Long non‑coding RNA GAS5 protects against Mycoplasma pneumoniae pneumonia by regulating the microRNA‑222‑3p/TIMP3 axis.

Mycoplasma pneumoniae pneumonia (MPP) is a type of pneumonia induced by M. pneumoniae (MP) infection. The present study investigated the effect of long non‑coding RNA growth arrest‑specific 5 (GAS5) in MPP and the underlying molecular mechanism of this. The expression of GAS5, microRNA‑222‑3p, (miR‑222‑3p) and tissue inhibitor of metalloproteinases‑3 (TIMP3) in MPP was investigated using reverse transcription‑quantitative PCR. Lipid‑associated membrane protein (LAMP)‑induced THP‑1 cells were used to model MPP. The viability of LAMP‑induced THP‑1 cells was analyzed using an MTT assay. Expression levels of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α (TNF‑α) pro‑inflammatory cytokines, and the anti‑inflammatory cytokine heme oxygenase‑1 (HO‑1) in LAMP‑induced THP‑1 cells were measured by ELISA. A dual‑luciferase reporter assay assessed the associations among GAS5, miR‑222‑3p and TIMP3. The expression of GAS5 and TIMP3 was downregulated in MPP. Expression of miR‑222‑3p was upregulated. GAS5‑overexpression increased the viability of LAMP‑induced THP‑1 cells. GAS5 upregulation decreased the levels of IL‑1β, IL‑6, TNF‑α and HO‑1 levels in LAMP‑induced THP‑1 cells. GAS5 directly interacted with miR‑222‑3p. TIMP3 was a target of miR‑222‑3p. miR‑222‑3p upregulation or TIMP3‑knockdown reversed the promotion effect on cell viability as well as the inhibitory effect on inflammation caused by GAS5‑overexpression in LAMP‑induced THP‑1 cells. GAS5‑overexpression increased the viability and decreased the inflammation of LAMP‑induced THP‑1 cells by regulating the miR‑222‑3p/TIMP3 axis. These results demonstrated a potential therapeutic target for MPP treatment.