Elevation of IL-6 in the allergic asthmatic airway is independent of inflammation but associates with loss of central airway function.
Respir Res
; 11: 28, 2010 Mar 08.
Article
in En
| MEDLINE
| ID: mdl-20205953
ABSTRACT
BACKGROUND:
Asthma is a chronic inflammatory disease of the airway that is characterized by a Th2-type of immune response with increasing evidence for involvement of Th17 cells. The role of IL-6 in promoting effector T cell subsets suggest that IL-6 may play a functional role in asthma. Classically IL-6 has been viewed as an inflammatory marker, along with TNFalpha and IL-1beta, rather than as regulatory cytokine.OBJECTIVE:
To investigate the potential relationship between IL-6 and other proinflammatory cytokines, Th2/Th17 cytokines and lung function in allergic asthma, and thus evaluate the potential role of IL-6 in this disease.METHODS:
Cytokine levels in induced sputum and lung function were measured in 16 healthy control and 18 mild-moderate allergic asthmatic subjects.RESULTS:
The levels of the proinflammatory biomarkers TNFalpha and IL-1beta were not different between the control and asthmatic group. In contrast, IL-6 levels were specifically elevated in asthmatic subjects compared with healthy controls (p < 0.01). Hierarchical regression analysis in the total study cohort indicates that the relationship between asthma and lung function could be mediated by IL-6. Among Th2 cytokines only IL-13 (p < 0.05) was also elevated in the asthmatic group, and positively correlated with IL-6 levels (rS = 0.53, p < 0.05).CONCLUSIONS:
In mild-moderate asthma, IL-6 dissociates from other proinflammatory biomarkers, but correlates with IL-13 levels. Furthermore, IL-6 may contribute to impaired lung function in allergic asthma.
Full text:
1
Collection:
01-internacional
Health context:
4_TD
Database:
MEDLINE
Main subject:
Pneumonia
/
Respiratory Hypersensitivity
/
Asthma
/
Cytokines
/
Interleukin-6
/
Lung
Type of study:
Risk_factors_studies
Limits:
Adult
/
Female
/
Humans
/
Male
Language:
En
Journal:
Respir Res
Year:
2010
Document type:
Article