Inflammatory response and Th1/Th2 immune response in children with Mycoplasma pneumonia and their correlation with pathogen load

• Main Authors: Bao-Qiang Xue, Ting-Zhi Wang
• Format: Article
• Language: English
• Published: Editorial Board of Journal of Hainan Medical University 2018-03-01
• Series: Journal of Hainan Medical University
• Subjects: Mycoplasma pneumonia; Pathogen load; Inflammatory response; Immune response; Transcription factor
• Online Access: http://www.hnykdxxb.com/PDF/201803/14.pdf
• ISSN: 1007-1237; 1007-1237

Objective: To study the inflammatory response and Th1/Th2 immune response in children with Mycoplasma pneumonia and their correlation with pathogen load. Methods: A total of 120 children who were diagnosed with Mycoplasma pneumonia in Zhidan County People’s Hospital between March 2014 and March 2017 were selected and divided into low load group and high load group according to the Mycoplasma pneumoniae DNA copy number in the induced sputum, and healthy children who received physical examination in Zhidan County People’s Hospital during the same period were selected as control group. The contents of inflammatory response cytokines and Th1/Th2 cytokines in serum as well as the expression of Th1/Th2 transcription factors in peripheral blood were detected. Results: Serum sTREM-1, CRP, sICAM-1, PCT, TNF-α, IFN-γ, IL-2, IL-4 and IL-10 levels as well as peripheral blood T-bet and GATA3 mRNA expression of low load group and high load group were significantly higher than those of control group while peripheral blood SOCS1 and SOCS3 mRNA expression were significantly lower than those of control group; serum sTREM-1, CRP, sICAM-1, PCT, TNF-α, IFN-γ, IL-2, IL-4 and IL-10 levels as well as peripheral blood T-bet and GATA3 mRNA expression of high load group were significantly higher than those of low load group while peripheral blood SOCS1 and SOCS3 mRNA expression were significantly lower than those of low load group. Conclusion: The increase of pathogen load in children with Mycoplasma pneumoniae can cause the overactivation of inflammatory response and Th1/Th2 immune response.