Background
Increased intestinal permeability, either due to the exposure to antigens in asthmatic patients or due to a barrier defect, plays a critical role in susceptibility to environmental allergens. House dust mite allergy occurs more commonly than any other type of allergy among Egyptian asthmatic patients.
Aim
To assess the relation between serum zonulin level as a marker of increased intestinal permeability and the severity of house dust mite allergic asthma.
Methods
A case–control study which included 48 patients with house dust mite allergic asthma and 48 healthy control subjects attending the Allergy and Immunology Unit, Microbiology and Immunology Department, Faculty of Medicine, Zagazig University.
Results
A statistically significant difference was detected between the two studied groups with respect to serum IgE and serum zonulin levels (p ˂ 0.001 and ˂ 0.001, respectively). The mean serum zonulin was equal to 258.3 ± 153.01 ng/ml in the asthmatic group and 80 ± 13 ng/ml in the control group. Serum zonulin level significantly increased with the increase of asthma severity (p ˂ 0.001). The cut off value of serum zonulin was ≥ 198 ng/ml, and the area under the curve was 0.76. It displayed sensitivity equal to 80% and specificity equal to 71.4%. Its negative predictive value was equal to 83.3%.
Conclusion
Intestinal barrier dysfunction contributes to the pathogenesis of allergic asthma. Serum zonulin level reflects an increase in intestinal permeability. Zonulin acts as prognostic factor of severity in asthma. Correction of the gut barrier defect may have a potential positive prognostic effect in asthma.
Trichinosis is a parasitic disease, caused by a nematode worm of the genus Trichinella. Infection is caused by ingestion of undercooked contaminated meat with infective parasitic larvae. The study assessed the muscle apoptotic and vascular changes in T. spiralis infected mice after intra-muscular artemether injection. This study included 80 clean laboratory-bred Swiss albino mice orally infected with 200 T. spiralis larvae/mouse. Four groups of mice (20 mice each), GI: non-infected (control normal); GII: infected untreated (control infected); GIII: infected then treated with artemether injection 1.25mg/kg 45days post-infection (dpi) and GIV: infected then treated with artemether injection 25mg/kg 45dpi. On the 60 th dpi, mice were sacrificed. All groups were evaluated parasitologically by assessing the number of intestinal worms and muscular encysted larvae, histopathological assessment of intestinal and muscle changes and immune-histochemical assessment of BAX marker for apoptotic changes and CD34 marker for vascular changes.
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