ArticleInfection and immunity2002
Role of caspase 1 in murine antibacterial host defenses and lethal endotoxemia.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Species-Specific Endotoxin Stimulus Determines Toll-Like Receptor 4- and Caspase 11-Mediated Pathway Activation Characteristics.mSystems · 2021Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
- Evodiamine Augments NLRP3 Inflammasome Activation and Anti-bacterial Responses Through Inducing α-Tubulin Acetylation.Frontiers in pharmacology · 2019Article
- A high concentration of DMSO activates caspase-1 by increasing the cell membrane permeability of potassium.Cytotechnology · 2018Article
- Interleukin-18: Biological properties and role in disease pathogenesis.Immunological reviews · 2018Review
- Berberine augments ATP-induced inflammasome activation in macrophages by enhancing AMPK signaling.Oncotarget · 2017Article
- Target deletion of complement component 9 attenuates antibody-mediated hemolysis and lipopolysaccharide (LPS)-induced acute shock in mice.Scientific reports · 2016Article
- Expression of Nucleotide-oligomerization Domain (NOD) and Related Genes in Mouse Tissues Infected with Mycobacterium leprae.Immune network · 2015Article
- Macrophages sense and kill bacteria through carbon monoxide-dependent inflammasome activation.The Journal of clinical investigation · 2014Article
- Article
- Polyacetylene Compound from Cirsium japonicum var. ussuriense Inhibited Caspase-1-mediated IL-1β Expression.Immune network · 2012Article
- Selective deletion of CD8(+) cells upregulated by caspases-1 via IL-18 in mice immunized with major outer membrane protein of Shigella dysenteriae 1 following infection.Journal of clinical immunology · 2010Article
- IL-1beta processing in host defense: beyond the inflammasomes.PLoS pathogens · 2010Review
- Comparison of two mice strains, A/J and C57BL/6, in caspase-1 activity and IL-1beta secretion of macrophage to Mycobacterium leprae infection.Mediators of inflammation · 2010Article
- Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors.The Journal of biological chemistry · 2009Article
- Neutrophil chemokines and their role in IL-18-mediated increase in neutrophil O2- production and intestinal edema following alcohol intoxication and burn injury.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
- Crystal structure of procaspase-1 zymogen domain reveals insight into inflammatory caspase autoactivation.The Journal of biological chemistry · 2009Article
- Evidence of the involvement of caspase-1 under physiologic and pathologic cellular stress during human pregnancy: a link between the inflammasome and parturition.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2008Article
- Bacillus anthracis spores and lethal toxin induce IL-1beta via functionally distinct signaling pathways.European journal of immunology · 2008Article
- Sepsis: links between pathogen sensing and organ damage.Current pharmaceutical design · 2008Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Sepsis is thought to result from an exaggerated innate immune response to microbial components such as lipopolysaccharide (LPS), but the involvement of a specific mechanism(s) has not been identified. We studied the role of caspase 1 (Cas-1) in the murine innate immune response to infection with gram-negative bacteria and to nonlethal and lethal doses of LPS. cas-1(-/-) and Cas-1 inhibitor (Ac-YVAD-CHO)-treated cas-1(+/+) mice were two- to threefold more susceptible to lethal Escherichia coli infection than cas-1(+/+) mice. Administration of Cas-1 products, interleukin-18 (IL-18) or IL-1beta, protected three of three and six of seven mice, respectively, from lethal infection with E. coli compared to none of six of untreated mice (P = 0.0082). Therefore, cas-1 is essential for antibacterial host defense. Nonlethal (75 micro g) and lethal (500 micro g) doses of LPS induce different patterns of gamma interferon, IL-1beta, and IL-18 expression. Consequently, the role of Cas-1, which cleaves pro-IL-18 and pro-IL-1beta to their active forms, was investigated in these disparate conditions by using enzymatic assay and reverse transcription-PCR. At 75 micro g, LPS induced a transient increase in IL-1beta and IL-18 levels in serum, whereas at 500 micro g it induced a 1.5-fold-higher IL-18 level in serum, which increased till death. At 75 micro g of LPS, splenic cas-1 mRNA expression remained unchanged at all time points, but activity increased transiently at 3 h. In lethally treated mice, Cas-1 activity remained elevated until death; however, cas-1 mRNA levels increased at 3 h and decreased to basal levels by 8 h. Treatment with Cas-1 inhibitor protected mice from lethal endotoxemia. Thus, Cas-1 is essential for innate antibacterial host defenses and may represent a mechanism of innate immunity that upon excessive stimulation by microbial components may lead to endotoxic shock.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.