High mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) in Kawasaki disease
T Hoshina1, K Kusuhara, K Ikeda
1Department of Paediatrics, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hoshina@pediatr.med.kyushu-u.ac.jp
Insights
High mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) are elevated in Kawasaki disease (KD). These proinflammatory cytokines and their receptors play a significant role in KD immune responses.
Area of Science:
- Immunology
- Pediatric Medicine
Background:
- Kawasaki disease (KD) is an acute febrile illness affecting young children.
- The pathogenesis of KD involves complex immune responses.
- Proinflammatory cytokines are implicated in KD development.
Purpose of the Study:
- To investigate the role of high mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) in Kawasaki disease (KD).
Main Methods:
- Serum levels of HMGB1 and MIF were measured using ELISA in 27 KD patients, 11 sepsis patients, and 28 healthy children.
- Gene expression of HMGB1 receptor (RAGE) and MIF receptor (CD74) was quantified in peripheral blood mononuclear cells (PBMCs) via real-time PCR.
Main Results:
- Serum HMGB1 and MIF levels were significantly higher in KD patients compared to controls (p<0.001 and p<0.01, respectively).
- Levels peaked in the early acute phase and decreased after defervescence.
- RAGE and CD74 gene expression was also significantly elevated in KD patients (p<0.001 and p<0.01, respectively).
Conclusions:
- HMGB1 and MIF are significantly elevated in Kawasaki disease.
- These cytokines and their receptors are involved in the immune response during KD.
- HMGB1 and MIF may play crucial roles in the pathogenesis of KD.
Objective:
To investigate whether two proinflammatory cytokines, high mobility group box 1 (HMGB1) and macrophage migration inhibitory factor (MIF) are involved in the development of Kawasaki disease (KD).
Methods:
Twenty-seven patients with KD were included in this study. Eleven patients with sepsis and 28 healthy children served as controls. Serum levels of HMGB1 and MIF were measured by corresponding enzyme-linked immunosorbent assay (ELISA) kits, respectively. Real-time polymerase chain reaction (PCR) was used to quantify the expression levels of genes encoding receptor for advanced glycation end-products (RAGE), an HMGB1 receptor, and CD74, an MIF receptor in peripheral blood mononuclear cells (PBMCs).
Results:
Serum levels of HMGB1 and MIF in KD patients were the highest in the early acute phase and gradually decreased after defervescence. Serum HMGB1 and MIF levels in KD patients were significantly higher than those in controls (HMGB1, p<0.001; MIF, p<0.01). The expression levels of the RAGE gene and CD74 gene in KD patients were significantly higher than those in controls (RAGE, p<0.001; CD74, p<0.01).
Conclusion:
These data suggest that HMGB1 and MIF play an important role in immune responses in KD patients.