Abstract
Asthma is a chronic inflammatory disease affecting 5% of the world population. FKBP51 is an important immunophilin modular protein of the glucocorticoid receptor (GC).
 The aim of the present study was to evaluate the levels and immunocytochemical distribution of FKBP51 and GR in lymphocyte cells of asthmatic patients, by use of immunocytochemistry method, and to assesslevels ofstress hormones (cortisol and ACTH) by radioimmuniassay (RIA).
 The results showed significantly increased nuclear localization and decreasedcytoplasmic distribution of FKBP51, while they showed a significant increase in nuclear localization and a non-significant decrease in cytoplasmic distribution of GRin asthmatic patients(P<0.05).
 Cortisol and ACTH levels were also measured and showedinsignificant increases(P<0.05)in steroid treated (338.85 ±139.5 mMol/L, 35.05±3.77 ng/ml, respectively)and non steroid treated asthmatics(280.5 ± 74.6 mMol/L, 32.0±6.43 ng/ml, respectively)as compared with the control group (234.33±29.13 mMol/L, 29.0±7.02 ng/ml, respectively).
Highlights
Asthma could be defined as a chronic airway inflammation which is often associated with eosinophilic, TH2-mediated immunopathology
The results showed significantly increased nuclear localization and decreasedcytoplasmic distribution of FKBP51, while they showed a significant increase in nuclear localization and a non-significant decrease in cytoplasmic distribution of GRin asthmatic patients(P
Glucocorticoid effects depend on the binding of the hormone to the Glucocorticoid receptor (GR) in the cytoplasm and their translocation to the nucleus where they interact with glucocorticoid responsive elements (GRE) of different genes and inhibit the transcription of pro-inflammatory genes
Summary
Asthma could be defined as a chronic airway inflammation which is often associated with eosinophilic, TH2-mediated immunopathology. High levels of FKBP51 correlate with resistance to GC therapies for asthma[3] and chronic obstructive pulmonary disease, while diagnostic assays are being developed using FKBP51 as a marker of GC sensitivity[4] Adrenocorticotropic hormone (ACTH), or corticotropin, is a 39 amino acid peptide hormone produced by cells of the anterior pituitary gland and carried by the peripheral circulation to its effector organ (the adrenal cortex) where it stimulates the synthesis and secretion of glucocorticoids, mineralocorticoids and adrenal androgens [5]. Patients were recruited from the out-patient clinic at the Department of Respiratory Diseases, AL –Imamain Al-Kadhumain Teaching Hospital in Baghdad They were prescribed with a maintenance inhaled corticosteroid treatment and remained uncontrolled with an Asthma Control Test (ACT)
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