endothelin-1 and Rhinitis--Allergic--Seasonal

Hay fever is one of the most frequent upper airway diseases. The nasal epithelium is considered to play and active role in the allergic inflammation through its capacity to synthesize and release a wide range of cytokines and mediators. One substance of potential relevance in this regard is endothelin (ET). We postulated that ET-1 could contribute to pathomechanism of seasonal allergic rhinitis. The aim of this study was to demonstrate release of this peptide and bradykinin into the nasal lavage fluid (NLF) of tree pollen allergic patients in response to allergen challenge. 16 subjects aged 25.5 +/- 3.3 years with clinical history of tree pollen allergic rhinitis participated in the study. Nasal allergen provocation with following lavage was performed in all subjects. Ten of them were hyposensitized preseasonally by allergic vaccine Allergovit (Allergopharma, Germany). Six patients received treatment with antihistamines, cromoglicates or steroids. Bradykinin and endothelin-1 in the nasal secretion were assayed before starting immunotherapy and early during tree pollen season. Increase in concentration of bradykinin in nasal lavage fluid from hyposensitized patients were significantly lower than from second group, 509.4 +/- 110.4 before 942.9 +/- 234.89 pg/ml after allergen provocation versus 417.8 +/- 100.4 and 2001.6 +/- 223.6 pg/ml (p < 0.05). We noticed lower concentration of ET-1 in NLF of hay fever patients, 17.5 +/- 3.9 versus 13.9 +/- 2.7 pmol/ml. We conclude that bradykinin and endothelin-1 could be involved in the pathogenesis of hay fever.

Topics: Adult; Biomarkers; Bradykinin; Bronchial Provocation Tests; Endothelin-1; Female; Humans; Male; Nasal Lavage Fluid; Rhinitis, Allergic, Seasonal

The nasal epithelium is considered to play an active role in the allergic inflammation through its capacity to synthesize and release a wide range of cytokines and mediators. Few studies have investigated the involvement of endothelin-1 in the pathogenesis of inflammatory diseases of the upper airways. To examine the release of endothelin-1 from nasal mucosa after allergen challenge we investigated 24 patients. 15 subjects (7 male, 8 female) allergic to birch pollen aged 37.1 +/- 4.9 years participated in the study. Nasal birch allergen provocation with following lavage was performed in all subjects. Endothelin-1 in the nasal secretion were assayed before and after challenge. Increase in concentration of endothelin-1 in nasal lavage fluid from allergic patients were significantly higher than in control group respectively from 18.33 +/- 5.47 fmol/ml to 26.41 +/- 6.92 fmol/ml versus 18.8 +/- 3.99 to 19.80 +/- 4.18 fmol/ml (p < 0.05) in controls. We conclude that endothelin-1 could be involved in the pathogenesis of seasonal allergic rhinitis.

Topics: Adolescent; Adult; Biomarkers; Case-Control Studies; Endothelin-1; Female; Humans; Male; Nasal Lavage Fluid; Nasal Mucosa; Nasal Provocation Tests; Rhinitis, Allergic, Seasonal

Various peptidases, including angiotensin-converting enzyme (ACE), inactivate some inflammatory peptides that are considered to influence the pathogenesis of atopic diseases. This enzyme is also involved in the conversion or activation of 2 bronchoconstriction mediators: angiotensin II from angiotensinogen and endothelin (ET), respectively.. We tested a hypothesis that asthma or other atopic diseases are associated with insertion/deletion ACE, M235T angiotensinogen, and TaqI ET-1 gene polymorphisms.. A case-control approach was used in the study. Healthy subjects (141 persons) were used as control subjects, and 231 patients with histories of atopic asthma, allergic rhinitis, atopic dermatitis, or a combination thereof were studied. ACE genotype was determined by PCR, angiotensinogen M235T and ET-1 by PCR, and restriction analysis by AspI and TaqI, respectively.. We found the significant association of the insertion/deletion polymorphism of the ACE, as well as that of M235T polymorphism of the angiotensinogen genes, with the group of patients with atopic diseases ( P =.0025 and P =.0204, respectively). No difference was proved for the intron 4 (position 8000) polymorphism in the ET-1 gene when comparing the atopic patients with the control group (P =.1774). A significant difference was found between groups of patients with both asthma and rhinitis and patients without both respiratory atopic diseases (P =.0033).. It follows that the examined polymorphisms in the genes for ACE, angiotensinogen, and ET-1 could participate in the etiopathogenesis of atopic diseases.

Topics: Adolescent; Adult; Alleles; Angiotensinogen; Asthma; Case-Control Studies; Dermatitis, Atopic; Endothelin-1; Female; Gene Frequency; Genotype; Humans; Hypersensitivity, Immediate; Male; Middle Aged; Mutation, Missense; Peptidyl-Dipeptidase A; Point Mutation; Polymerase Chain Reaction; Polymorphism, Genetic; Restriction Mapping; Rhinitis, Allergic, Seasonal