Impact of Mycobacterium vaccae immunization on lung histopathology in a murine model of chronic asthma.

BACKGROUND: Therapeutic modalities of asthma have not been proved to be successful in reversing the already established chronic changes of airways. OBJECTIVE: We aimed to determine the impact of heat-killed Mycobacterium vaccae immunization, a potent Th1 stimulant, on chronic changes of asthma. METHODS: Newborn BALB/c mice were divided into three groups; mice in M. vaccae group received 107 colony-forming units (CFU)/50 micro L of heat-killed M. vaccae subcutaneously on days 3, 14 and 42 before the development of chronic asthma model, whereas mice in control and chronic asthma groups received saline. Subsequently, mice in M. vaccae and chronic asthma groups were administered 10 micro g/100 micro L of ovalbumin (OVA) on days 43, 45, 47, 49, 51, 53 and 55 intraperitoneally, and 20 micro g/10 micro L of OVA on days 83, 86 and 89 intratracheally. Mice in control group received saline on the same days. RESULTS: Comparison of M. vaccae and chronic asthma groups showed statistically significant differences in goblet cell numbers, thickness of basement membrane and subepithelial smooth muscle of small, medium and large airways and epithelial thickness of medium airways. There was no significant difference between the control and M. vaccae groups except for goblet cell numbers of medium and large airways, and epithelial thickness of medium airways. CONCLUSION: Results of our study suggested that immunization by M. vaccae of newborn mice would prevent some of the chronic changes of airways due to asthma.

Parental smoking behavior and the urinary cotinine levels of asthmatic children.

To determine whether parental reports of smoking habits and modifications in smoking behavior are associated with urinary cotinine levels (UCLs), UCLs were measured in 77 asthmatic children. Parental reports and UCLs agreed for 58 of the 77 children (75%). Although UCLs of children whose parents smoked indoors and outdoors were significantly higher than UCLs of children whose parents did not smoke (p<0.0001, p<0.002, respectively), there was no statistically significant difference between the UCLs of children whose parents smoked indoors and outdoors (p = 0.286). We concluded that encouraging smoking parents of asthmatic children to smoke outdoors may not be an effective way to lessen exposure.

Thorax high resolution computerized tomography findings in asthmatic children with unusual clinical manifestations.

BACKGROUND: It has been consistently observed in high resolution computerized tomography (HRCT) scans that asthmatic patients manifest more abnormalities related to airways remodeling than do normal subjects. OBJECTIVE: To find the underlying abnormalities in the lungs of asthmatic children with unusual manifestations. METHOD: Asthmatic children not responding as expected to inhaled steroid therapy with or without localized permanent or temporary recurrent auscultation findings (rales) were evaluated with chest radiographs and HRCT scans. Bronchoscopy was performed on the ones with localized rales. RESULTS: The sample consisted of 16 asthmatic children (6 girls and 10 boys, mean age = 7.75+/-4.43 years). Chest radiograph abnormality rate was 44% and the thorax HRCT scan abnormality rate was 75% (56% fibrotic retractions, 38% atelectasis, 19% bronchiectasis, and 19% bronchial wall thickening). Two patients with localized permanent rales and with right middle lobe (RML) atelectasis in HRCT scan underwent bronchoscopy which revealed RML syndrome due to mucus plugging in one and lymph node pressure in the other. In one patient with localized temporary recurrent rales and major bronchiectasis in HRCT scan, bronchoscopy revealed bronchitis. The patient with RML syndrome due to mucus plugging required lobectomy. CONCLUSION: We conclude with this experience that thorax HRCT scanning may be a helpful adjunct in the evaluation of an asthmatic children with atypical clinical findings.

Serum TNF-alpha, sCD8 and sIL-2R levels in childhood tuberculosis.

In this study we have determined the serum tumor necrosis factor-alpha (TNF-alpha), soluble CD8 (sCD8) and soluble interleukin-2 receptor (sIL-2R) levels in children with active pulmonary tuberculosis (n = 66) and healthy controls (n = 20). Measurable serum TNF-alpha levels were detected in nine of 86 children (10.5%), all of whom belonged to the group with active disease. Serum sCD8 and sIL-2R determinations revealed a significant difference between the group with active pulmonary tuberculosis and the controls (p < 0.05). Deeper insight into the involvement of cytokines and T cells will provide a better understanding

Serum tumor necrosis factor levels in acute myocardial infarction and unstable angina pectoris.

Tumor necrosis factor (TNF) enhances leukocyte adherence to vascular endothelium and increases procoagulant activity in the endothelial cells. Thus it may be implicated in the pathogenesis of acute vascular occlusions. To study the role of TNF in the early stages of acute myocardial infarction (MI), the authors measured circulating TNF levels in the sera of patients with acute MI and unstable angina pectoris. Blood samples were obtained within six hours after onset of chest pain and stored at -70 degrees until tested. A sensitive sandwich enzyme-linked immunosorbent assay (ELISA) test was used for TNF measurement. C-reactive protein (CRP) levels were determined semiquantitatively. Immediate complications such as heart failure, arrhythmia, and shock were also noted. Twenty-four patients with electrocardiographically and biochemically confirmed acute MI and 14 patients with unstable angina pectoris were included in the study. TNF levels were serially assessed at the time of admission and at hours 6, 24, 48, 72, and 96 after onset of chest pain in 2 patients with acute MI. Detectable TNF was found in 13 sera of the acute MI group (range; 10-1510 pg/mL) and 4 sera of the angina pectoris group (range; 15-240 pg/mL). There was no correlation between the serum TNF levels and the occurrence of complications and the extent of myocardial damage. CRP response was unrelated to TNF levels. Contrary to previous reports, serial measurement of TNF revealed that peak values were reached within six hours and disappeared after twenty-four hours.(ABSTRACT TRUNCATED AT 250 WORDS)