ArticleRespiratory research2011
Impaired neonatal macrophage phagocytosis is not explained by overproduction of prostaglandin E2.
Article in Respiratory research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Developmental impact of peripheral injury on neuroimmune signaling.Brain, behavior, and immunity · 2023Review
- The BCG Moreau Vaccine Upregulates In Vitro the Expression of TLR4, B7-1, Dectin-1 and EP2 on Human Monocytes.Vaccines · 2022Article
- IRF5 Is a Key Regulator of Macrophage Response to Lipopolysaccharide in Newborns.Frontiers in immunology · 2018Article
- Innate Immunity to Respiratory Infection in Early Life.Frontiers in immunology · 2017Review
- Prostaglandin E2 production during neonatal respiratory infection with mouse adenovirus type 1.Virus research · 2016Article
- Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and Disease.Frontiers in immunology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNeonates and young infants manifest increased susceptibility to bacterial, viral and fungal lung infections. Previous work has identified a role for eicosanoids in mediating host defense functions of macrophages. This study examines the relationship between alveolar macrophage (AM) host defense and production of lipid mediators during the neonatal period compared to adult AMs.
methodsAMs were harvested from young (day 7 and day 14) and adult (~10 week) rats. The functionality of these cells was assessed by examining their ability to phagocytose opsonized targets, produce cytokines, eicosanoids and intracellular cAMP measured by enzyme immunoassays, and gene expression of proteins, enzymes and receptors essential for eicosanoid generation and phagocytosis measured by real time RT-PCR.
resultsAMs from young animals (day 7 and 14) were defective in their ability to phagocytose opsonized targets and produce tumor necrosis factor (TNF)- α. In addition, young AMs produce more prostaglandin (PG) E(2), a suppressor of host defense, and less leukotriene (LT) B(4), a promoter of host defense. Young AMs express higher levels of enzymes responsible for the production of PGE(2) and LTB(4); however, there was no change in the expression of E prostanoid (EP) receptors or LT receptors. Despite the similar EP profiles, young AMs are more responsive to PGE(2) as evidenced by their increased production of the important second messenger, cyclic AMP. In addition, young AMs express higher levels of PDE3B and lower levels of PDE4C compared to adult AMs. However, even though the young AMs produced a skewed eicosanoid profile, neither the inhibition of PGE(2) by aspirin nor the addition of exogenous LTB(4) rescued the defective opsonized phagocytosis. Examination of a receptor responsible for mediating opsonized phagocytosis showed a significant decrease in the gene expression levels of the Fcgamma receptor in young (day 7) AMs compared to adult AMs.
conclusionThese results suggest that elevated production of PGE(2) and decreased production of LTB(4) do not contribute to impaired opsonized macrophage phagocytosis and highlight an important difference between young and adult AMs.
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