ArticleBMC veterinary research2021
Induction of macrophage pyroptosis-related factors by pathogenic E. coli high pathogenicity island (HPI) in Yunnan Saba pigs.
Article in BMC veterinary research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- Escherichia coli HPI-induced duodenitis through ubiquitin regulation of the TLR4/NF-κB pathway.BMC veterinary research · 2025Article
- Review
- Yersiniabactin-ProducingInternational journal of molecular sciences · 2023Article
- Exogenous 8-Hydroxydeoxyguanosine Attenuates PMAntioxidants (Basel, Switzerland) · 2023Article
- Global Genomic Epidemiology ofMicroorganisms · 2022Article
- Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes.BMC molecular and cell biology · 2022Article
- The current landscape of microRNAs (miRNAs) in bacterial pneumonia: opportunities and challenges.Cellular & molecular biology letters · 2022Review
- Porcine Gasdermin D Is a Substrate of Caspase-1 and an Executioner of Pyroptosis.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPyroptosis plays a pivotal role in the pathogenesis of many inflammatory diseases. The molecular mechanism by which pyroptosis is induced in macrophages following infection with pathogenic E. coli high pathogenicity island (HPI) will be evaluated in our study.
resultsAfter infection with the HPI
conclusionOur findings indicate that pathogenic E. coli HPI infection of Saba pigs causes pyroptosis of macrophages characterized by upregulated expression of pyroptosis key factors in the NLRP3/ASC/caspase-1 signaling pathway, direct cell membrane pore formation, and secretion of the inflammatory factor IL-1β and IL-18 downstream of NLRP3 and caspase-1 activation to enhance the inflammatory response.
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Registered trials
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