ArticleInfection and immunity1989
Production of interleukin-1 but not tumor necrosis factor by human monocytes stimulated with pneumococcal cell surface components.
Article in Infection and immunity, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 162 citations in OpenAlex.
- Acute otitis media with spontaneous tympanic membrane perforation.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017Review
- Lipoteichoic acids, phosphate-containing polymers in the envelope of gram-positive bacteria.Journal of bacteriology · 2014Review
- Interleukin-1β regulates CXCL8 release and influences disease outcome in response to Streptococcus pneumoniae, defining intercellular cooperation between pulmonary epithelial cells and macrophages.Infection and immunity · 2012Article
- Streptococcus pneumoniae causing septic arthritis with shock and revealing multiple myeloma.BMJ case reports · 2011Article
- Pneumococcal lipoteichoic acid (LTA) is not as potent as staphylococcal LTA in stimulating Toll-like receptor 2.Infection and immunity · 2003Article
- ZmpB, a novel virulence factor of Streptococcus pneumoniae that induces tumor necrosis factor alpha production in the respiratory tract.Infection and immunity · 2003Article
- Teichoic acids are not required for Streptococcus pneumoniae and Staphylococcus aureus cell walls to trigger the release of tumor necrosis factor by peripheral blood monocytes.Infection and immunity · 2003Article
- Streptococcus pneumoniae strain-dependent lung inflammatory responses in a murine model of pneumococcal pneumonia.Intensive care medicine · 2003Article
- Role of inflammatory mediators in resistance and susceptibility to pneumococcal infection.Infection and immunity · 2002Article
- Modulation of release of proinflammatory bacterial compounds by antibacterials: potential impact on course of inflammation and outcome in sepsis and meningitis.Clinical microbiology reviews · 2002Review
- Commercial preparations of lipoteichoic acid contain endotoxin that contributes to activation of mouse macrophages in vitro.Infection and immunity · 2001Article
- Failure To detect muramic acid in normal rat tissues but detection in cerebrospinal fluids from patients with Pneumococcal meningitis.Infection and immunity · 2000Article
- Pathogenesis of gram-positive bacterial endophthalmitis.Infection and immunity · 1999Article
- Effects of polysaccharide fucoidin on cerebrospinal fluid interleukin-1 and tumor necrosis factor alpha in pneumococcal meningitis in the rabbit.Infection and immunity · 1999Article
- Lactobacilli and streptococci induce interleukin-12 (IL-12), IL-18, and gamma interferon production in human peripheral blood mononuclear cells.Infection and immunity · 1998Article
- Pharmacokinetic optimisation of the treatment of bacterial central nervous system infections.Clinical pharmacokinetics · 1998Review
- Coexistence of CD14-dependent and independent pathways for stimulation of human monocytes by gram-positive bacteria.Infection and immunity · 1997Article
- Cancer immunotherapy: potential involvement of mediators.Mediators of inflammation · 1997Article
- Production of human tumor necrosis factor alpha, interleukin-6, and interleukin-10 is induced by lactic acid bacteria.Infection and immunity · 1996Article
- Roles of proinflammatory and anti-inflammatory cytokines in pathophysiology of bacterial meningitis and effect of adjunctive therapy.Infection and immunity · 1996Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
While there is considerable evidence that both interleukin-1 (IL-1) and tumor necrosis factor (TNF) are central mediators of inflammation caused by gram-negative bacteria and endotoxin, the roles of these two mediators in gram-positive infection are unknown. Pneumococcal infections are characterized by an intense inflammatory reaction in infected tissues. Current evidence suggests that the component of the pneumococcus which causes this inflammation in many body sites is the cell wall. We determined the ability of native pneumococcal cell wall, lipoteichoic acid, and cell wall subcomponents to stimulate secretion of IL-1 and TNF from human monocytes. Each pneumococcal cell surface component was found to have a different specific activity for induction of IL-1. Teichoication was an important determinant of this activity: teichoicated species were at least 10,000-fold more potent than endotoxin and 100-fold more potent than teichoic acid-free peptidoglycan. IL-1-inducing activity was greatly reduced by chemical alteration of the teichoic acid. In contrast to endotoxin, cell wall did not induce production of TNF. This dissociation of the production of IL-1 and TNF during the response of the human monocyte to pneumococcal surface components suggests that, in at least some circumstances, the mechanisms for generation of an inflammatory response to infection may be fundamentally different between gram-positive and gram-negative disease.
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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.