Hai Lee Chung

Deposition of eosinophil-granule major basic protein and expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the mucosa of the small intestine in infants with cow’s milk–sensitive enteropathy ☆ ☆☆

BACKGROUND Cows milk-sensitive enteropathy (CMSE) is an important cause of chronic diarrhea and failure to thrive in infancy. The immunopathology of the mucosal lesion associated with CMSE has not yet been described. OBJECTIVES This study investigated the eosinophil activation and the role of adhesion molecules in the pathogenesis of intestinal mucosal damage associated with CMSE. METHODS Twenty-one patients with chronic diarrhea and abnormal mucosa on duodenal biopsy specimens were included. The patients had negative responses to skin prick tests and RASTs with milk. Fourteen patients were diagnosed with CMSE by milk challenge test and were designated as the CMSE group. Seven patients with no milk intolerance were defined as the non-CMSE group. Four infants with frequent vomiting and no mucosal abnormalities were also studied as the control group. Immunohistochemical stains for eosinophil major basic protein (MBP), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 on endoscopic duodenal biopsy specimens were performed. RESULTS The degree of eosinophil degranulation, as evidenced by localization of extracellular MBP, was significantly greater in the CMSE group compared with the non-CMSE and control groups (P <.05). Expression of VCAM-1 on mononuclear cells was higher in the CMSE group compared with the non-CMSE and control groups (P <.05). The severity of villous atrophy was positively correlated with the deposition of MBP (r = 0.79, P <.001). CONCLUSION These results strongly suggest eosinophils and VCAM-1 are implicated in the pathogenesis of mucosal damage associated with CMSE.

Increased epidermal growth factor in nasopharyngeal aspirates from infants with recurrent wheeze

Airway remodeling is known to be a consequence of repeated injury and thought to be involved in early stage of asthma. We aimed to investigate the mediators associated with airway remodeling in recurrent early wheezers. Thirty‐three infants, aged 2 years or less, admitted with exacerbation of wheezing were enrolled. All of them had experienced three or more episodes of wheezing before admission. They were categorized into two groups: those who had been hospitalized two or more times for severe wheezing (N = 19) and those who had only once or never been hospitalized (N = 14). Epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF)‐β1 levels in nasopharyngeal aspirates (NPA) collected on admission were measured. The difference between two patients groups divided based on their hospitalization history was assessed. We also examined these mediators in older asthmatic children (N = 15) admitted with exacerbation and their relationship with lung function parameters measured after stabilization. NPA EGF levels were significantly increased in recurrent early wheezers compared to controls. EGF, VEGF, and TGF‐β1 levels were significantly higher in those with a previous history of multiple hospitalizations than in those without. In older asthmatic children, EGF levels were related with age and duration of asthma, but showed an inverse correlation with forced expiratory volume in 1 sec and forced expiratory flow between 25% and 75% of vital capacity. Our study shows that there might be significant damage during exacerbation in wheezy infants as levels of the mediators, EGF, VEGF, and TGF‐β1 were higher in those who had been frequently hospitalized. It seems to suggest that those infants with severe recurrent wheezing might have chronic airway obstruction. Pediatr Pulmonol. 2015; 50:841–847.

Decreased interleukin-18 response in asthmatic children with severe Mycoplasma pneumoniae pneumonia.

Abstract Purpose Mycoplasma pneumoniae (M. pneumoniae) is a common causative agent of pneumonia in children. The aim of this study is to determine whether there is any difference in selected cytokine or chemokines response in asthmatic children compared to non-asthmatic children during acute M. pneumoniae pneumonia. Methods Seventy-five children, 6–12years of age, admitted with M. pneumoniae pneumonia were enrolled. Two patient groups were defined: the children with known asthma (N =40) and non-asthmatic children (N =35). Interleukin (IL)-18 and selected chemokines, IL-8, CXCL9, CXCL10, and regulation upon activation normal T-cell expressed and secreted (RANTES) were measured by means of ELISA in the plasma samples of the patients collected on admission. We investigated the values of these mediators in relation to the asthma status and symptom severity of the patients. Twenty age-matched, non-infected controls were also studied. Results Plasma levels of IL-18 and the chemokines increased significantly in the patients with M. pneumoniae pneumonia compared to non-infected, age-matched controls (P <0.01). However, the asthmatic patients showed significantly reduced IL-18 and CXCL10 responses (P <0.01, <0.05, respectively) and had more severe pneumonia symptoms (P <0.01) compared to non-asthmatic patients. IL-18 was significantly lower in severe pneumonia group than in non-severe group (P <0.05). Conclusions Our study suggests that IL-18 and the chemokines are importantly involved in the pathogenesis of M. pneumoniae pneumonia. It also indicates that some asthmatic children have deficient IL-18 response when affected by M. pneumoniae pneumonia, which might be associated with more severe pneumonia observed in this group of patients.