Study on the Earlier Inflammatory and Antiinflammatory and Immune Mechanism Change of Children With Hand, Foot and Mouth Disease
2014
Objective
To investigate the changes of tumor necrosis factor (TNF)-α, interleukin (IL)- 6, IL - 10 and nti-i functions of children with hand, foot and mouth disease (HFMD).
Methods
Fifty-six out-patients and in-patients who were diagnosed as HFMD in the department of Pediatrics, People's Hospital of Jimo City from May to October 2012, were included into this study as experiment group. At the same time, another 20 healthy children were recruited into this study as control group. There were no significant differences on age and gender between two groups (P>0.05). The levels of following items were detected of two groups: immunoglobulin (Ig)A, IgG, IgM, T cell subgroup (CD3+ , CD4+ , CD8+ , CD4+ /CD8+ ) and cytokines(TNF-α, IL-6, IL -10). The study protocol was approved by the Ethical Review Board of Investigation of People's Hospital of Jimo City. Informed consent was obtained from all participates' patients.
Results
The significant differences were found in the levels of IgA, CD4+ , IL-6 and IL-10 between experiment group and control group [(1.06±0.61) g/L vs (1.50±0.54) g/L, (30.79±8.87)% vs (35.15±5.18)%, (14.71±16.29) pg/mL vs (3.76±1.03) pg/mL, (15.38±8.77) pg/mL vs (11.39±4.99) pg/mL](t=2.849, 2.070, 2.991, 1.921; P<0.05). There were significant differences in IL-6, IL-10 between severe HFMD patients and common HFMD patients [(8.02±8.91) pg/mL vs (16.75±18.01) pg/mL, (23.17±10.06) pg/mL vs (11.86±7.01) pg/mL](t=1.792, 4.739; P<0.05). There was a positive correlation between IL-6 and IgG, IgM (r=0.411, 0.899; P<0.05), IL-10 and IgA (r=-0.325, P<0.05), IL-6 and CD3, CD4 (r=0.720, 0.764; P<0.05).
Conclusions
The immune function disorder was found at the early stage of HFMD, especially the decline of IgA and CD4+ levels. Furthermore, the inflammatory and nti-inflammatory mechanism disorder may play an important role in the development of severe HFMD.
Key words:
Hand, foot and mouth disease; Immun function; Cytokines; Systemic inflammatory response syndrome; Compensatory anti-inflammatory response syndrome
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