The role of circTMOD3 in regulating LPS-induced acute inflammation and injury in human lung fibroblast WI-38 cells.

BACKGROUND: Circular RNAs (circRNAs) have been implicated in the molecular etiology of pediatric pneumonia. Here, we investigated the precise action of circRNA tropomodulin 3 (circTMOD3, hsa_circ_0035292) in cell injury and inflammation induced by lipopolysaccharide (LPS). Methods: Cell viability was gauged by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis and cycle distribution were assessed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was used to measure interleukin-6 (IL-6), IL-1ß and tumor necrosis factor alpha (TNF-α) production. The levels of circTMOD3, microRNA (miR)-146b-3p, and C-X-C motif chemokine receptor 1 (CXCR1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Ribonuclease (RNase) R, Actinomycin D and subcellular localization assays were done to characterize circTMOD3. The direct relationship between miR-146b-3p and circTMOD3 or CXCR1 was confirmed by dual-luciferase reporter assays. Results: Our data showed that LPS induced the expression of circTMOD3 in WI-38 cells. CircTMOD3 was resistant to RNase R and was mainly present in the cytoplasm. Silencing endogenous circTMOD3 alleviated WI-38 cell injury and inflammation triggered by LPS. Mechanistically, circTMOD3 directly targeted miR-146b-3p, and CXCR1 was a direct and functional target of miR-146b-3p. CircTMOD3 regulated LPS-induced cell inflammation and injury by targeting miR-146b-3p, and miR-146b-3p-mediated suppression of CXCR1 impacted LPS-evoked cytotoxicity and inflammation. Furthermore, circTMOD3 functioned as a competing endogenous RNA (ceRNA) for miR-146b-3p to induce CXCR1 expression. Conclusion: Our findings demonstrated the regulation of circTMOD3 in LPS-induced cell injury and inflammation at least partially via miR-146b-3p-independent modulation of CXCR1.

[Effect of low-dose methylprednisolone on serum TNF-α level in children with Mycoplasma pneumoniae pneumonia].

OBJECTIVE: To investigate the effect of low-dose methylprednisolone on serum tumor necrosis factor alpha (TNF-α) level in children with Mycoplasma pneumoniae pneumonia (MPP). METHODS: A case-control study was conducted among 38 children with MPP who received treatment in the Affiliated Hospital of Yan'an University between January and December 2012, and who had not received glucocorticoids before hospitalization. They were randomly divided into methylprednisolone treatment (n=20) and conventional treatment groups (n=18). The methylprednisolone treatment group was administered with methylprednisolone (1 mg/kg·d) by intravenous drip for three days in addition to conventional treatment. Serum samples were collected from both groups before treatment and on days 4 and 7 of treatment. Twenty-five children who underwent physical examination in the healthcare clinic during the same period were randomly selected as a normal control group, and serum samples were collected on the same day that the physical examination was performed. Serum TNF-α levels in the three groups were measured using enzyme-linked immunosorbent assay. RESULTS: On admission, the methylprednisolone treatment and conventional treatment groups had significantly higher serum TNF-α levels than the normal control group (P<0.01), but there was no significant difference between the methylprednisolone treatment and conventional treatment groups. On days 4 and 7 of treatment, the methylprednisolone treatment group had significantly lower serum TNF-α levels than the conventional treatment group (P<0.05; P<0.01). On day 7 of treatment, there was no significant difference in serum TNF-α level between the methylprednisolone treatment and normal control groups, but the conventional treatment group still had a significantly higher serum TNF-α level than the normal control group (P<0.01). CONCLUSIONS: Low-dose methylprednisolone can significantly decrease serum TNF-α level and inhibit inflammatory response in children with MPP, and may reduce damage caused by inflammatory response.

Association between inflammation factors and Mycoplasma pneumoniae in children: Protocol for a systematic review.

BACKGROUND: Several clinical studies have reported that inflammation factors (IF) are associated with Mycoplasma pneumoniae in children. However, no study systematically investigated the association between IF and M pneumoniae in pediatric population. Thus, this study will explore the association between IF and pediatric M pneumoniae systematically. METHODS: This study will search following databases of PUBMED, PsycINFO, Scopus, Cochrane Library, EMBASE, Web of Science, and Chinese Biomedical Literature Database from inception to the February 28, 2019 without any language limitations. We will cover clinical studies of M pneumoniae that report associations between IF and M pneumoniae. In addition, reference lists of relevant studies will also be identified to avoid missing any eligible studies. Two investigators will independently screen and select studies, and will assess the methodological quality for each study, which is evaluated by using Newcastle Ottawa Scale. Any disagreements will be settled down through discussion with a third investigator until consensus is reached. RESULTS: This study will explore the associations between IF and M pneumoniae by assessing the changes of IF, such as interleukin (IL)-4, IL-5, IL-6, IL-10, IL-13, and IL-17 at different stages of M pneumoniae. CONCLUSION: The findings of this study may provide most recent evidence for the associations between IF and M pneumoniae in pediatric populations. ETHICS AND DISSEMINATION: Ethical approval is not needed in this study, because no individual patient data will be utilized in this study. The findings of this study are expected to be published at peer-reviewed journal or will be presented at professional conference. PROSPERO REGISTRATION NUMBER: PROSPERO CRD42019125359.