Premium
Circulating levels of tumor necrosis factor and interleukin‐1 in cystic fibrosis
Author(s) -
Brown Mark A.,
Morgan Wayne J.,
Finley Paul R.,
Scuderi Philip
Publication year - 1991
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950100209
Subject(s) - medicine , cachexia , pathophysiology , tumor necrosis factor alpha , cystic fibrosis , inflammation , interleukin , interleukin 6 , cytokine , endocrinology , immunology , respiratory disease , lung , cancer
To assess the role of tumor necrosis factor (TNF) and interleukin‐1 (IL‐1) in the pathophysiology of cystic fibrosis (CF)‐associated growth failure/cachexia and lung disease we measured height, weight, triceps skin fold, forced vital capacity, forced expiratory volume in 1 second, and plasma levels of TNF, interleukin‐1‐alpha (IL‐1α), interleukin‐1‐beta (IL‐1β), and alpha‐1‐antitrypsin (A 1 AT) in 12 patients with CF, and in 12 age‐ and gender‐matched healthy controls. The patients as a group had significantly lower values for the anthropomorphic measurements and lung function parameters as compared to controls. They also had higher circulating levels of A 1 AT than controls. TNF, however, was detected less frequently in patients than in controls. Neither group had detectable levels of circulating IL‐1α or IL‐1β, which is consistent with the observation that CF patients infrequently present with fever. Potential explanations for these findings include compartmentalization of secreted TNF/IL‐1, altered regulation of TNF/IL‐1 secretion as a result of the chronic inflammatory state seen in CF, or increased degradation of TNF/IL‐1, also a result of chronic inflammation. The role of these cytokines in the pathophysiology of CF remains unclear, but should be explored further; however it seems unlikely that circulating TNF plays a role in the growth failure/cachexia associated with CF. Pediatr Pulmonol 1991; 10:86–91.