NDLI: Hydrogen sulfide increases survival during sepsis: Protective effect of CHOP inhibition

Please wait, while we are loading the content...

Year: 2017 Volume: 198

Year: 2016 Volume: 197

Year: 2016 Volume: 196

Year: 2015 Volume: 195

Year: 2015 Volume: 194

Year: 2014 Volume: 193

Year: 2014 Volume: 192

Year: 2014 Volume: 192 Issue: 12

Year: 2014 Volume: 192 Issue: 11

Year: 2014 Volume: 192 Issue: 10

Year: 2014 Volume: 192 Issue: 9

Year: 2014 Volume: 192 Issue: 8

Year: 2014 Volume: 192 Issue: 7

Year: 2014 Volume: 192 Issue: 6

Year: 2014 Volume: 192 Issue: 5

Year: 2014 Volume: 192 Issue: 4

Dual-specificity phosphatase 14 (DUSP14/MKP6) negatively regulates TCR signaling by inhibiting TAB1 activation.

Mutagenesis of Ly49B reveals key structural elements required for promiscuous binding to MHC class I molecules and new insights into the molecular evolution of Ly49s.

Hydrogen sulfide increases survival during sepsis: Protective effect of CHOP inhibition

IDO-independent suppression of T cell effector function by IFN-Î³-licensed human mesenchymal stromal cells.

The aryl hydrocarbon receptor promotes IL-10 production by NK cells.

Autoimmune vitiligo does not require the ongoing priming of naive CD8 T cells for disease progression or associated protection against melanoma.

KLRG1+ NK cells protect T-bet-deficient mice from pulmonary metastatic colorectal carcinoma.

Noncore RAG1 regions promote Vß rearrangements and ß T cell development by overcoming inherent inefficiency of Vß recombination signal sequences.

Enforced expression of Gata3 in T cells and group 2 innate lymphoid cells increases susceptibility to allergic airway inflammation in mice.

Posttranscriptional modulation of cytokine production in T cells for the regulation of excessive inflammation by TFL.

Fetal intervention increases maternal T cell awareness of the foreign conceptus and can lead to immune-mediated fetal demise.

Transcriptional regulator CTR9 inhibits Th17 differentiation via repression of IL-17 expression.

Tetraacylated lipid A and paclitaxel-selective activation of TLR4/MD-2 conferred through hydrophobic interactions.

Second-generation Langerhans cells originating from epidermal precursors are essential for CD8+ T cell priming.

Induced resistance to ofatumumab-mediated cell clearance mechanisms, including complement-dependent cytotoxicity, in chronic lymphocytic leukemia.

Excess IL-1 signaling enhances the development of Th17 cells by downregulating TGF-ß-induced Foxp3 expression.

Heterotropic modulation of selectin affinity by allosteric antibodies affects leukocyte rolling.

Pathogen-related differences in the abundance of presented antigen are reflected in CD4+ T cell dynamic behavior and effector function in the lung.

Serum and glucocorticoid-regulated kinase 1 regulates neutrophil clearance during inflammation resolution.

Gr1+ cells suppress T-dependent antibody responses in (NZB x NZW)F1 male mice through inhibition of T follicular helper cells and germinal center formation.

Induction of endotoxin tolerance by pathogenic Neisseria is correlated with the inflammatory potential of lipooligosaccharides and regulated by microRNA-146a.

CD19 and CD32b differentially regulate human B cell responsiveness.

A genetic defect in mice that impairs missing self recognition despite evidence for normal maturation and MHC class I-dependent education of NK cells.

Human cytomegalovirus infection promotes rapid maturation of NK cells expressing activating killer Ig-like receptor in patients transplanted with NKG2C-/- umbilical cord blood.

Casein kinase 1Î³1 inhibits the RIG-I/TLR signaling pathway through phosphorylating p65 and promoting its degradation.

NFIL3-deficient mice develop microbiota-dependent, IL-12/23-driven spontaneous colitis.

Cleavage of the T cell protein tyrosine phosphatase by the hepatitis C virus nonstructural 3/4A protease induces a Th1 to Th2 shift reversible by ribavirin therapy.

CXCL1 but not IL-6 is required for recurrent herpetic stromal keratitis.

Flagellin induces antibody responses through a TLR5- and inflammasome-independent pathway.

Anti-CD79 antibody induces B cell anergy that protects against autoimmunity.

Conventional NK cells can produce IL-22 and promote host defense in Klebsiella pneumoniae pneumonia.

PC3-secreted microprotein is a novel chemoattractant protein and functions as a high-affinity ligand for CC chemokine receptor 2.

Role of neutrophils in IL-17-dependent immunity to mucosal candidiasis.

Cutting edge: FYCO1 recruitment to dectin-1 phagosomes is accelerated by light chain 3 protein and regulates phagosome maturation and reactive oxygen production.

Cutting edge: Self-antigen controls the balance between effector and regulatory T cells in peripheral tissues.

Role of Th1/Th17 balance regulated by T-bet in a mouse model of Mycobacterium avium complex disease.

Mechanism of neutrophil dysfunction: neutrophil serine proteases cleave and inactivate the C5a receptor.

IL-21 contributes to fatal inflammatory disease in the absence of Foxp3+ T regulatory cells.

Islet antigen-specific Th17 cells can induce TNF- -dependent autoimmune diabetes.

IL-17A promotes the exacerbation of IL-33-induced airway hyperresponsiveness by enhancing neutrophilic inflammation via CXCR2 signaling in mice.

CD8+ T cells are activated in an antigen-independent manner in HIV-infected individuals.

TNF- -dependent hematopoiesis following Bcl11b deletion in T cells restricts metastatic melanoma.

Intradermal delivery of Shigella IpaB and IpaD type III secretion proteins: kinetics of cell recruitment and antigen uptake, mucosal and systemic immunity, and protection across serotypes.

IL-37 ameliorates the inflammatory process in psoriasis by suppressing proinflammatory cytokine production.

Bruton's tyrosine kinase promotes persistence of mature anti-insulin B cells.

Embryonic trophoblasts induce decidual regulatory T cell differentiation and maternal-fetal tolerance through thymic stromal lymphopoietin instructing dendritic cells.

FLT3-ligand treatment of humanized mice results in the generation of large numbers of CD141+ and CD1c+ dendritic cells in vivo.

KIR3DL01 recognition of Bw4 ligands in the rhesus macaque: maintenance of Bw4 specificity since the divergence of apes and Old World monkeys.

Dectin-2 regulates the effector phase of house dust mite-elicited pulmonary inflammation independently from its role in sensitization.

Oral combined therapy with probiotics and alloantigen induces B cell-dependent long-lasting specific tolerance.

CD4+ T cell responses to the Plasmodium falciparum erythrocyte membrane protein 1 in children with mild malaria.

B cell depletion curtails CD4+ T cell memory and reduces protection against disseminating virus infection.

Binding of HLA-G to ITIM-bearing Ig-like transcript 2 receptor suppresses B cell responses.

Mst1/Mst2 regulate development and function of regulatory T cells through modulation of Foxo1/Foxo3 stability in autoimmune disease.

A spliced antigenic peptide comprising a single spliced amino acid is produced in the proteasome by reverse splicing of a longer peptide fragment followed by trimming.

MMTV superantigens coerce an unconventional topology between the TCR and MHC class II.

FADD and caspase-8 mediate priming and activation of the canonical and noncanonical Nlrp3 inflammasomes.

PTPN22 controls the germinal center by influencing the numbers and activity of T follicular helper cells.

Infection and cellular defense dynamics in a novel 17ß-estradiol murine model of chronic human group B streptococcus genital tract colonization reveal a role for hemolysin in persistence and neutrophil accumulation.

Mast cells contribute to bleomycin-induced lung inflammation and injury in mice through a chymase/mast cell protease 4-dependent mechanism.

Computational approach to characterize causative factors and molecular indicators of chronic wound inflammation.

Modulation of nonneutralizing HIV-1 gp41 responses by an MHC-restricted TH epitope overlapping those of membrane proximal external region broadly neutralizing antibodies.

Probiotic Lactobacillus rhamnosus inhibits the formation of neutrophil extracellular traps.

-Galactosylceramide but not phenyl-glycolipids induced NKT cell anergy and IL-33-mediated myeloid-derived suppressor cell accumulation via upregulation of egr2/3.

HIV Nef expression favors the relative preservation of CD4+ T regulatory cells that retain some important suppressive functions.

Endogenous retroviruses and the development of cancer.

Year: 2014 Volume: 192 Issue: 3

Year: 2014 Volume: 192 Issue: 2

Year: 2014 Volume: 192 Issue: 1

Year: 2013 Volume: 191

Year: 2013 Volume: 190

Year: 2012 Volume: 189

Year: 2012 Volume: 188

Year: 2011 Volume: 187

Year: 2011 Volume: 186

Year: 2010 Volume: 185

Year: 2010 Volume: 184

Year: 2009 Volume: 183

Year: 2009 Volume: 182

Year: 2008 Volume: 181

Hydrogen sulfide increases survival during sepsis: Protective effect of CHOP inhibition

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Paolocci, Nazareno Marchionni, Luigi Fox-Talbot, Karen Steenbergen, Charles Wang, Qihong Ferlito, Marcella Fulton, William B. Colombani, Paul M.
Description	Author Affiliation: Ferlito M ( Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205)
Abstract	Sepsis is a major cause of mortality, and dysregulation of the immune response plays a central role in this syndrome. H2S, a recently discovered gaso-transmitter, is endogenously generated by many cell types, regulating a number of physiologic processes and pathophysiologic conditions. We report that H2S increased survival after experimental sepsis induced by cecal ligation and puncture (CLP) in mice. Exogenous H2S decreased the systemic inflammatory response, reduced apoptosis in the spleen, and accelerated bacterial eradication. We found that C/EBP homologous protein 10 (CHOP), a mediator of the endoplasmic reticulum stress response, was elevated in several organs after CLP, and its expression was inhibited by H2S treatment. Using CHOP-knockout (KO) mice, we demonstrated for the first time, to our knowledge, that genetic deletion of Chop increased survival after LPS injection or CLP. CHOP-KO mice displayed diminished splenic caspase-3 activation and apoptosis, decreased cytokine production, and augmented bacterial clearance. Furthermore, septic CHOP-KO mice treated with H2S showed no additive survival benefit compared with septic CHOP-KO mice. Finally, we showed that H2S inhibited CHOP expression in macrophages by a mechanism involving Nrf2 activation. In conclusion, our findings show a protective effect of H2S treatment afforded, at least partially, by inhibition of CHOP expression. The data reveal a major negative role for the transcription factor CHOP in overall survival during sepsis and suggest a new target for clinical intervention, as well potential strategies for treatment.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1300835
Journal	The Journal of Immunology
Issue Number	4
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bacteria Immunology Hydrogen Sulfide Metabolism Sepsis Transcription Factor Chop Antagonists & Inhibitors Animals Apoptosis Drug Effects Caspase 3 Cecum Surgery Cytokines Biosynthesis Endoplasmic Reticulum Stress Enzyme Activation Lipopolysaccharides Macrophages Mice Mice, Inbred C57bl Mice, Knockout Nf-e2-related Factor 2 Drug Therapy Spleen Genetics Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Central Library (ISO-9001:2015 Certified)
Indian Institute of Technology Kharagpur
Kharagpur, West Bengal, India | PIN - 721302

See location in the Map
03222 282435
Mail: support@ndl.gov.in

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in