ArticleIranian journal of basic medical sciences2018
The effect of down-regulation of CCL5 on lipopolysaccharide-induced WI-38 fibroblast injury: a potential role for infantile pneumonia.
Article in Iranian journal of basic medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- The Concentration and Duration of Lipopolysaccharide Stimulation Produce Different Cytokine Responses in an Ex Vivo Whole Blood Model in Horses.Veterinary sciences · 2025Article
- Curcumin alleviates LPS-induced WI-38 cell inflammation injury by regulating PTGS2 expression.Hereditas · 2025Article
- Oridonin alleviates inflammation and endoplasmic reticulum stress in pediatric pneumonia via regulating the SIRT1-mediated Wnt/β-catenin signaling pathway.Histology and histopathology · 2024Article
- Downregulation of circ_0035292 Alleviates LPS-Induced WI-38 Cell Injury via Targeting miR-494-3p/TLR4 Pathway in Infantile Pneumonia.Biochemical genetics · 2024Article
- FOXA2 attenuates lipopolysaccharide‑induced pneumonia by inhibiting the inflammatory response, oxidative stress and apoptosis through blocking of p38/STAT3 signaling.Experimental and therapeutic medicine · 2023Article
- The Effect of Natural-Based Formulation (NBF) on the Response of RAW264.7 Macrophages to LPS as an In Vitro Model of Inflammation.Journal of fungi (Basel, Switzerland) · 2022Article
- Circ_0026579 alleviates LPS-induced WI-38 cells inflammation injury in infantile pneumonia.Innate immunity · 2022Article
- Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway.BMC pharmacology & toxicology · 2021Article
- let7f‑5p attenuates inflammatory injury in iMolecular medicine reports · 2021Article
- Knockdown XIST alleviates LPS-induced WI-38 cell apoptosis and inflammation injury via targeting miR-370-3p/TLR4 in acute pneumonia.Cell biochemistry and function · 2019Article
- miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway.International journal of molecular medicine · 2019Article
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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
objectivesAberrant expression of CCL5 has been found in several kinds of inflammatory diseases, and the roles of CCL5 in these diseases have also been reported. However, the role of CCL5 in infantile pneumonia is still unclear. Thus, the function and acting mechanism of CCL5 in the MATERIALS AND
methodsHuman fetal lung fibroblast WI-38 cells were subjected with lipopolysaccharide (LPS) to mimic an in vitro model of pneumonia. CCL5 was silenced by transfection with CCL5-targeted siRNA, and then cell viability, apoptosis, and the expressions of apoptosis-associated factors were respectively assessed by CCK-8 assay, flow cytometry and Western blot. Besides, expressions of CCL5 and pro-inflammatory factors were analyzed by qRT-PCR and Western blot. The secretions of pro-inflammatory factors were measured by ELISA. Finally, the expressions of main factors in JNK and NF-κB pathways were detected.
resultsLPS treatment suppressed cell viability, promoted cell apoptosis, and enhanced the secretion of IL-6, MCP-1, and TNF-α. Overexpression of CCL5 was found in LPS-treated cells. CCL5 silence protected WI-38 cells from LPS-induced inflammatory damage, with increasing cell viability, inhibiting cell apoptosis, and reducing the production of pro-inflammatory cytokines. Besides, CCL5 silence inhibited LPS-induced activations of JNK and NF-κB pathways.
conclusionDown-regulation of CCL5 could protect WI-38 cells from LPS-induced inflammatory damage via inactivating JNK and NF-κB pathways.
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