Circular RNAs have emerged as important regulators in the pathogenesis of human diseases, including infantile pneumonia (IP). In this study, we aimed to explore the effects of circ_0035292 on lipopolysaccharide (LPS)-treated Wistsar Institute (WI)-38 cells.
Quantitative real-time polymerase chain reaction and western blot were executed to detect the levels of circ_0035292, microRNA-370-3p (miR-370-3p) and transducin β-like 1X related protein 1 (TBL1XR1). Cell counting kit-8, 5-ethynyl-2\'-deoxyuridine, and flow cytometry assessed cell proliferation and apoptosis. Concentrations of inflammatory factors were examined with enzyme linked immunosorbent assay kits. Dual-luciferase reporter assay and RNA immunoprecipitation were adopted to analyze binding between miR-370-3p and circ_0035292 or TBL1XR1.
Circ_0035292 level was increased in IP patients and LPS-triggered WI-38 cells. Circ_0035292 knockdown rescued LPS-mediated WI-38 cell proliferation suppression and WI-38 cell apoptosis and inflammation promotion. Circ_0035292 interacted with miR-370-3p and miR-370-3p directly targeted TBL1XR1. Moreover, miR-370-3p overexpression alleviated LPS-induced WI-38 cell apoptosis and inflammatory injury, which was abrogated via TBL1XR1 upregulation. Circ_0035292 absence inhibited the NF-κB pathway.
Knockdown of circ_0035292 rescued LPS-triggered WI-38 cell injury via miR-370-3p/TBL1XR1 axis and NF-κB pathway.

This study designed to investigate the potential role of lncRNA NEAT1/miR-146b in infantile pneumonia. In this study, 58 children with pneumonia and 58 healthy children collected for routine examination from December 2016 to January 2019. The lncRNA NEAT1 and miR-146b expression levels were detected by qPCR in both groups. The pneumonia model was established by inducing human embryonic lung fibroblasts HFL1 with LPS, and then transfected with lncRNA NEAT1 inhibition and miR-146b over-expression vector to observe the effect on cell viability and apoptosis after induction. Starbase predicted the binding site between lncRNA NEAT1 and miR-146b, and the targeted relationship between them was detected by dual luciferase reporter gene. The relative expression of lncRNA NEAT1 in serum of infantile pneumonia was up-regulated. Knocking down lncRNA NEAT1 promotes cell growth and reduces apoptosis in LPS-induced HFL1 cells. Results showed that the fluorescence activity of lncRNA NEAT1 obviously reduced when combined with miR-146b. In conclusion, the relative expression of miR-146b in serum of infantile pneumonia decreased, and over-expressing it could promote LPS-induced cell viability and reduce apoptosis. Taken together, this study demonstrated that the lncRNA NEAT1 regulates infantile pneumonia by sponging miR-146b.

BACKGROUND: Infantile pneumonia (IP) is a usual disease in infants and young children. The function and underlying mechanism of circZNF652 on lipopolysaccharide (LPS)-triggered inflammatory damage in WI-38 cells were detected in this article.
METHODS: WI-38 cells were induced by dosages of LPS to construct inflammatory injury model. WI-38 cell viability and apoptosis were detected by CCK-8 assay and flow cytometry, respectively. CircZNF652 and miR-181a levels were changed and detected by cell transfection and qRT-PCR. The levels of apoptosis and JNK/p38 and NF-κB pathways-related proteins, as well as the level of Cox-2 were detected by western blot. Finally, the concentrations of inflammatory factors were detected by ELISA.
RESULTS: LPS induced inflammatory injury showing as notably decreased the viability, while increased the numbers of apoptotic cells, as well as the levels of apoptosis and inflammatory factors in a dose dependent way. Besides, LPS inducement remarkably enhanced the expression of circZNF652. However, knockdown of circZNF652 remitted LPS-triggered inflammatory damage and restrained NF-κB and JNK/p38 pathways. Moreover, circZNF652 knockdown promoted miR-181a expression. Whereas, miR-181a inhibition markedly relieved circZNF652 knockdown-induced impacts.
CONCLUSIONS: Knockdown of circZNF652 remitted LPS-triggered WI-38 cells inflammatory damage through deactivation of NF-κB and JNK/p38pathways by up-regulating miR-181a.

CircRNA derived from vacuolar ATPase assembly factor (circVMA21) is a newly-researched circRNA, which is reported to adjust the degeneration of intervertebral disc. But, function of circVMA21 in infantile pneumonia is yet to be explored. The research surveyed the role of circVMA21 in lipopolysaccharide (LPS)-caused WI-38 cell inflammatory injury. LPS (10 μg/ml, 12 hr) was exploited to arouse WI-38 cell inflammatory injury. Subsequently, the mediatory impacts of microRNA (miR)-142-3p and circVMA21 in LPS-evoked cell injury were detected after transfection with the inhibited or overexpressed vectors. In above processes, cell behaviors of cell viability, apoptosis, and pro-inflammatory factors were monitored. NF-κB and JNK pathways were elucidated to showcase the feasible molecular mechanisms. Results displayed that LPS engendered WI-38 cell inflammatory injury was alleviated as well as activated NF-κB and JNK pathways was interdicted by miR-142-3p suppression. Importantly, restrained miR-142-3p expression was discovered in WI-38 cells after overexpressing circVMA21. Moreover, overexpressed circVMA21 exerted the similar functions as miR-142-3p suppression in LPS-triggered WI-38 cell injury. But, the influence was clearly reversed by miR-142-3p overexpression. Hindered NF-κB and JNK pathways caused by overexpressed circVMA21 was also crippled by miR-142-3p overexpression. The research discolsed that circVMA21 protected WI-38 cells to resist LPS-triggered inflammatory injury via miR-142-3p-NF-κB/JNK axis.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the authors, as they state that the data are not reproducible. The author states that the original data of the experiments do not possess reproductivity in their recent study, and that the obtained Figures 2-4 vary under different experiments.

UNASSIGNED: Aberrant 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 in vitro model of infantile pneumonia were researched in this study.
UNASSIGNED: Human 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.
UNASSIGNED: LPS 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.
UNASSIGNED: Down-regulation of CCL5 could protect WI-38 cells from LPS-induced inflammatory damage via inactivating JNK and NF-κB pathways.

The present study explored the functional role of microRNA (miR)-194 in lipopolysaccharide (LPS) induced lung cell injury, along with the underlying mechanisms and to reveal the potential role in infantile pneumonia. Human fibroblasts WI38 cells were transfected with miR-194 mimic or miR-194 inhibitor, and the transfection efficiency was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Thereafter, the cells were treated with or without LPS, and then cell viability, cell apoptosis and mRNA and protein expressions of key proteins of nuclear factor kappa B (NF-κB) pathway including inhibitor of NF-κB (IκB) α, p-65, and B-cell CLL/lymphoma (Bcl) 3 were analyzed. Results showed that overexpression and suppression of miR-194 was effective. Administration of LPS significantly decreased the cell viability and statistically promoted the percentages of apoptotic cells and increased the mRNA and protein expressions of p-65 and Bcl-3 but downregulated IκBα compared to the control group (P < 0.05 or P < 0.01). LPS in combination with miR-194 suppression further enhanced the effects of LPS on cell viability and cell apoptosis compared to the LPS group (P < 0.05). In contrast, LPS in combination with miR-194 overexpression observably reversed the effects of LPS on cell viability, cell apoptosis and mRNA and protein expressions of the key proteins (P < 0.05 or P < 0.01). In conclusion, miR-194 increases the LPS-induced the inhibition of cell viability and increasing of the cell apoptosis by inhibition of NF-κB pathway in WI38 cells. MiR-194 might be a potential targeted therapy for treatment of infantile pneumonia.

Infantile pneumonia is a common disease in children, which affects cardiopulmonary function and even threats to life. Therefore, overall analysis about the mechanism of pathogenesis may be provided a new slight for the treatment of infantile pneumonia. This study aimed to investigate the role of p300 in lipopolysaccharide (LPS)-induced inflammatory injuries in A549 cells. MTT, flow cytometry, qRT-PCR and western blot assays were used to assess the effect of p300 on A549 cells viability, apoptosis and inflammatory cytokines expressions. Furthermore, RhoA/ROCK/NF-κB signaling pathways were analyzed by qRT-PCR and western blot. Results showed that p300 was significantly up-regulated in LPS-treated A549 cells. Knockdown of p300 promoted cell viability, inhibited apoptosis and decreased the expression levels of IL-1β, IL-6 and TNF-α in LPS-treated A549 cells. In addition, knockdown of p300 abolished the activation of the downstream RhoA/ROCK/NF-κB signaling pathways induced by LPS exposure via regulation of RhoA. In conclusion, p300 might be involved in progression of cell inflammatory response and could serve as a novel therapeutic target for clinical treatment of infantile pneumonia.

Human parechoviruses (HPeVs) belong to the Parechovirus genus of the large and growing family of Picornaviridae with a non-enveloped, single-stranded and positive-sense RNA. An HPeV strain was isolated from the nasopharyngeal aspirate specimen of a 2 months old infant hospitalized with pneumonia in Beijing, China and nominated as BJ-37359 followed the code of the specimen. Strain BJ-37359 was identified as HPeV1 by whole genome sequencing. The full genome of strain BJ-37359 consisted of 7336 nucleotides (nt), excluding a poly (A) tail and contained an ORF of 6537 nt flanked by 5\'UTR of 709 nt and 3\'UTR of 90 nt. Phylogenetic analyses revealed that strain BJ-37359 were clustered together with HPeV1 strains in the structural capsid protein region, while uncoupling in the non-structural gene regions. Analyses with Simplot and Bootscan indicated that multiple recombination events occurred in the non-structural region and VP0 region of strain BJ-37359 with other HPeV1, and other types might have contributed to the recombination, especially HPeV6 and HPeV7 strains. Recombination analyses indicated that strain BJ-37359 may have a mosaic genome with new genomic recombination breakpoints.