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High expression of HMGB1 in children with refractory Mycoplasma pneumoniae pneumonia
Ying Ding1, Chu Chu1, Yuqin Li1
1Department of Infectious Disease, Children's Hospital of Soochow University, Suzhou, 215003, China.
Background:
Increasing numbers of refractory or severe, even fatal, cases of Mycoplasma pneumoniae infections have been reported in recent years. Excessive inflammatory responses play a vital role in the pathogenesis of refractory M. pneumoniae pneumonia (RMPP). HMGB1 is an actively secreted cytokine produced by macrophages and other inflammatory cells that participates in various infectious diseases. The present study aimed to explore the role and clinical significance of HMGB1 in children with RMPP and the potential mechanism of HMGB1 expression.
Methods:
Four hundred and fifty-two children diagnosed with M. pneumoniae pneumonia, including 108 children with RMPP, were enrolled from January 2013 to December 2015 at the Children's Hospital of Soochow University. HMGB1, TNF-α, and IL-6 in peripheral blood from RMPP and non-RMPP (NRMPP) cases were detected by real-time PCR and ELISA. Lipid-associated membrane proteins (LAMPs) were extracted from live M. pneumoniae and prepared at different concentrations for stimulation of THP-1 cells. After coculture with LAMPs, HMGB1, TNF-α, IL-6, RAGE, TLR2, and TLR4 in THP-1 cells were detected by real-time PCR.
Results:
Occurrences of cough, fever, and abnormal lung signs were more frequent in RMPP cases compared with NRMPP cases (all p < 0.05). Children with RMPP had longer hospital stays than children with NRMPP (p < 0.05). Different distributions of lymphocytes were noted between RMPP and NRMPP cases. HMGB1, TNF-α, and IL-6 levels were significantly higher in RMPP cases compared with NRMPP cases (all p < 0.05). HMGB1 had good diagnostic ability to differentiate RMPP with AUC of 0.876, sensitivity of 0.833, and specificity of 0.824 compared with TNF-α and IL-6. HMGB1 expression in THP-1 cells was increased by stimulation with 10 μg/ml LAMPs. TLR2 expression was increased after stimulation with 6 μg/ml LAMPs. HMGB1 level was positively associated with TNF-α, IL-6, and TLR2 levels.
Conclusions:
HMGB1 is a good diagnostic biomarker for differentiating RMPP and NRMPP. LAMPs from M. pneumoniae may induce HMGB1 expression in immune cells through the TLR2 pathway. Further in vitro and in vivo studies are needed for the development of a new treatment strategy to inhibit the HMGB1 pathway, thereby preventing the inflammation in RMPP.
Insights
High mobility group box 1 (HMGB1) is a promising biomarker for diagnosing refractory Mycoplasma pneumoniae pneumonia (RMPP) in children. HMGB1 may be induced by M. pneumoniae lipid-associated membrane proteins via the TLR2 pathway, suggesting potential therapeutic targets.
Area of Science:
- Pediatric Infectious Diseases
- Immunology
- Molecular Biology
Background:
- Refractory Mycoplasma pneumoniae pneumonia (RMPP) cases are increasing, often driven by excessive inflammatory responses.
- High mobility group box 1 (HMGB1) is a cytokine implicated in infectious disease pathogenesis.
- Understanding HMGB1's role in RMPP is crucial for developing targeted treatments.
Purpose of the Study:
- To investigate the clinical significance and diagnostic value of HMGB1 in pediatric RMPP.
- To explore the potential mechanism of HMGB1 expression induced by M. pneumoniae.
Main Methods:
- Recruited 452 children with M. pneumoniae pneumonia (108 RMPP).
- Measured HMGB1, TNF-α, and IL-6 levels in RMPP and non-RMPP (NRMPP) groups using real-time PCR and ELISA.
- Stimulated THP-1 cells with M. pneumoniae lipid-associated membrane proteins (LAMPs) to assess HMGB1, TLR2, and TLR4 expression.
Main Results:
- RMPP cases showed higher HMGB1, TNF-α, and IL-6 levels compared to NRMPP cases.
- HMGB1 demonstrated good diagnostic ability for differentiating RMPP (AUC=0.876).
- M. pneumoniae LAMPs stimulated HMGB1 expression in THP-1 cells, potentially via the TLR2 pathway.
Conclusions:
- HMGB1 serves as a valuable diagnostic biomarker for distinguishing RMPP from NRMPP.
- M. pneumoniae LAMPs may induce HMGB1 expression through the TLR2 pathway.
- Inhibiting the HMGB1 pathway could be a future therapeutic strategy for RMPP.
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