ArticlePediatric surgery international2016
Surfactant protein-D attenuates the lipopolysaccharide-induced inflammation in human intestinal cells overexpressing toll-like receptor 4.
Article in Pediatric surgery international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Limited effect of surfactant protein D ablation on doxorubicin-induced intestinal toxicity in mice.Frontiers in immunology · 2026Article
- The Extracellular Matrix and the Immune System in Acute Lung Injury: Partners in Damage and Repair.Biomedicines · 2025Review
- Surfactant protein a attenuates generalized and localized neuroinflammation in neonatal mice.Brain research · 2023Article
- Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways.Iranian journal of basic medical sciences · 2022Article
- Innate/Inflammatory Bioregulation of Surfactant Protein D Alleviates Rat Osteoarthritis by Inhibiting Toll-Like Receptor 4 Signaling.Frontiers in immunology · 2022Article
- Necrotizing enterocolitis intestinal barrier function protection by antenatal dexamethasone and surfactant-D in a rat model.Pediatric research · 2021Article
- The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease.Frontiers in immunology · 2019Review
- Structure, genetics and function of the pulmonary associated surfactant proteins A and D: The extra-pulmonary role of these C type lectins.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2017Review
- Non-Pulmonary Immune Functions of Surfactant Proteins A and D.Journal of innate immunity · 2017Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeNecrotizing enterocolitis (NEC) is a devastating inflammatory disease of preterm infants that may depend on overexpression of toll-like receptor-4 (TLR4) in the immature intestine. Surfactant protein (SP)-D is a member of the collectin family and plays an important role in innate immunity, particularly in the airways. Although SP-D also exists in the intestines, little is known about its function. This study investigated whether SP-D can attenuate the inflammatory response of TLR4-overexpressing embryonal intestinal cells.
methodsAll experimental procedures were performed using the human intestinal cell line INT407 originally derived from human embryonal intestines. Platelet-activating factor (PAF), reported to be elevated in NEC patients, was used to induce TLR4 overexpression in the human embryonal intestinal cell line INT407. TLR4 expression was measured using quantitative real-time PCR. Inflammatory responses to PAF (5 µM), the TLR4 agonist lipopolysaccharide (LPS, 100 ng/ml), PAF + LPS, and PAF + LPS following SP-D pretreatment (20 µg/ml) were assessed by enzyme-linked immunosorbent assay (ELISA) of interleukin-8 (IL-8) release (in pg/ml).
resultsExpression of TLR4 mRNA (mean ± SD) was upregulated by PAF (369 % ± 28 %, p < 0.001). Stimulation with PAF + LPS resulted in higher IL-8 release (1959.3 ± 52.3) than control (141.2 ± 12.4), LPS (167.3 ± 65.8), or PAF (1527.2 ± 129.4) treatment (p < 0.05). Release in response to PAF + LPS (1590.1 ± 319.3) was attenuated by SP-D pretreatment (1161.6 ± 131.6; p < 0.05).
conclusionSP-D attenuates LPS-induced IL-8 production in TLR4-overexpressing intestinal cells, suggesting that SP-D may have a protective effect in the development of NEC in preterm infants.
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