Level of eosinophil cationic protein in sputum of chemical warfare victims

Considering fair response to inhaled corticosteroids and reports of severe air way hyper responsiveness in chemical warfare victims [CWV], a role for eosinophilic inflammation [i.e. asthma] was postulated. The objective of this study was to determine the presence of eosinophilic inflammation in CWV by evaluation of Sputum cellularity and eosinophil cationic protein [ECP]. Forty CWV and 15 control subjects entered this cross sectional study. Demographic data, dyspnea severity scale, spirometry results and 6 min walk test were determined. Sputum was collected with inducing by nebulizing hypertonic saline and analyzed for total inflammatory cell count, the cellular differential count and ECP level. Control group was normal volunteers with PC[20] more than 8 mg/ml. Mean +/- SD of eosinophil percentage [11.7 +/- 11.1%] and ECP level in sputum of CWV [46.1 +/- 19.5 ng/ml] were significantly more than control group. Regression analysis showed significant correlation between ECP level and percentage of eosinophils in sputum [r= +0.43, P< 0.01]. ECP level of CWV subjects with obstructive pattern did not show any significant difference from CWV with normal spirometry. ECP level in CWV subjects who revealed more than 12% improvement in forced expiratory volume in one second [FEV1] was significantly higher than CWV who had improvement less than 12% [P= 0.01]. BO and asthma as final clinical diagnosis of CWV did not show any significant difference of sputum ECP. Bronchial inflammation in different types of pulmonary complication of CWV is eosinophil dependent. ECP level of sputum in CWV could guide physician to select CWV who would respond to corticosteroids

Acute effect of water pipe smoke on sensitized animals

This study aimed to compare the inflammatory effects of water pipe smoke with cigarette smoke on inducing exacerbation in asthmatic murine model, under similar conditions of exposure. Thirty-six BALB-C mice in six different groups [one control group, one asthmatic group and four groups of asthmatic exposed to smoke] were entered the study. Animals were exposed to cigarette and water pipe smokes and samples were obtained after 6 and 24 hours. Bronchoalveolar lavage fluid [BALF] was collected and analyzed for neutrophils, eosinophils, nitric oxide, Interferon-gamma [IFN-delta] and lnterleukin-4 [IL-4]. Serum Interferon-gamma and IL-4 were also evaluated. Both lungs were sent for histopathological examination. In all sensitized animals, BALF cytology showed a significant decrease in neutrophils and lymphocyte percentage and significant increase of eosinophils. The level of nitric oxide in all smoke exposed animals was significantly higher than sensitized controls. Water pipe smoke did not affect the IL-4 level, but cigarette smoke decreased IL-4 after 6 hours. The level of IFN-gamma in BALF decreased after 6 hours of exposure in both exposed groups and returned to baseline after 24 hours. Exacerbation of asthma by water pipe smoke is comparable to that of cigarette smoke. The mechanism of action may be through the suppression of the type 1 T helper cells

Level of nitric oxide in bronchoalveolar lavage fluid of asthmatic mice model

Asthma is a chronic inflammatory disease with multifactorial and complicated mechanisms. Elevated level of exhaled Nitric Oxide [NO] in asthma and other inflammatory lung diseases has led to many studies examining NO as a potential marker of airway inflammation. This study was designed to determine the level of NO in Bronchoalveolar Lavage [BAL] fluid during early and late stages of asthmatic attack in mouse model. In this study male BALB/c mice were used. The level of NO was determined in BAL fluid of asthmatic mice five minutes, six and sixteen hours after challenge with methacholine, as irritant and smoke and 5% ovalbumin as allergens, using colorimetric assay. The level of NO increased upon exposure to all three irritants used in this study [52.3 microM for smoke and 49.5 [microMfor methacholine] as compared to 22.8 microM for the baseline. Our results showed that NO levels were increased during early phase of asthmatic condition and reached to its maximum level after six hours and decreased at the late stage of asthma [16hrs] possibly by activating a feedback regulatory loop. In addition, high level of NO led to the hypertrophy of smooth muscle that can account for the pathological changes associated with asthma. Thus, NO is an inflammatory marker in asthma and its measurement, as a non-invasive method during asthmatic attack is suggested. A careful development of specific inhibitors for iNOS enzyme during asthmatic attack is also necessary