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Published on: July 30, 2016
CD14 down-modulation as a real-time biomarker in Kawasaki disease
Yutaro Inada1, Motoshi Sonoda2,3, Yumi Mizuno1
1Kawasaki Disease Center Fukuoka Children's Hospital Fukuoka Japan.
Insights
Kawasaki disease (KD) involves immune cell changes and oxidative stress. CD14 down-modulation on monocytes and elevated oxidative stress markers are key indicators in KD patients, aiding treatment assessment.
Area of Science:
- Immunology
- Oxidative Stress Research
- Pediatric Infectious Diseases
Background:
- Kawasaki disease (KD) pathophysiology involves complex immunological responses and oxidative stress.
- Identifying real-time biomarkers for innate immunity and oxidative stress in KD is crucial for effective management.
Purpose of the Study:
- To investigate the pathophysiology of Kawasaki disease (KD) through immunological and oxidative stress lenses.
- To identify real-time biomarkers associated with innate immunity and oxidative stress in KD patients.
Main Methods:
- Prospective enrollment of 85 KD patients and 135 controls.
- Flow cytometry analysis of monocyte surface markers (CD14, CD38, CD62L) and CD14 down-modulation.
- Assessment of oxidative stress using d-ROMs and antioxidant capacity via a free radical elective evaluator system.
Main Results:
- Significant CD14 down-modulation observed on monocytes during acute KD, indicating innate immune patterns.
- KD patients exhibited higher CD14 down-modulation and elevated d-ROM levels compared to controls.
- Monocyte CD14 expression normalized with intravenous immunoglobulin (IVIG) and infliximab treatment; oxidative stress decreased post-IVIG.
Conclusions:
- CD14 down-modulation on monocytes serves as a valuable real-time biomarker for assessing KD treatment response and differentiating relapse from infection.
- The interplay between inflammation and oxidative stress is critical in KD pathogenesis.
- Monitoring these biomarkers can guide second-line therapy selection post-IVIG in KD.
Objectives:
The objectives of this study were to investigate the pathophysiology of Kawasaki disease (KD) from immunological and oxidative stress perspectives, and to identify real-time biomarkers linked to innate immunity and oxidative stress in KD.
Methods:
We prospectively enrolled 85 patients with KD and 135 patients with diverse conditions including immune, infectious and non-infectious diseases for this investigation. Flow cytometry was used to analyse the surface expression of CD14, CD38 and CD62L on monocytes, along with a quantitative assessment of CD14 down-modulation. Additionally, oxidative stress levels were evaluated using derivatives of reactive oxygen metabolites (d-ROMs) and antioxidant capacity measured by a free radical elective evaluator system.
Results:
During the acute phase of KD, we observed a prominent CD14 down-modulation on monocytes, reflecting the indirect detection of circulating innate immune molecular patterns. Moreover, patients with KD showed a significantly higher CD14 down-modulation compared with infectious and non-infectious disease controls. Notably, the surface expression of CD14 on monocytes was restored concurrently with responses to intravenous immunoglobulin and infliximab treatment in KD. Furthermore, d-ROM levels in patients with KD were significantly elevated compared with patients with infectious and non-infectious diseases. Following intravenous immunoglobulin treatment, oxidative stress levels decreased in patients with KD.
Conclusion:
Monitoring CD14 down-modulation on monocytes in real-time is a valuable strategy for assessing treatment response, distinguishing KD relapse from concomitant infections and selecting second-line therapy after IVIG treatment in KD patients. The interplay between inflammation and oxidative stress likely plays a crucial role in the development of KD.
