneganti
Activation of the multimeric inflammasome complex leads to inflammatory responses to biotic and abiotic triggers. The inflammasome sensor, Nod-like receptor family pyrin domain containing 3 (NLRP3), is activated by a range of stimuli and is tightly regulated to restrict excessive inflammation. Because NLRP3 responds broadly to cellular insults and regulates cell death similar to the stress-activated apoptosis signal-regulating kinases 1 and 2 (ASK1/2), we hypothesized that ASK1/2 may regulate NLRP3 activity...
April 2018: American Journal of Pathology
https://www.readbyqxmd.com/read/29348507/stressed-out-ros-take-a-silent-death-route
#7
Sannula Kesavardhana, Thirumala-Devi Kanneganti
No abstract text is available yet for this article.
February 2018: Nature Immunology
https://www.readbyqxmd.com/read/29343431/gasdermin-d-flashes-an-exit-signal-for-il-1
#8
Teneema Kuriakose, Thirumala-Devi Kanneganti
The IL-1 family of cytokines follows an unconventional pathway of secretion mostly associated with inflammatory cell death. In this issue of Immunity, (Evavold et al., 2017) report gasdermin D pores as channels for active IL-1 release in live phagocytic cells.
January 16, 2018: Immunity
https://www.readbyqxmd.com/read/29321274/irf1-is-a-transcriptional-regulator-of-zbp1-promoting-nlrp3-inflammasome-activation-and-cell-death-during-influenza-virus-infection
#9
Teneema Kuriakose, Min Zheng, Geoffrey Neale, Thirumala-Devi Kanneganti
Innate immune sensing of influenza A virus (IAV) induces activation of various immune effector mechanisms, including the nucleotide and oligomerization domain, leucine-rich repeat-containing protein family, pyrin domain containing 3 (NLRP3) inflammasome and programmed cell death pathways. Although type I IFNs are identified as key mediators of inflammatory and cell death responses during IAV infection, the involvement of various IFN-regulated effectors in facilitating these responses are less studied. In this study, we demonstrate the role of IFN regulatory factor (IRF)1 in promoting NLRP3 inflammasome activation and cell death during IAV infection...
February 15, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29262324/caspase-1-engagement-and-tlr-induced-c-flip-expression-suppress-asc-caspase-8-dependent-apoptosis-by-inflammasome-sensors-nlrp1b-and-nlrc4
#10
Nina Van Opdenbosch, Hanne Van Gorp, Maarten Verdonckt, Pedro H V Saavedra, Nathalia M de Vasconcelos, Amanda Gonçalves, Lieselotte Vande Walle, Dieter Demon, Magdalena Matusiak, Filip Van Hauwermeiren, Jinke D'Hont, Tino Hochepied, Stefan Krautwald, Thirumala-Devi Kanneganti, Mohamed Lamkanfi
The caspase activation and recruitment domain (CARD)-based inflammasome sensors NLRP1b and NLRC4 induce caspase-1-dependent pyroptosis independent of the inflammasome adaptor ASC. Here, we show that NLRP1b and NLRC4 trigger caspase-8-mediated apoptosis as an alternative cell death program in caspase-1-/- macrophages and intestinal epithelial organoids (IECs). The caspase-8 adaptor FADD was recruited to ASC specks, which served as cytosolic platforms for caspase-8 activation and NLRP1b/NLRC4-induced apoptosis...
December 19, 2017: Cell Reports
https://www.readbyqxmd.com/read/29247991/function-and-regulation-of-il-1%C3%AE-in-inflammatory-diseases-and-cancer
#11
REVIEW
Ankit Malik, Thirumala-Devi Kanneganti
The interleukin (IL)-1 family of cytokines is currently comprised of 11 members that have pleiotropic functions in inflammation and cancer. IL-1α and IL-1β were the first members of the IL-1 family to be described, and both signal via the same receptor, IL-1R. Over the last decade, much progress has been made in our understanding of biogenesis of IL-1β and its functions in human diseases. Studies from our laboratory and others have highlighted the critical role of nod-like receptors (NLRs) and multi-protein complexes known as inflammasomes in the regulation of IL-1β maturation...
January 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29247654/mechanisms-and-consequences-of-inflammasome-activation
#12
EDITORIAL
Kate Schroder, Thirumala-Devi Kanneganti, Feng Shao, Petr Broz
No abstract text is available yet for this article.
January 19, 2018: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29236673/zbp1-innate-sensor-regulating-cell-death-and-inflammation
#13
REVIEW
Teneema Kuriakose, Thirumala-Devi Kanneganti
Z-DNA-binding protein 1 (ZBP1), initially reported as an interferon (IFN)-inducible tumor-associated protein, harbors nucleic acid-binding domains for left-handed helix (Z-form) and receptor-interacting protein homotypic interaction motif (RHIM) domains for protein homotypic interactions. Recent studies have identified ZBP1 as an innate sensor of viral infections and a target of viral evasion strategies, regulating cell death, inflammasome activation, and proinflammatory responses. ZBP1 also functions during development and can trigger perinatal lethality when its RHIM-dependent interactions are not restricted...
November 24, 2017: Trends in Immunology
https://www.readbyqxmd.com/read/29203515/-brucella-abortus-triggers-a-cgas-independent-sting-pathway-to-induce-host-protection-that-involves-guanylate-binding-proteins-and-inflammasome-activation
#14
Miriam M Costa Franco, Fernanda Marim, Erika S Guimarães, Natan R G Assis, Daiane M Cerqueira, Juliana Alves-Silva, Jerome Harms, Gary Splitter, Judith Smith, Thirumala-Devi Kanneganti, Nina M G P de Queiroz, Delia Gutman, Glen N Barber, Sergio C Oliveira
Immunity against microbes depends on recognition of pathogen-associated molecular patterns by innate receptors. Signaling pathways triggered by Brucella abortus DNA involves TLR9, AIM2, and stimulator of IFN genes (STING). In this study, we observed by microarray analysis that several type I IFN-associated genes, such as IFN-β and guanylate-binding proteins (GBPs), are downregulated in STING knockout (KO) macrophages infected with Brucella or transfected with DNA. Additionally, we determined that STING and cyclic GMP-AMP synthase (cGAS) are important to engage the type I IFN pathway, but only STING is required to induce IL-1β secretion, caspase-1 activation, and GBP2 and GBP3 expression...
January 15, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29203393/pyrin-inflammasome-regulates-tight-junction-integrity-to-restrict-colitis-and-tumorigenesis
#15
Deepika Sharma, Ankit Malik, Clifford S Guy, Rajendra Karki, Peter Vogel, Thirumala-Devi Kanneganti
BACKGROUND & AIMS: Inflammatory bowel diseases (IBD) increase risk for colorectal cancer. Mutations in the Mediterranean fever gene (MEFV or pyrin) are associated with hereditary autoinflammatory disease and severe IBD. Expression of MEFV, a sensor protein that the initiates assembly of the inflammasome complex, is increased in colon biopsies from patients with IBD. We investigated the role of pyrin in intestinal homeostasis in mice. METHODS: Mefv-/- mice and C57/BL6 mice (controls) were given azoxymethane followed by multiple rounds of dextran sodium sulfate (DSS) to induce colitis and tumorigenesis...
March 2018: Gastroenterology
https://www.readbyqxmd.com/read/29196474/inflammasome-activation-and-assembly-at-a-glance
#16
REVIEW
Ankit Malik, Thirumala-Devi Kanneganti
Inflammasomes are multimeric protein complexes that typically comprise a sensor, an adaptor and the zymogen procaspase-1. An inflammasome assembles in response to a diverse range of pathogen-associated or danger-associated molecular patterns (PAMPs or DAMPs). The inflammasome platform leads to activation of caspase-1 through proximity-induced self-cleavage, which further induces maturation of interleukins 1β and 18 (IL-1β and IL-18) through proteolytic cleavage of pro-IL-1β and pro-IL-18. Activated caspase-1 also cleaves gasdermin D, which leads to a particular form of cell death called pyroptosis...
December 1, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/29150429/cgamp-a-tale-of-two-signals
#17
Teneema Kuriakose, Thirumala-Devi Kanneganti
In this issue of JEM, Swanson et al. (https://doi.org/10.1084/jem.20171749) report an unanticipated role for cGAMP in priming and activation of inflammasomes in addition to its well-characterized function as an endogenous second messenger inducing type I interferons in the cytosolic DNA-sensing pathway.
December 4, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29128729/recent-advances-in-inflammasome-biology
#18
REVIEW
David E Place, Thirumala-Devi Kanneganti
The inflammasome is a complex of proteins that through the activity of caspase-1 and the downstream substrates gasdermin D, IL-1β, and IL-18 execute an inflammatory form of cell death termed pyroptosis. Activation of this complex often involves the adaptor protein ASC and upstream sensors including NLRP1, NLRP3, NLRC4, AIM2, and pyrin, which are activated by different stimuli including infectious agents and changes in cell homeostasis. Here we discuss new regulatory mechanisms that have been identified for the canonical inflammasomes, the most recently identified NLRP9b inflammasome, and the new gasdermin family of proteins that mediate pyroptosis and other forms of regulated cell death...
February 2018: Current Opinion in Immunology
https://www.readbyqxmd.com/read/29027223/inflammatory-cell-death-in-intestinal-pathologies
#19
REVIEW
Deepika Sharma, Thirumala-Devi Kanneganti
The intestinal tract is a site of intense immune cell activity that is poised to mount an effective response against a pathogen and yet maintain tolerance toward commensal bacteria and innocuous dietary antigens. The role of cell death in gut pathologies is particularly important as the intestinal epithelium undergoes self-renewal every 4-7 days through a continuous process of cell death and cell division. Cell death is also required for removal of infected, damaged, and cancerous cells. Certain forms of cell death trigger inflammation through release of damage-associated molecular patterns...
November 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28974614/inflammasome-activation-by-bacterial-outer-membrane-vesicles-requires-guanylate-binding-proteins
#20
Ryan Finethy, Sarah Luoma, Nichole Orench-Rivera, Eric M Feeley, Arun K Haldar, Masahiro Yamamoto, Thirumala-Devi Kanneganti, Meta J Kuehn, Jörn Coers
The Gram-negative bacterial cell wall component lipopolysaccharide (LPS) is recognized by the noncanonical inflammasome protein caspase-11 in the cytosol of infected host cells and thereby prompts an inflammatory immune response linked to sepsis. Host guanylate binding proteins (GBPs) promote infection-induced caspase-11 activation in tissue culture models, and yet their in vivo role in LPS-mediated sepsis has remained unexplored. LPS can be released from lysed bacteria as "free" LPS aggregates or actively secreted by live bacteria as a component of outer membrane vesicles (OMVs)...
October 3, 2017: MBio
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