Elevation of IL-6 in the allergic asthmatic airway is independent of inflammation but associates with loss of central airway function

Abstract

BackgroundAsthma 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 TNFα and IL-1β, rather than as regulatory cytokine.ObjectiveTo 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.MethodsCytokine levels in induced sputum and lung function were measured in 16 healthy control and 18 mild-moderate allergic asthmatic subjects.ResultsThe levels of the proinflammatory biomarkers TNFα and IL-1β 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).ConclusionsIn 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.

Opuntia humifusamodulates morphological changes characteristic of asthma via IL-4 and IL-13 in an asthma murine model

“…Both IL-6 and IL-13 levels are usually elevated in asthma patients and are presumed to be closely correlated [19]; we found that IL-6 levels were similar to IL-13 levels, supporting this idea. IL-13 and IL-6 levels after treatment with 500 mg/kg O. humifusa were notably lower than their levels after dexamethasone treatment.…”

“…Mast cells respond to inflammatory inducers in the early phase and release TNF-α to bring on typical asthma characteristics, such as contracting smooth muscles [14], attracting neutrophils and eosinophils [17], and activating T cells [18]. IL-6 is an important factor that regulates asthma induction via CD4+ cell modulation [19]. …”

Cellular cytotoxic response induced by highly purified multi-wall carbon nanotube in human lung cells

“…IL-6 is linked to allergic responses involving asthma [21], while IL-8 is associated with chronic obstructive pulmonary disease (COPD) [22]. IL-6 stimulates the acutephase reaction, which enhances the innate immune system and protects against tissue damage [23].…”

Let-7a is differentially expressed in bronchial biopsies of patients with severe asthma

“…It was found to be down-regulated in human asthmatic T cells 26 , and in mice elevated pro-inflammatory cytokines IL-6 and IL-1b were found as a result of miR-223 down-regulation upon induction with LPS 35 . In humans, IL-6 levels are known to be elevated in asthma and also correlate with lung function and IL-13 levels 36 . MiRNAs let-7a, miR-21, and miR-223 were shown to either directly or indirectly repress the translation of several crucial factors with well-defined roles in asthma pathogenesis, such as signal transducer and activator of transcription 3 (STAT3), interleukins (IL-6, IL-1b, IL-13), interferon gamma (IFN-c), transforming growth factor, beta receptor (TGF-b receptor), toll-like receptor 4 (TLR4), and vascular endothelial growth factor (VEGF) 3,4,[10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] .…”