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Published on: August 7, 2017
Nasal Mucosal Cytokines as Potential Biomarkers for Assessing Disease Severity and Class of Pathogen in Children With
Rouba Sayegh1,2, Li Tang3, Ki Wook Yun2,4
1Division of Infectious Diseases, Department of Pediatrics, Nationwide Children's Hospital.
Insights
Identifying mucosal biomarkers like MCP-2 and IFN-γ in children with community-acquired pneumonia (CAP) can help determine disease severity and identify pathogens, aiding clinical classification.
Area of Science:
- Pediatric infectious diseases
- Respiratory medicine
- Immunology
Background:
- Community-acquired pneumonia (CAP) is a major cause of childhood illness and death.
- Accurate assessment of CAP severity and cause is clinically difficult.
- Novel biomarkers are needed for improved patient classification.
Purpose of the Study:
- To identify mucosal biomarkers for classifying pediatric CAP.
- To correlate cytokine concentrations with disease severity and pathogens.
Main Methods:
- Analyzed nasopharyngeal cytokine concentrations in 182 children with CAP and 26 controls.
- Identified pathogens using cultures and molecular assays.
- Defined severe CAP by hospitalization duration or PICU admission.
Main Results:
- Children with atypical bacteria or influenza showed higher levels of MCP-2, IFN-γ, and CXCL10 compared to typical bacterial infections.
- Severe CAP cases had elevated CCL23 levels, independent of pathogen type.
- Specific cytokines differed based on pathogen and disease severity.
Conclusions:
- Mucosal cytokine profiles vary with CAP etiology and severity in children.
- Mucosal biomarkers show promise for assessing pediatric CAP severity and identifying causative agents.
Background:
Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality in children. Assessing disease severity and etiology remains challenging in the clinical setting. The objective of this study was to identify mucosal biomarkers that could potentially assist with patient classification.
Methods:
We analyzed mucosal concentrations of cytokines in nasopharyngeal samples obtained from a convenience sample of 182 children with CAP and 26 matched healthy controls. Pathogens were identified by cultures and molecular assays. Severe disease was defined by hospital stay ≥3 days and/or pediatric intensive care unit admission. Data were analyzed according to identified pathogens and disease severity.
Results:
Children with CAP and detected atypical bacteria had significantly higher concentrations of monocyte chemotactic protein 2 (MCP-2), interferon gamma (IFN-γ), and CXCL10, among others, compared with those with typical bacteria. Children with influenza virus had significantly higher concentrations of MCP-2, CXCL10, CXCL11, CX3CL1, and IFN-γ than those with typical bacteria. Additionally, children with severe CAP had significantly higher concentrations of CCL23 than children with mild/moderate disease, irrespective of the pathogen(s) identified.
Conclusions:
We identified differences in mucosal concentrations of inflammatory and antiviral cytokines in children with CAP according to disease severity and detected pathogens. Mucosal biomarkers represent a promising approach to help assess disease severity and etiology.
