Allergic rhinitis (AR) is one of the most common allergic diseases around the world [1]. Typical symptoms of AR include nasal itching, sneezing, rhinorrhea, nasal stuffiness, and/or red, itchy, and watery eyes which last throughout the year in perennial AR [2].
AR is an IgE-mediated allergic inflammation associated with T helper 2 (Th2) cells polarization, which is attributed to a functional defect of T regulatory (Treg) cells. Treg produce IL-10 and transforming growth factor (TGF)-, while Th2 cells produce interleukin (IL)-4, IL-5, and IL-13, which finally activate effector cells of allergic inflammation such as eosinophils and mast cells.
IgE-mediated allergic inflammation is the main pathophysiologic mechanism of allergic rhinitis, and drives the T helper 2 (Th2) cell polarization. Th2 cells produce interleukin (IL)-4, IL-5, and IL-13 and these mediators activate various effectors cells of allergic inflammation such as eosinophils and mast cells.
In contrast, activation of Th2 derived allergic inflammation is attributed to a functional defect of T regulatory (Treg) cells. The production of IL-10 and transforming growth factor (TGF)- produced from Treg was decreased, and subsequently leading to skewing into Th2-inflammation.
Main pharmacologic treatment of AR includes antihistamines, inhaled nasal corticosteroids, and leukotriene receptor antagonists, which are effective to control AR symptoms and allergic inflammation.
Main pharmacologic treatment of AR includes intranasal corticosteroids (INS), antihistamines and leukotrien receptor antagonists. INS is the mainstream of the treatment of AR by effectively reducing the Th2-drived allergic inflammation. Antihistamines relieve the symptoms of allergic rhinitis by blocking the action of histamine released from mast cells. However, pharmacotherapy only reduces the symptoms of AR and do not change the pathologic immunologic profiles of AR. On the other hands, Allergen-sepcific immunotherapy (AIT) can induce the allergen-specific Treg cells and subsequently the production of IL1- and TGF-b. These changes of immune profiles exertd counter-regulatry inhibition of Th2-inflammations. However, AIT has been implicated limitedly in clinical practice. AIT has several disadvantages such as inconvenience and needs to risk of systemic adverse reaction. Though AIT is a potential disease-modifying immune-modulatory treatment option, there are still unmed needs for the treatment of AR. It is necessary to develop new immunomodulatory treatment with overcoming the limitation of pharmacologic treaments and AIT.
Many clinical trials have reported that various probiotics were effective to control symptoms and quality of life in perennial and seasonal AR.(Ref) However, the study protocols of outcome measurements were heterogeneous, where the probiotics improved Rhinitis Quality of Life Questionnaires (RQLQ) in several studies, while they had no effects on Rhinitis Total Symptom Scores (RTSS) or symptom medication scores (SMS) in other studies(Ref). Furthermore, the mechanism of anti-allergic activity for probiotics have been investigated with the peripheral blood mononuclear cells (PBMCs) from the AR patients. Bifidobacterium lactis NCC2818 [22], Lactobacillus gasseri A5 [23], Lactobacillus paracasei ST11 [24], and Lactobacillus rhamnosus GG [25] reduced IL-5, IL-13, and TNF- production from the PBMC of the AR patients, but do not affect serum total IgE, serum allergen-specific IgE, and IL-10 production. In a randomized, open-label, crossover study of Lactobacillus johnsonii EM1 in 7- to 12-year-old children with perennial AR, the combined treatment group of EM1 with levocetirizine significantly increased serum TGF-β levels compared with levocetirizine alone at 12 weeks [26]. We previously reported that NVP-1703, a mixture of Bifidobacterium longum IM55 and Lactobacillus plantarum IM76, mitigated OVA- or house dust mite allergen (HDMA)-induced AR in mice, where NVP-1703 reduced IL-4, IL-5, IL-13, and IgE levels in nasal mucosa, BALF and blood, whereas the level of IL-10 was increased [27,28]. Taken together, probiotics may suppress Th2 response by way of promoting Treg activity.