Abstract
Lunasin is a naturally occurring peptide isolated from soybeans and has been explored in cancer treatment. Lunasin inhibits NF-κB activation and thus pro-inflammatory cytokine and mediator production in macrophages. In this study we demonstrate that lunasin can effectively suppress allergic airway inflammation in two murine models of asthma. In an OVA+Alum sensitization model, intranasal lunasin treatment at the time of OVA challenges significantly reduced total cells counts in bronchoalveolar lavage (BAL) fluid and eosinophilia, peribronchiolar inflammatory infiltration, goblet cell metaplasia and airway IL-4 production. In an OVA+LPS intranasal sensitization model, lunasin treatment either at the time of sensitization or challenge has similar effects in suppress allergic airway inflammation including significantly reduced total cell and eosinophil counts in BAL fluid, inflammatory gene Fizz1 expression in the lung, and IL-4 production by OVA re-stimulated cells from mediastinal lymph nodes. We further show that intranasal instillation of OVA+lunasin significantly increases OVA-specific regulatory T cell (Treg) accumulation in the lung comparing to OVA only treatment. Taken together, our results suggest lunasin as an anti-inflammatory agent can be potentially used in asthma therapy or as an adjuvant to enhance the induction of antigen-specific Tregs and thus boost the efficacy of allergy immunotherapy.
Highlights
Prevalence of asthma has increased over the past 2–3 decades affecting 5–10% of the population in many developed countries and is associated with a large socioeconomic burden [1]
To study the effects of lunasin in suppressing allergic airway inflammation, we sensitized BALB/c mice with OVA and Alum followed by intranasal (i.n.) OVA challenge (Fig. 1A). 20 mg lunasin was mixed with 100 mg OVA to intranasally challenge the treatment group of mice while control group was treated OVA or PBS only
Gene found in inflammatory zone 1 (Fizz1) encodes a cysteine-rich secreted protein associated with pulmonary inflammation and is capable of promoting expression of a-SMA and type I collagen at the early stages of airway remodeling in murine model of asthma [23]
Summary
Prevalence of asthma has increased over the past 2–3 decades affecting 5–10% of the population in many developed countries and is associated with a large socioeconomic burden [1]. Majority of asthma is associated with dysregulated T helper type-2 (Th2) immunity leading to chronic eosinophilic inflammation in the airways. Recent studies demonstrated that asthma is PLOS ONE | DOI:10.1371/journal.pone.0115330. Treatments for asthma have been improved substantially in recent years. Current treatments such as antihistamines, leukotriene receptor antagonists and glucocorticoids are effective in temporarily relieve symptoms by suppressing inflammation but do not change the chronic course of disease [3]. These therapies failed to control the symptoms in 5–10% severe persistent asthma patients.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
