Possible role of plasminogen activator inhibitor-1 in bronchial asthma

Asthma represents a chronic inflammatory process of the airways. The plasminogen activator inhibitor-1 gene [PAI-1] has an essential role in promoting fibrosis after inflammation. The tissue-type plasminogen activator [t-PA] and urokinasc type plasminogen activator [u-PA] convert plasminogen to plasmin, which enhance proteolytic degradation of the extracellular matrix [ECM]. Among the inhibitors of plasminogen activators, PAI-1 is the most important in the process of lung fibrosis. The main role in the inhibition of fibrinolysis through the blockade of activators is ascribed to PAI-1. It is synthesized in endothelium, megakaryocytes, smooth muscle cells of vessels, and in the liver, with the help of cytokines, growth factors, cyclic nucleotides. hormones including glycocorticosteriods and bacterial endotoxins. The study is designed to investigate the correlation between plasma PAI-1 and bronchial asthma severity and whether steroid medications could affect its levels. The study included 40 children with bronchial asthma and 20 healthy children as control subjects. Estimation of plasma PAI-1 carried out for them using ELISA technique. There was a significant lowering of PAI-1 in all asthmatic groups in comparison to control group. The moderate asthmatic subgroups showed highly significant difference in comparison to mild asthmatic and to control group. The mild subgroups showed also significant difference to control group but with lesser mean value compared to moderate subgroups. The results suggest that PAI-1 may play an important role in the pathogenesis of bronchial asthma

Serum ICAM-1 in asthmatic children

The recruitment of leukocytes to inflamed tissues depends on the function of adhesive molecules of the leukocytes and of vascular endothelium. Intercellular adhesion molecules-1 [ICAM-1, CD.54] is a number of the immunoglobulin super-family of adhesion proteins. It is expressed by a number of blood cells and by endothclial, fibroblastic, and epithelial cells. The expression of ICAM-1 is upregulated by a number of cytokines that are released at sites of inflammation. It is probable that ICAM-1 participates in the recruitment of eosmophils to asthmatic airways and contributes to the pathogenesis of asthma. Serum ICAM-1 contains most of the structure of the extracellular portion of membrane-bound ICAM-1 could potentially have physiologic function, perhaps as a modifier of lymphocyte function-associated antigen-1 [LFA-1] dependent leukocyte adhesion. The principle objective of this work is to assess serum soluble intercellular adhesion molecules-1 [slCAM-1] level in asthmatic children during acute asthma exacerbation of their symptoms. We will pay attention to the effect of corticosteroid therapy on serum ICAM-1 level when administered for a short period of time during the acute episode. The study included 30 wheezy children with age from [6 months to 12 year] and 10 normal controls with the same age range. All children and controls undergo good history taking and thorough clinical examination, plain chest X-ray and laboratory investigations including; serum IgE, CBC with differential, serum ICAM-1 determination. Bacterial infection is excluded by clinical examination, leukocytic count, and chest X-ray. Our results showed that serum soluble intercellular adhesion molecules-1 [sICAM-1] level is significantly higher during acute asthma exacerbation in comparison to its level in serum of healthy controls. Also the level of serum soluble adhesion molecules-1 [slCAM-1] is reduced significantly 10 days following the acute episode after a short period of oral corticosteroid therapy

Diagnostic accuracy of sepsis score, CRP, G-CSF and blood culture in Egyptian neonates with suspected bacterial infection

To elucidate the diagnostic accuracy of granulocyte colony stimulating factor [G-CSF] in identifying sepsis among neonates with suspected bacterial infection, in comparison with clinical sepsis score, blood culture and C-reactive protein. It is a case control study. 83 neonates were recruited from tertiary level neonatal intensive care unit over five months period. They are subdivided into 2 groups. 42 cases [29 were septic with positive blood culture + 13 were probably septic with negative blood culture] and 41 healthy controls. Sepsis score, CRP using Chemiluminescent Technique, G-CSF using [ELISA] and Blood culture were determined. Plasma G-CSF was markedly elevated in cases with blood culture positive [310 +/- 734 pg/ml] and in cases with blood culture negative [280 +/- 736 pg/ml] but not in controls [20 +/- 13 pg/ml]. There is statistical significant difference [p=<0.05] of G-CSF level between all cases and controls. There is also highly statistical significant difference [p=<0.01] between cases and controls regarding sepsis score. There is highly statistical significant difference [p=<0.01] between number of positives versus negatives regarding the 4 parameters between cases and controls. The cut off point of G-CSF was 37 pg/ml for discrimination between the presence or absence of infection. The area under the receiver operating characteristic curve was 0.847 with sensitivity of 50% and specificity of 90%.Although G-CSF determination is not superior over other parameters to role in or out infection in neonates, but combining G-CSF and sepsis score increases the sensitivity to 79%, whereas, sepsis score has the highest specificity [100%].Measuring plasma G-CSF is helpful for diagnosis of bacterial sepsis in hetcrogcnous ill newborn. A combined measure of G-CSF and clinical sepsis score, improve the diagnostic accuracy over any single parameter