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Harmonizing to Tantisira & A ; Weiss ( 2006 ) , an estimated 300 million persons worldwide are affected with asthma ( Tantisira & A ; Weiss, 2006 ) . Asthma is a clinical disease characterized by the redness, reversible air passages obstructor, and bronchial hyperresponsiveness ( Tantisira & A ; Weiss, 2006 ) , Umetsu & A ; Dekruyff ( 2006 ) , added that asthma was an immunological disease and that it has increased dramatically in it prevalence over the past two decennaries. They continued by stating that this statistics is common in the United States and other Westernized states. With one in five to ten persons affected, they concluded that asthma has reached an epidemic proportion, and that current health care outgos for asthma in industrialized are tremendous ( Umetsu & A ; Dekruyff, 2006 ) . Harmonizing to Umetsu & A ; Dekruyff ( 2006 ) , asthma and allergic reaction are inflammatory diseases, caused by the dysregulated immune responses in the respiratory mucous membrane, Umetsu & A ; Dekruyff ( 2006 ) besides suggested that asthma originates from fanatic T-helper 2 ( th2 ) -driven responses result in the development of asthma. Umetsu & A ; Dekruyff ( 2006 ) posited that it was CD+4 T cells bring forthing th2 cytokines that plays a outstanding function in the lungs of asthma sick persons, due to interleukin-4 ( IL-4 ) and IL-13 enhance Ig E ( IgE ) production, while IL-4, IL-9, and IL-10, heightening mast growing cell, so as IL-5 enhances eosinophil accretion, they concluded that both IL-9 and IL-13 straight were precursors for mucous secretion hypersecretion and airway hyperactivity ( AHR ) ( Umetsu & A ; Dekruyff, 2006 ) . Allergen tolerance is the system that confers the preventative belongings of these responses, but the existent immunological events that brings about the tolerance in these scenes are non to the full understood ( Umetsu & A ; Dekruyff, 2006 ) . Certain factors disposes one to hold an asthma onslaught. Because asthma is a complex disease, there is no individual cistron responsible for it. Alternatively, it is likely consequences from the influence of multiple familial, environmental, and developmental factors ( Tantisira & A ; Weiss, 2006 ) .

Hygiene Hypothesis

Harmonizing to Han et Al ( 2008 ) , the hygiene hypothesis suggests that infections of microbic beginning or microbic substance may modify host ‘s immune system, therefore modulating the patterned advance of allergic diseases ( Han et al. , 2008 ) . They demonstrated that certain intracellular bacterial infection or bacterial merchandises are capable of suppressing airway eosinophilic redness, mucous secretion overrun, allergen -specific IgE production, airway hyperresponsiveness, and airway reconstructing ( Han et al. , 2008 ) . This hypothesis was earlier demonstrated Tantisira & A ; Weiss, 2006 ; Umetsu & A ; Dekruyff 2006 ) . Han et Al ( 2008 ) concluded that the alteration of cytokine design and initiation of immunosuppressive or regulative T Cell look to be of import precursor for infection-mediated suppression of allergic reaction ( Han et al. , 2008 ) . This mechanism of protection is besides supported by Umetsu & A ; Dekruyff ( 2006 ) that because Th1 cells crossregulate Th2 cells in certain systems, allergen-specific Th1 cells is thought to be responsible for the ordinance of allergic diseases and asthma ( Umetsu & A ; Dekruyff, 2006 ) . Harmonizing to these writers, T-helper 1 cells inhibit the patterned advance and production of Th2 cells, and IgE proliferation is complimentarily modulated by IL-4 and interferon-I? ( IFN-I? ) , deducing that unsusceptibility from allergic reaction was due to the development of repressive allergen-specific Th1 cell ( Umetsu & A ; Dekruyff, 2006 ) .

Recent Research on Hygiene Hypothesis and Asthma

Han et Al ( 2008 ) , carried out a survey to find that NK Cells was responsible for intracellular bacterial infection-mediated suppression of Allergic responses. Experimentally the writers researched on the consequence of chlamydial infection on the development of allergic responses induced by egg white and the activities of NK cells in this procedure utilizing a mouse theoretical account of airway redness. Their consequences of findings was that anterior Chlamydial exposure can hinder airway eosinophilic redness and mucous secretion production induced by allergen sensitisation and challenge ( Han et al. , 2008 ) . In this research lab survey, Han et Al ( 2008 ) demonstrated that the suppression was synonymous with an change of allergen-driven cytokine- bring forthing forms of T cells, deducing that NK cells were activated following chlamydial infection, demoing both cell enlargement and secernment ( Han et al.,2008 ) . While carry oning this survey, they observed that transferred NK cells that were isolated from septic mice showed a important repressive consequence on allergic responses, compared to their observation in natural infection. Their survey concluded that the innate immune cells such as NK cells may play an of import function in infection- mediated suppression of allergic responses ( Han et al. , 2008 ) . One restriction of this survey is that when these research workers tried to clear up the mechanisms by which NK cells from septic mice inhibit allergy response, they observed that transportation of infection activated NK cells after sensitisation, but before challenge could non militate against airway allergic responses. This is consistent with a survey done by Broide et Al ( 2001 ) who demonstrated that the lessening of NK cells during the allergen challenge phase, had no consequence in the ability of immunostimulatory DNA sequences to suppress allergic eosinophilic redness and airway hyperreactivity ( Broide et al. , 2001 ) .

Heaton et Al ( 2003 ) , conducted another survey on the occurence of Staphylococcus aureus ( S. aureus ) colonisation on the tegument of patients with atopic eczema/dermatitis syndrome ( AEDS ) and the function of staphylococcal enterotoxin B ( SEB ) in atopic disease. Their purpose was to clarify the regulative effects of Sag SEB on production of cytokines in peripheral blood mononuclear cells ( PBMC ) from patients with AEDS. The method used for this survey was the isolation of PBMC from normal nonatopic grownups, who were symptomless atopic persons, and patients with active allergic asthma. Cells used for this survey was cultured for 24 or 96hrs with house dust touch ( HDM ) , SEB and phytohaemaglutitinin were assayed for cytokine degrees. Their consequences indicated that SEB meagerly stimulates the production of interleukin ( IL ) -5 in AEDS sick persons but non in symptomless atopic persons. These research workers every bit observed comparative exposure to the IL-5- stimulatory belongingss of SEB in allergic asthmatics ( Heaton et al. , 2003 ) . The consequences of this survey correlates with earlier findings by Umetsu et Al ( 2006 ) that IL-5 enhances eosinophilic accretion.

In drumhead the above survey demonstrated that IL-5-driven eosinophilia plays a function in the patterned advance of mild immediate allergy to severe disease therefore supplying a plausible theoretical account for AEDS- effects of Staphs antigens. Their findings is implicative that SEB could hold similar maps in atopic respiratory disease. One restriction in this survey is the restrictive form of the simulatory effects of SEB on IL-5, which is different for what is gettable on IL-4 and IFN-I? production nowadays merely in individuals with current atopic disease ( Heaton et al. , 2003 ) .

Application of These Findingss to Public Health

About 300 million people throughout the whole universe are plagued with asthma, this has well resulted in high morbidity, mortality, and healthcare bringing ( Tantisira & A ; Weiss, 2006 ) . The two surveies presented above has demonstrated that micro-organism ( S.aureus and Chlamydia ) in the context of this research plays a important function in triping responses against asthma and allergic diseases. Again, these surveies are in line with the hygiene hypothesis theory which proposes that there is a lessening of/ or altered exposure of micro-organisms in the environment which may be as a direct consequence of improved sanitation, hygiene, childhood immunisation in a manner confers unsusceptibility on the person against asthma and allergic diseases ( Umetsu & A ; Dekruyff, 2006 ) . In the survey of Heaton et Al ( 2003 ) , it may be a possibility that topical agent made from Bacterial SAg can be developed by scientist, because it has been found in this survey to exercise some authority in carnal theoretical accounts and adult male when applied to the tegument for the initiation of inflammatory reaction ( Heaton et al. , 2003 ) . I think that the cognition of this theory which has shown the patterned advance of Th2 to Th1 cytokines at early phase in life can ensue in allergic responses. It therefore implies that unsusceptibility during childhood is conferred by Th2, which will be complimented by Ig E and subsequent hyperresponsiveness of the respiratory piece of land ( Umetsu & A ; Dekruyff, 2006 ) .

I will strongly urge that research scientist and public wellness continue to experiment to research the possibility of developing a vaccinum, which could in bend be utile in the stimulation of allergen-specific Th 1. Knowledge of hygiene hypothesis can be used in the readying of homogenous allergen and recolte allergen proteins, could broaden the safety and specificity of immunotherapy and later the diagnosing of specified allergic reactions ( Umetsu & A ; Dekruyff, 2006 ) .

In decision therefore, attention should be taken when these processs are effected in worlds as we are non about certain what will go of allergen-specific Th1 if long period of exposure may do chronic redness of the respiratory piece of lands. More research is needed here. Research has shown that hygiene hypothesis has been studied for over 10 old ages now, evenso, the mechanisms with which infections regulate allergic reactions are still obscure. ( Han et al. , 2008 ) .

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