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According to Tantisira & Weiss(2006), an estimated 300 million individuals worldwide are affected with asthma (Tantisira &Weiss, 2006). Asthma is a clinical disease characterized by the inflammation, reversible airways obstruction, and bronchial hyperresponsiveness (Tantisira & Weiss, 2006), Umetsu & Dekruyff(2006) , added that asthma was an immunological disease and that it has increased dramatically in it prevalence over the past two decades. They continued by saying that this statistics is common in the United States and other Westernized nations. With one in five to ten individuals affected, they concluded that asthma has reached an epidemic proportion, and that current healthcare expenditures for asthma in industrialized are enormous (Umetsu & Dekruyff, 2006). According to Umetsu &Dekruyff(2006), asthma and allergy are inflammatory diseases, caused by the dysregulated immune responses in the respiratory mucosa, Umetsu& Dekruyff (2006) also suggested that asthma originates from overzealous T-helper 2(th2)-driven responses result in the development of asthma. Umetsu&Dekruyff (2006)posited that it was CD+4 T cells producing th2 cytokines that plays a prominent role in the lungs of asthma sufferers, due to interleukin-4(IL-4) and IL-13 enhance immunoglobulin E(IgE) production, while IL-4,IL-9, and IL-10, enhancing mast growth cell, so as IL-5 enhances eosinophil accumulation, they concluded that both IL-9 and IL-13 directly were precursors for mucus hypersecretion and airway hyperactivity(AHR) (Umetsu & Dekruyff, 2006). Allergen tolerance is the system that confers the preventive property of these responses, but the actual immunological events that brings about the tolerance in these settings are not fully understood (Umetsu & Dekruyff, 2006). Certain factors disposes one to have an asthma attack. Because asthma is a complex disease, there is no single gene responsible for it. Instead, it is likely results from the influence of multiple genetic, environmental, and developmental factors (Tantisira & Weiss, 2006).
According to Han et al (2008), the hygiene hypothesis suggests that infections of microbial origin or microbial substance may modify host's immune system, hence regulating the progression of allergic diseases (Han et al., 2008). They demonstrated that certain intracellular bacterial infection or bacterial products are capable of inhibiting airway eosinophilic inflammation, mucus overproduction, allergen -specific IgE production, airway hyperresponsiveness, and airway remodeling (Han et al., 2008). This hypothesis was earlier demonstrated Tantisira &Weiss, 2006; Umetsu & Dekruyff 2006). Han et al (2008) concluded that the modification of cytokine design and induction of immunosuppressive or regulatory T Cell appear to be important precursor for infection-mediated inhibition of allergy (Han et al ., 2008). This mechanism of protection is also supported by Umetsu & Dekruyff(2006) that because Th1 cells crossregulate Th2 cells in certain systems, allergen-specific Th1 cells is thought to be responsible for the regulation of allergic diseases and asthma(Umetsu &Dekruyff, 2006). According to these authors, T-helper 1 cells inhibit the progression and production of Th2 cells, and IgE proliferation is complimentarily modulated by IL-4 and interferon-Î³ (IFN-Î³), inferring that immunity from allergy was due to the development of inhibitory allergen-specific Th1 cell (Umetsu & Dekruyff, 2006).
Recent Research on Hygiene Hypothesis and Asthma
Han et al (2008), carried out a study to determine that NK Cells was responsible for intracellular bacterial infection-mediated inhibition of Allergic responses. Experimentally the authors researched on the effect of chlamydial infection on the development of allergic responses induced by ovalbumin and the activities of NK cells in this process using a mouse model of airway inflammation. Their results of findings was that prior Chlamydial exposure can impede airway eosinophilic inflammation and mucus production induced by allergen sensitization and challenge (Han et al., 2008). In this laboratory study, Han et al(2008) demonstrated that the inhibition was synonymous with an alteration of allergen-driven cytokine- producing patterns of T cells, inferring that NK cells were activated following chlamydial infection, showing both cell expansion and secretion (Han et al.,2008). While conducting this study, they observed that transferred NK cells that were isolated from infected mice showed a significant inhibitory effect on allergic responses, compared to their observation in natural infection. Their study concluded that the innate immune cells such as NK cells may play an important role in infection- mediated inhibition of allergic responses (Han et al., 2008). One limitation of this study is that when these researchers tried to clarify the mechanisms by which NK cells from infected mice inhibit allergy response, they observed that transfer of infection activated NK cells after sensitization, but before challenge could not militate against airway allergic responses. This is consistent with a study done by Broide et al( 2001) who demonstrated that the decrease of NK cells during the allergen challenge stage, had no effect in the ability of immunostimulatory DNA sequences to inhibit allergic eosinophilic inflammation and airway hyperreactivity (Broide et al., 2001) .
Heaton et al (2003), conducted another study on the occurence of Staphylococcus aureus (S. aureus) colonization on the skin of patients with atopic eczema/dermatitis syndrome (AEDS) and the role of staphylococcal enterotoxin B (SEB) in atopic disease. Their aim was to elucidate the regulatory effects of Sag SEB on production of cytokines in peripheral blood mononuclear cells(PBMC) from patients with AEDS. The method used for this study was the isolation of PBMC from normal nonatopic adults, who were asymptomatic atopic individuals, and patients with active allergic asthma. Cells used for this study was cultured for 24 or 96hrs with house dust mite (HDM), SEB and phytohaemaglutitinin were assayed for cytokine levels. Their results indicated that SEB sparingly stimulates the production of interleukin (IL)-5 in AEDS sufferers but not in asymptomatic atopic individuals. These researchers equally observed relative vulnerability to the IL-5- stimulatory properties of SEB in allergic asthmatics (Heaton et al., 2003). The results of this study correlates with earlier findings by Umetsu et al (2006) that IL-5 enhances eosinophilic accumulation.
In summary the above study demonstrated that IL-5-driven eosinophilia plays a role in the progression of mild atopy to severe disease thus providing a plausible model for AEDS- effects of Staphs antigens. Their findings is suggestive that SEB could have similar functions in atopic respiratory disease. One limitation in this study is the restrictive pattern of the simulatory effects of SEB on IL-5, which is different for what is obtainable on IL-4 and IFN-Î³ production present only in persons with current atopic disease ( Heaton et al., 2003).
Application of These Findings to Public Health
About 300 million people throughout the whole world are plagued with asthma, this has substantially resulted in high morbidity, mortality, and healthcare delivery (Tantisira &Weiss, 2006). The two studies presented above has demonstrated that microorganisms (S.aureus and Chlamydia) in the context of this research plays a significant role in triggering responses against asthma and allergic diseases. Again, these studies are in line with the hygiene hypothesis theory which proposes that there is a decrease of/ or altered exposure of microorganisms in the environment which may be as a direct result of improved sanitation, hygiene, childhood immunization in a way confers immunity on the individual against asthma and allergic diseases( Umetsu & Dekruyff, 2006). In the study 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 study to exert some potency in animal models and man when applied to the skin for the induction of inflammatory reaction( Heaton et al., 2003). I think that the knowledge of this theory which has shown the progression of Th2 to Th1 cytokines at early stage in life can result in allergic responses. It therefore implies that immunity during childhood is conferred by Th2, which will be complimented by immunoglobulin E and subsequent hyperresponsiveness of the respiratory tract( Umetsu &Dekruyff, 2006).
I will strongly recommend that research scientist and public health continue to experiment to explore the possibility of developing a vaccine, which could in turn be useful in the stimulation of allergen-specific Th 1. Knowledge of hygiene hypothesis can be used in the preparation of homogeneous allergen and recolte allergen proteins, could broaden the safety and specificity of immunotherapy and subsequently the diagnosis of specified allergies (Umetsu & Dekruyff, 2006).
In conclusion therefore, care should be taken when these procedures are effected in humans as we are not almost certain what will become of allergen-specific Th1 if long period of exposure may cause chronic inflammation of the respiratory tracts. More research is needed here. Research has shown that hygiene hypothesis has been studied for over ten years now, evenso, the mechanisms with which infections regulate allergy are still vague.(Han et al., 2008).