ArticlePLoS pathogens2009
Anthrax lethal toxin impairs IL-8 expression in epithelial cells through inhibition of histone H3 modification.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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
30 citing papers in PubMed, 56 citations in OpenAlex.
- Reprogramming host histone modifications by bacterial pathogens.Molecules and cells · 2026Review
- Loss of cPLA2α function attenuates inflammation and epithelial thickening in a mouse model ofCurrent research in microbial sciences · 2026Article
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- Future applications of host direct therapies for infectious disease treatment.Frontiers in immunology · 2024Review
- Functional differences and similarities in activated peripheral blood mononuclear cells by lipopolysaccharide or phytohemagglutinin stimulation between human and cynomolgus monkeys.Annals of translational medicine · 2021Article
- Epigenetic interaction of microbes with their mammalian hosts.Journal of biosciences · 2021Article
- Trained immunity and host-pathogen interactions.Cellular microbiology · 2020Review
- Prospects of NSAIDs administration as double-edged agents against endometrial cancer and pathological species of the uterine microbiome.Cancer biology & therapy · 2020Review
- Impact of Bacterial Toxins in the Lungs.Toxins · 2020Review
- Revealing eukaryotic histone-modifying mechanisms through bacterial infection.Seminars in immunopathology · 2020Review
- Epigenetic regulation in bacterial infections: targeting histone deacetylases.Critical reviews in microbiology · 2018Review
- HDAC8 Prevents Anthrax Lethal Toxin-induced Cell Cycle Arrest through Silencing PTEN in Human Monocytic THP-1 Cells.Toxins · 2017Article
- Bacterial Virulence Factors: Secreted for Survival.Indian journal of microbiology · 2017Review
- Inhibition of Interleukin 1β (IL-1β) Expression by Anthrax Lethal Toxin (LeTx) Is Reversed by Histone Deacetylase 8 (HDAC8) Inhibition in Murine Macrophages.The Journal of biological chemistry · 2016Article
- Chemokine-Releasing Microparticles Improve Bacterial Clearance and Survival of Anthrax Spore-Challenged Mice.PloS one · 2016Article
- Review
- Genome-wide immunity studies in the rabbit: transcriptome variations in peripheral blood mononuclear cells after in vitro stimulation by LPS or PMA-Ionomycin.BMC genomics · 2015Article
- Crossing of the epithelial barriers by Bacillus anthracis: the Known and the Unknown.Frontiers in microbiology · 2015Review
- AhR and Arnt differentially regulate NF-κB signaling and chemokine responses in human bronchial epithelial cells.Cell communication and signaling : CCS · 2014Article
- Bacterial SET domain proteins and their role in eukaryotic chromatin modification.Frontiers in genetics · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lethal toxin (LT) is a critical virulence factor of Bacillus anthracis, the etiological agent of anthrax, whose pulmonary form is fatal in the absence of treatment. Inflammatory response is a key process of host defense against invading pathogens. We report here that intranasal instillation of a B. anthracis strain bearing inactive LT stimulates cytokine production and polymorphonuclear (PMN) neutrophils recruitment in lungs. These responses are repressed by a prior instillation of an LT preparation. In contrast, instillation of a B. anthracis strain expressing active LT represses lung inflammation. The inhibitory effects of LT on cytokine production are also observed in vitro using mouse and human pulmonary epithelial cells. These effects are associated with an alteration of ERK and p38-MAPK phosphorylation, but not JNK phosphorylation. We demonstrate that although NF-kappaB is essential for IL-8 expression, LT downregulates this expression without interfering with NF-kappaB activation in epithelial cells. Histone modifications are known to induce chromatin remodelling, thereby enhancing NF-kappaB binding on promoters of a subset of genes involved in immune response. We show that LT selectively prevents histone H3 phosphorylation at Ser 10 and recruitment of the p65 subunit of NF-kappaB at the IL-8 and KC promoters. Our results suggest that B. anthracis represses the immune response, in part by altering chromatin accessibility of IL-8 promoter to NF-kappaB in epithelial cells. This epigenetic reprogramming, in addition to previously reported effects of LT, may represent an efficient strategy used by B. anthracis for invading the host.
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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.