ArticleInfection and immunity2012
Global effect of interleukin-10 on the transcriptional profile induced by Neisseria meningitidis in human monocytes.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- RNA profiles in extracellular vesicles from severe sepsis and meningitis patients reveal pathogen-specific immune signatures in meningococcal versus pneumococcal infections.Frontiers in cellular and infection microbiology · 2026Article
- Review
- Aryl hydrocarbon receptor activity downstream of IL-10 signaling is required to promote regulatory functions in human dendritic cells.Cell reports · 2023Article
- Article
- Transcriptomic changes in the large organs in lethal meningococcal shock are reflected in a porcine shock model.Frontiers in cellular and infection microbiology · 2022Article
- Loss of IL-10 signaling in macrophages limits bacterial killing driven by prostaglandin E2.The Journal of experimental medicine · 2020Article
- Extensive Changes in Transcriptomic "Fingerprints" and Immunological Cells in the Large Organs of Patients Dying of Acute Septic Shock and Multiple Organ Failure Caused byFrontiers in cellular and infection microbiology · 2020Article
- CD19+IgM+ cells demonstrate enhanced therapeutic efficacy in type 1 diabetes mellitus.JCI insight · 2018Article
- Large-scale reduction of tyrosine kinase activities in human monocytes stimulated in vitro with N. meningitidis.PloS one · 2018Article
- Article
- Traceability and distribution ofBMC clinical pathology · 2017Article
- Combined inhibition of C5 and CD14 efficiently attenuated the inflammatory response in a porcine model of meningococcal sepsis.Journal of intensive care · 2017Article
- Human hepatocytes express absent in melanoma 2 and respond to hepatitis B virus with interleukin-18 expression.Virus genes · 2016Article
- Haemophilus ducreyi infection induces activation of the NLRP3 inflammasome in nonpolarized but not in polarized human macrophages.Infection and immunity · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In meningococcal septic shock, the dominant inducer of inflammation is lipopolysaccharide (LPS) in the outer membrane of Neisseria meningitidis, while interleukin-10 (IL-10) is the principal anti-inflammatory cytokine. We have used microarrays and Ingenuity Pathway Analysis to study the global effects of IL-10 on gene expression induced by N. meningitidis, after exposure of human monocytes (n = 5) for 3 h to N. meningitidis (10(6) cells/ml), recombinant human IL-10 (rhIL-10) (25 ng/ml), and N. meningitidis combined with rhIL-10. N. meningitidis and IL-10 differentially expressed 3,579 and 648 genes, respectively. IL-10 downregulated 125 genes which were upregulated by N. meningitidis, including NLRP3, the key molecule of the NLRP3 inflammasome. IL-10 also upregulated 270 genes which were downregulated by N. meningitidis, including members of the leukocyte immunuglobulin-like receptor (LIR) family. Fifty-three genes revealed a synergistically increased expression when N. meningitidis and IL-10 were combined. AIM2 (the principal molecule of the AIM2 inflammasome) was among these genes (fold change [FC], 18.3 versus 7.4 and 9.4 after stimulation by N. meningitidis and IL-10, respectively). We detected reduced concentrations (92% to 40%) of six cytokines (IL-1b, IL-6, IL-8, tumor necrosis factor alpha [TNF-α], macrophage inflammatory protein alpha [MIP-α], MIP-β) in the presence of IL-10, compared with concentrations with stimulation by N. meningitidis alone. Our data analysis of the effects of IL-10 on gene expression induced by N. meningitidis suggests that high plasma levels of IL-10 in meningococcal septic shock plasma may have a profound effect on a variety of functions and cellular processes in human monocytes, including cell-to-cell signaling, cellular movement, cellular development, antigen presentation, and cell death.
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