ArticlePloS one2016
Reduced PICD in Monocytes Mounts Altered Neonate Immune Response to Candida albicans.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 13 citations in OpenAlex.
- TLR7/8 signaling balances cytokine responses in neonatal monocytes.Scientific reports · 2026Article
- Preterm ETs Are Significantly Reduced Compared with Adults and Partially Reduced Compared with Term Infants.Children (Basel, Switzerland) · 2022Article
- Leucine Reconstitutes Phagocytosis-Induced Cell Death inInternational journal of molecular sciences · 2021Article
- Evaluation of the Induction of Cell-Mediated Immunity Against Candida albicans in a Model of Cutaneous Infection in Newborn 0-Day-Old Mice.Mycopathologia · 2019Article
- Functional analysis of granulocyte and monocyte subpopulations in neonates.Molecular and cellular pediatrics · 2019Article
- Pattern recognition receptors in fungal immunity.Seminars in cell & developmental biology · 2019Review
- Review
- Immunomodulation to Prevent or Treat Neonatal Sepsis: Past, Present, and Future.Frontiers in pediatrics · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInvasive fungal infections with Candida albicans (C. albicans) occur frequently in extremely low birthweight (ELBW) infants and are associated with poor outcome. Phagocytosis of C.albicans initializes apoptosis in monocytes (phagocytosis induced cell death, PICD). PICD is reduced in neonatal cord blood monocytes (CBMO). HYPOTHESIS: Phagocytosis of C. albicans causes PICD which differs between neonatal monocytes (CBMO) and adult peripheral blood monocytes (PBMO) due to lower stimulation of TLR-mediated immune responses.
methodsThe ability to phagocytose C. albicans, expression of TLRs, the induction of apoptosis (assessment of sub-G1 and nick-strand breaks) were analyzed by FACS. TLR signalling was induced by agonists such as lipopolysaccharide (LPS), Pam3Cys, FSL-1 and Zymosan and blocked (neutralizing TLR2 antibodies and MYD88 inhibitor).
resultsPhagocytic indices of PBMO and CBMO were similar. Following stimulation with agonists and C. albicans induced up-regulation of TLR2 and consecutive phosphorylation of MAP kinase P38 and expression of TNF-α, which were stronger on PBMO compared to CBMO (p < 0.005). Downstream, TLR2 signalling initiated caspase-3-dependent PICD which was found reduced in CBMO (p < 0.05 vs PBMO).
conclusionOur data suggest direct involvement of TLR2-signalling in C. albicans-induced PICD in monocytes and an alteration of this pathway in CBMO.
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Registered trials
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