AI Article Synopsis
- Leukotriene signaling is crucial in various diseases, such as asthma and inflammatory bowel disease, but its role in nasal polyps (NPs) and chronic rhinosinusitis is not well understood.
- The study found that cysteinyl leukotrienes (CysLTs) and their receptors (CYSLTRs) were significantly elevated in patients with chronic rhinosinusitis with nasal polyps (CRSwNP), particularly in a subgroup associated with higher IL-5 levels.
- Montelukast, a leukotriene receptor antagonist, effectively reduced the expression of certain inflammatory markers and improved patient outcomes when added to standard treatment for those with refractory CRSwNP.
Article Abstract
Leukotriene signaling is essential in many diseases, including asthma, allergic rhinitis, atherosclerosis and inflammatory bowel disease. Nevertheless, the expression of cysteinyl leukotrienes (CysLTs) and its receptors (CYSLTRs) in different types of nasal polyps (NPs), and the role of their antagonist in the treatment of refractory chronic rhinosinusitis with nasal polyps (CRSwNP) are not well understood. The following study investigates the expression of CysLTs and CYSLTRs in different types of NPs, as well as the role of leukotriene receptor antagonist (montelukast) in refractory NPs. Our data showed that CysLTs and CYSLTRs were significantly elevated in CRSwNP group (p < 0.05), particularly in IL-5NP patients compared to patients with chronic rhinosinusitis but without NPs (CRSsNP) and the control group. Furthermore, montelukast have shown the ability to inhibit the expression of MUC5AC, TSLP, IL-4, IL-5, IL-13, and TGF-β in NP explants after treatment with Staphylococcal Enterotoxins B (SEB). In addition, the patients treated by additional montelukast have better outcomes compared to those with INCS only. To conclude, our results demonstrate that the inhibition of CysLTs signaling by montelukast decreases the expression of cytokines and mucin in polyp explants, and in turn promotes the recovery in patients with refractory CRSwNP.
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| http://dx.doi.org/10.1016/j.plefa.2017.09.009 | DOI Listing |
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