ArticleJournal of acquired immune deficiency syndromes (1999)2007
Chemokine responses are increased in HIV-infected Malawian children with invasive pneumococcal disease.
Article in Journal of acquired immune deficiency syndromes (1999), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- HIV-1 Infection Transcriptomics: Meta-Analysis of CD4+ T Cells Gene Expression Profiles.Viruses · 2021Pooled it
- Corticosteroid administration and outcome of adolescents and adults with acute bacterial meningitis: a meta-analysis.Mayo Clinic proceedings · 2009Pooled it
- The Effect of miRNA Gene Regulation on HIV Disease.Frontiers in genetics · 2022Review
- Immortalization of primary microglia: a new platform to study HIV regulation in the central nervous system.Journal of neurovirology · 2017Article
- Cytokine Profiles during Invasive Nontyphoidal Salmonella Disease Predict Outcome in African Children.Clinical and vaccine immunology : CVI · 2016Article
- Chemokine CXCL8 promotes HIV-1 replication in human monocyte-derived macrophages and primary microglia via nuclear factor-κB pathway.PloS one · 2014Article
- Article
- PCR improves diagnostic yield from lung aspiration in Malawian children with radiologically confirmed pneumonia.PloS one · 2011Article
- The role of angiogenic factors in predicting clinical outcome in severe bacterial infection in Malawian children.Critical care (London, England) · 2010Article
- Endotoxin-induced gene expression differences in the brain and effects of iNOS inhibition and norepinephrine.Intensive care medicine · 2009Article
- HIV-1-infected and/or immune-activated macrophages regulate astrocyte CXCL8 production through IL-1beta and TNF-alpha: involvement of mitogen-activated protein kinases and protein kinase R.Journal of neuroimmunology · 2008Article
- CD40-CD40 ligand interactions in human microglia induce CXCL8 (interleukin-8) secretion by a mechanism dependent on activation of ERK1/2 and nuclear translocation of nuclear factor-kappaB (NFkappaB) and activator protein-1 (AP-1).Journal of neuroscience research · 2008Article
- Successful downstream application of the Paxgene Blood RNA system from small blood samples in paediatric patients for quantitative PCR analysis.BMC immunology · 2007Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundChemokines play an important role in the recruitment and regulation of leukocyte traffic during bacterial infection. The aims of this study were to investigate the chemokine response to invasive pneumococcal disease (IPD) and to examine the influence of HIV infection on the chemokine response, pneumococcal bacterial loads, and outcome.
methodsWe prospectively studied 95 children with IPD, and blood and cerebrospinal fluid (CSF) samples were taken at admission for the determination of chemokines, interferon-gamma (IFNgamma), and pneumococcal bacterial loads.
resultsPlasma CXCL8 and CCL2, CSF CXCL8 and CCL4, and IFNgamma were significantly higher in HIV-infected children than in HIV-uninfected children. Blood and CSF pneumococcal bacterial loads correlated with plasma and CSF chemokines, respectively, and were higher in HIV-infected children compared with HIV-uninfected children. Among HIV-infected children, plasma concentrations of CXCL8 and CCL2 were significantly higher in nonsurvivors than in survivors, but CCL5 was significantly lower. HIV-infected and HIV-uninfected children with IPD had higher concentrations of chemokines (except CCL5) than acutely ill HIV-infected and HIV-uninfected children with no detectable bacterial infection. Male gender and low plasma CCL2 concentrations were shown to be independently associated with survival.
conclusionsChemokines, in particular CCL2, are associated with survival in IPD and correlate with pneumococcal bacterial loads, disease presentation, and outcome.
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