Chronic allergic airway disease (AAD) is a group of the diseases characterized by airway inflammation and airway hyperresponsiveness (AHR).
Airway inflammation is the hallmark of chronic obstructive pulmonary disease (COPD) associated with low-grade inflammation caused by the persistent production of proinflammatory cytokines by the immune system in the airway.
On the other hand, airway hyperresponsiveness (AHR) is a cardinal feature of asthma associated with the response of the immune system against pathogens.
The most common symptoms of coughing, wheezing, and shortness of breath in reactive airway disease (AAD) may not be due to asthma or other chronic airway conditions.
Conventionally, reactive airway inflammatory disease is treated with medication to control symptoms such as long-term use of an inhaler to relieve attacks and improve quality of life through avoidance of irritants.
If the cause of reactive airway disease is found, most cases of the condition may be cured by medication.
Dr. Jill R. Johnson, the lead scientist in the examination of Allergic Airway Disease: More than Meets the IgE? wrote, "After exposure, allergens crosslink with IgE on mast cells and induce histamine and leukotriene release (6), thereby initiating the allergic response and leading to the classic symptoms of allergy, i.e., sneezing and wheezing".
And, ". Omalizumab binds to the Ce3 domain of free IgE with high affinity (7), thereby inhibiting early- and late-phase asthmatic reactions (8) and decreasing the frequency of exacerbations in severe asthmatics (9). Omalizumab binding also prevents IgE from interacting with Fc«RI and Fc«RII1 on effector cells (mast cells, B cells, eosinophils, dendritic cells, and monocytes), thus impairing their activation and making them less sensitive to allergens, and disabling signaling cascades (10), with the end result of a reduction in symptoms".
In other words, allergic airway disease (AAD) is a result of an immune response upon exposure to the allergens, Therefore, by making the immune system less sensitive to allergens, symptoms of allergic airway disease (AAD) may be reduced.
Bromelain, a proteolytic enzyme found in pineapples (Ananas comosus) has been used in traditional medicine as an inflammatory agent and to treat pains, strains, muscle aches and pains and ease back pain and chronic joint pain, skin diseases, etc.
With an aim to discover a potential compound for the treatment of diseases associated with chronic inflammation, researchers examined the ability of bromelain to reduce the inflammation of preexisting asthma via ovalbumin (OVA)-induced murine model of allergic airway disease (AAD).
The study included female C57BL/6J mice with intraperitoneal OVA/alum and then challenged them with OVA aerosolization for 10 consecutive days.
On day 4, phosphate-buffered saline (PBS) was administrated to the control group (n = 10) and bromelain (6mg/kg) in PBS was administrated to the bromelain (intervention) group (n = 10).
According to the tested assays, bromelain treatment of AAD mice (bromelain group) showed a significant anti-inflammatory activity indicated by reduced BAL total leukocytes, eosinophils, and cellular infiltrates via lung pathology compared to the control group.
Furthermore, bromelain also significantly reduced bronchoalveolar lavage (BAL) CD4+ associated and CD8+ T cells d with the T helper 2 (TH2) cells in the promotion of allergic inflammation process without affecting cell numbers in the spleen or hilar lymph node.
The efficacy of bromelain in the inhibition was attributed to the decreased interleukins involved in the production of pro-inflammatory cytokines.
In other words, bromelain protects asthma patients against allergic airway inflammation through its strong anti-inflammatory properties.
Based on the results, researchers said, "bromelain has a therapeutic effect in established AAD, which may translate into an effective adjunctive therapy in patients with similar conditions, such as allergic asthma, who have chosen to initiate treatment after the onset of symptoms".
In order to find more information about bromelain anti-ADD activity, researchers investigated the effect of bromelain treatment in an ovalbumin (OVA)-induced murine model of allergic airway disease (AAD).
Selected mice were sensitized with intraperitoneal (i.p.) OVA/alum and challenged with daily OVA aerosols to induce ADD followed by the treatment of either saline, 2 or 6 mg/kg bromelain, twice daily for four consecutive days.
According to the findings, bromelain showed a similar effect as the aforementioned results in reduced total BAL leukocytes, eosinophils, CD4+, and CD8+ T lymphocytes, CD4+/CD8+ T cell ratio, and IL-13.
Taken altogether, bromelain may be considered a supplement for the prevention and treatment of allergic airway disease ADD, pending the confirmation of the larger sample size and multicenter human study.
Intake of bromelain in the form of supplements should be taken with extreme care to prevent overdose acute liver toxicity.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All rights reserved)
Health article writer and researcher; Over 10,000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, Best Before it's news, the karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for Shorty Award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Bromelain limits airway inflammation in an ovalbumin-induced murine model of established asthma by Secor ER Jr1, Shah SJ, Guernsey LA, Schramm CM, Thrall RS. (PubMed)
(2) Bromelain exerts anti-inflammatory effects in an ovalbumin-induced murine model of allergic airway disease by Secor ER Jr1, Carson WF 4th, Cloutier MM, Guernsey LA, Schramm CM, Wu CA, Thrall RS. (PubMed)
(3) Allergic Airway Disease: More than Meets the IgE? by Jill R. Johnson, Ph.D. and James A. Harker, Ph.D
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