Kawasaki disease was associated with higher IL-17A and IL-6, a cytokine profile similar to other autoimmune diseases. IVIG therapy resulted in increased expression of Treg-related FoxP3. IVIG resistance was associated with higher levels of IL-10 and IL-17A. Our findings provide further evidence that Kawasaki disease is an autoimmune-like disease.

Background Pneumonia, the leading reason underlying childhood deaths, may be triggered or exacerbated by air pollution. To date, only a few studies have examined the association of air pollution with emergency department (ED) visits for pediatric pneumonia, with inconsistent results. Therefore, we aimed to elucidate the impact of short-term exposure to particulate matter (PM) and other air pollutants on the incidence of ED visits for pediatric pneumonia. Methods PM 2.5 , PM 10 , and other air pollutant levels were measured at 11 air quality-monitoring stations in Kaohsiung City, Taiwan, between 2008 and 2014. Further, we extracted the medical records of non-trauma patients aged ≤17 years and who had visited an ED with the principal diagnosis of pneumonia. A time-stratified case–crossover study design was employed to determine the hazard effect of air pollution in a total of 4024 patients. Results The single-pollutant model suggested that per interquartile range increment in PM 2.5 , PM 10 , nitrogen dioxide (NO 2 ), and sulfur dioxide (SO 2 ) on 3 days before the event increased the odds of pediatric pneumonia by 14.0% [95% confidence interval (CI), 5.1–23.8%], 10.9% (95% CI, 2.4–20.0%), 14.1% (95% CI, 5.0–24.1%), and 4.5% (95% CI, 0.8–8.4%), respectively. In two-pollutant models, PM 2.5 and NO 2 were significant after adjusting for PM 10 and SO 2 . Subgroup analyses showed that older children (aged ≥4 years) were more susceptible to PM 2.5 (interaction p = 0.024) and children were more susceptible to NO 2 during warm days (≥26.5 °C, interaction p = 0.011). Conclusions Short-term exposure to PM 2.5 and NO 2 possibly plays an important role in pediatric pneumonia in Kaohsiung, Taiwan. Older children are more susceptible to PM 2.5 , and all children are more susceptible to NO 2 during warm days.

Background: Air pollution exposure is associated with greater risk for cardiovascular events. This study aims to examine the effects of increased exposure to short-term air pollutants on ST-segment elevation myocardial infarction (STEMI) and determine the susceptible groups. Methods: Data on particulate matter PM2.5 and PM10 and other air pollutants, measured at each of the 11 air-quality monitoring stations in Kaohsiung City, were collected between 2011 and 2016. The medical records of non-trauma adult (>17 years) patients who had visited the emergency department (ED) with a typical electrocardiogram change of STEMI were extracted. A time-stratified and case-crossover study design was used to examine the relationship between air pollutants and daily ED visits for STEMI. Results: An interquartile range increment in PM2.5 on lag 0 was associated with an increment of 25.5% (95% confidence interval, 2.6%–53.4%) in the risk of STEMI ED visits. Men and persons with ≥3 risk factors (male sex, age, hypertension, diabetes, current smoker, dyslipidemia, history of myocardial infarction, and high body mass index) for myocardial infarction (MI) were more sensitive to the hazardous effects of PM2.5 (interaction: p = 0.039 and p = 0.018, respectively). The associations between PM10, NO2, and O3 and STEMI did not achieve statistical significance. Conclusion: PM2.5 may play an important role in STEMI events on the day of exposure in Kaohsiung. Men and persons with ≥3 risk factors of MI are more susceptible to the adverse effects of PM2.5 on STEMI.