ArticleInfection and immunity1994
Group B streptococcus-induced nitric oxide production in murine macrophages is CR3 (CD11b/CD18) dependent.
Article in Infection and immunity, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 53 citations in OpenAlex.
- An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.FEMS microbiology reviews · 2024Review
- Polymyxin B-immobilized fiber column hemoperfusion mainly helps to constrict peripheral blood vessels in treatment for septic shock.Journal of intensive care · 2015Article
- NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Fcγ receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1.PLoS pathogens · 2010Article
- Herpes simplex virus as a tool to define the role of complement in the immune response to peripheral infection.Vaccine · 2008Review
- Recent advances in understanding the molecular basis of group B Streptococcus virulence.Expert reviews in molecular medicine · 2008Review
- Differential regulation of lipopolysaccharide and Gram-positive bacteria induced cytokine and chemokine production in macrophages by Galpha(i) proteins.Immunology · 2007Article
- Inhibition of nitric oxide synthase exacerbates group B streptococcus sepsis and arthritis in mice.Infection and immunity · 2004Article
- Role of the lectin domain of Mac-1/CR3 (CD11b/CD18) in regulating intercellular adhesion.Immunologic research · 2002Review
- Cytokine responses to group B streptococci induce nitric oxide production in respiratory epithelial cells.Infection and immunity · 2002Article
- Endothelial cell injury caused by Candida albicans is dependent on iron.Infection and immunity · 1998Article
- Regulation of interleukin-12 by complement receptor 3 signaling.The Journal of experimental medicine · 1997Article
- The role of nitric oxide in experimental murine sepsis due to pyrogenic exotoxin A-producing Streptococcus pyogenes.Infection and immunity · 1997Article
- CD18/ICAM-1-dependent oxidative NF-kappaB activation leading to nitric oxide production in rat Kupffer cells cocultured with syngeneic hepatoma cells.The Journal of clinical investigation · 1997Article
- Expression of inducible nitric oxide synthase and its involvement in pulmonary granulomatous inflammation in rats.The American journal of pathology · 1996Article
- Entry and intracellular survival of group B streptococci in J774 macrophages.Infection and immunity · 1996Article
- Interleukin-12 and tumor necrosis factor alpha mediate innate production of gamma interferon by group B Streptococcus-treated splenocytes of severe combined immunodeficiency mice.Infection and immunity · 1996Article
- Tumor necrosis factor alpha acts as an autocrine second signal with gamma interferon to induce nitric oxide in group B streptococcus-treated macrophages.Infection and immunity · 1995Article
- Modulation of nitric oxide synthase activity in macrophages.Mediators of inflammation · 1995Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is produced by murine macrophages in response to cytokines and/or gram-negative bacterial lipopolysaccharide. NO induction by gram-positive bacteria such as group B streptococci (GBS), the major etiologic agents of neonatal pneumonia and meningitis, has received little study. GBS as well as two other gram-positive bacterial species, Staphylococcus aureus and Staphylococcus epidermidis, were found to stimulate NO production in thioglycolate-elicited murine macrophages and in the mouse macrophage cell line J774A.1 in the presence of gamma interferon. Serotype Ia and III GBS were both stimulatory, as were asialo- and type antigen-deficient mutant strains of type III GBS. NO production was dose dependent, inhibitable by L-arginine analogs, and unaffected by polymyxin B. Since phagocytosis by murine and human phagocytes of GBS is dependent on complement receptor type 3 (CR3), the role of CR3 in the NO response to GBS was tested in the CR3-deficient myelomonocytic cell line WEHI-3. GBS did not induce NO, whereas S. aureus or lipopolysaccharide did induce NO in WEHI-3 cells. S. epidermidis, whose nonopsonic phagocytosis is also CR3 dependent, failed to induce NO in WEHI-3 cells. Monoclonal anti-CR3 (anti-CD11b or anti-CD18) in the presence of interferon also induced NO production in thioglycolate-elicited macrophages and in J774A.1 cells but not in WEHI-3 cells. This evidence suggests that ligated CR3 and gamma interferon act synergistically to induce NO production and that CR3 mediates the GBS-induced signal for NO production in interferon-treated macrophages.
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