ArticleMethods in molecular biology (Clifton, N.J.)2022
Analysis of Bacteria-Triggered Inflammasome: Activation in Neutrophils by Immunoblot.
Article in Methods in molecular biology (Clifton, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1.Life science alliance · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Detection of microbes relies on the expression of germline-encoded pattern recognition receptors (PRRs). While PRRs can directly sense conserved pattern expressed by various microbes, they can also induce effector-triggered immunity (ETI) by sensing pathogenic alterations of cellular homeostasis. One consequence of ETI is the death of the infected cell through the induction of inflammasome-dependent cell death, namely, pyroptosis. Such process can be easily studied in macrophages and epithelial cells, yet neutrophils encode an arsenal of proteolytic enzymes that imped easy and reliable study of ETI-triggered inflammasome response. Here, we describe an immunoblotting methodology to study both ETI- and PRR-driven inflammasome responses in neutrophils upon bacterial infections. This method is also transposable to other microbial pathogen- and toxin-induced inflammasome response in neutrophils.
Indexed as
Identifiers
What OpenQuestion holds
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.