Periostin Modulating Mycoplasma pneumoniae Pneumonia in Children Related to Th17 Cell Function

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Objective Mycoplasma pneumoniae pneumonia (MPP) is recognized as a significant respiratory tract infection in children. Periostin associates with airway remodeling, and the T helper 17 (Th17) cells play a crucial role against M. pneumoniae infection. This study investigates the effect of periostin in Th17 cells and the associated mechanism in MPP.

Methods The study investigated the role of periostin stimulated with pulmonary bronchoalveolar lavage fluid (BALF) from MPP. Levels of infection of M. pneumoniae were determined using quantitative real-time polymerase chain reaction. The periostin was cloned into vector, and siRNA fragment were synthesized. The Th17 cells were transfected with the vector and the fragment, and its expression and proinflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α, and IL-1β) were determined using western blot. The cell apoptosis, migration, and proliferation were measured using flow cytometer, transwell migration, and cell counting kit-8 assay, respectively.

Results The results showed that periostin expression had a positive correlation with MPP severity. Fluorescence-activated cell sorting analysis showed that the periostin inhibited the apoptosis of Th17 cells. Moreover, transwell migration showed a significant increased migration in Th17 cell was detected treated with BALF, and selective knockdown of periostin by specific siRNA had negative effect on cell migration. Western blot analysis showed the periostin induced the expression of the proinflammatory cytokines (IL-6, TNF-α, and IL-1β), and downregulation of periostin could decrease the expression of cytokines in MPP group.

Conclusion The study suggested that periostin is required for Th17 cells migration, and it also has effect on Th17 apoptosis and proinflammatory cytokines expression in MPP.

Keywords Mycoplasma pneumoniae - Th17 cell - periostin - migration - apoptosis - inflammatory cytokine Publication History

Received: 28 August 2023

Accepted: 29 December 2023

Article published online:
04 March 2024

© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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