Increased systemic and local interleukin 9 levels in patients with carotid and coronary atherosclerosis.

ABSTRACT:

Objective

Atherosclerosis is a chronic inflammatory disorder that involves a range of inflammatory mediators. Although interleukin (IL)-9 has been related to inflammation, there are at present no data on its role in atherosclerosis. Here we have examined IL-9 and IL-9 receptor (IL-9R) systemically and locally in patients with coronary and carotid atherosclerosis.

Methods

Plasma IL-9 was quantified by enzyme immunoassay and multiplex technology. IL-9 and IL-9R mRNA were quantified by real-time RT-PCR, and their localization within the lesion was assessed by immunohistochemistry.

Results

THE MAIN FINDINGS WERE: (i) Patients with carotid atherosclerosis had significantly raised IL-9 plasma levels compared with healthy controls (n?=?28), with no differences between asymptomatic (n?=?56) and symptomatic (n?=?88) patients. (ii) On admission, patients with acute ST-elevation myocardial infarction (STEMI) (n?=?42) had markedly raised IL-9 plasma levels which gradually declined during the first week post-MI. (iii) T cells and monocytes from patients with unstable angina (n?=?17) had increased mRNA levels of IL-9 as compared with controls (n?=?11). (iv) Carotid plaques (n?=?68) showed increased mRNA levels of IL-9 and IL-9R compared to non-atherosclerotic vessels (n?=?10). Co-localization to T cells (IL-9 and IL-9R) and macrophages (IL-9) were shown by immunohistochemistry. (v) IL-9 increased IL-17 release in peripheral blood mononuclear cells from patients with unstable angina (n?=?5) and healthy controls (n?=?5) with a particularly enhancing effect in cells from the patient group.

Conclusion

Our findings show increased IL-9 levels in different atherosclerotic disorders both systemically and within the lesion, suggesting a role for the IL-9/IL-9R axis in the atherosclerotic process, potentially involving IL-17 mediated mechanisms. However, the functional consequences of these findings should be further investigated.

SUBMITTER: Gregersen I 

PROVIDER: S-EPMC3758349 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature