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Clinical significance of serum miR-95 in children with Mycoplasma pneumoniae infection complicated with diarrhea.

Created on 28 Sep 2026

Authors

Hongliang Zhang, Mengyang Cai, Qing Gong

Published in

Annals of agricultural and environmental medicine : AAEM. Volume 33. Issue 3. Pages 407-412. Sep 21, 2026. Epub Mar 05, 2026.

Abstract

Mycoplasma pneumoniae infection (MPI) can lead to extrapulmonary diseases, in which diarrhea occurs frequently. The role and impact of microRNA-95 (miR-95) in MPI and MPI with diarrhea (MPI+DIA) remain elusive. The aim of the study is to investigate miR-95 expression and its functional impact in paediatric MPI with diarrhea.
The study enrolled 80 MPI patients (53 without diarrhea, 27 with diarrhea) and 80 matched healthy controls. Expression of miR-95 was quantified using reverse transcription quantitative polymerase chain reaction (RT -qPCR). Predictors of disease status were analyzed through binary logistic regression. An in vitro pneumonia model (MP-BEAS-2B) was generated by infecting BEAS-2B cells with Mycoplasma pneumoniae (MP). In parallel, an intestinal epithelial injury model was generated by treating Caco-2 cells with 4 μg/mL lipid-associated membrane proteins (LAMPs). Cell proliferation was measured with cell counting kit-8 (CCK-8), apoptosis by flow cytometry, and interleukin -8 (IL-8) and tumour necrosis factor-alpha (TNF-α) levels were determined via RT-qPCR.
The study revealed that miR-95 was significantly elevated in the MPI group, with a further increase observed in MPI patients complicated with diarrhea. Additionally, miR-95 served as a discriminator among healthy controls, MPI patients, and MPI+DIA patients. In MP-BEAS-2B and LAMPs-Caco-2 cells, miR-95 was highly expressed. However, downregulating miR-95 significantly enhanced cell proliferation, inhibited apoptosis, and reduced the expression of IL-8 and TNF-α.
MiR-95 expression was significantly elevated in MPI patients, and further increased in those with MPI complicated by diarrhea. Downregulating miR-95 significantly protected BEAS-2B and Caco-2 cells from MP damage and alleviated cellular inflammation.

PMID:
42802963
Bibliographic data and abstract were imported from PubMed on 28 Sep 2026.

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