According to Tantisira Weiss, 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 proportions, 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). "Tolerance to allergens is a mechanism that normally prevents such responses, but the specific immunological events that mediates tolerance in this settings are poorly 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).
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According to Han et al(2008), "the hygiene hypothesis proposes that microbial infection or microbial products may alter host's immune system, thus modulating the development 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 alteration of cytokine patterns and induction of immune suppressive or regulatory T lymphocytes appear to be important mechanisms 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 some systems, allergen -specific Th1 cells have been assumed to regulate allergic disease and asthma(Umetsu &Dekruyff, 2006). According to these authors, T-helper 1 cells inhibit the development and proliferation of Th2 cells, and IgE production is complimentarily regulated by IL-4 and interferon-Î³ (IFN-Î³), inferring that protection from allergy is due to the development of inhibitory allergen-specific Th1 cell (Umetsu & Dekruyff, 2006).
Recent Research on Hygiene Hypothesis and Asthma
Han et al (2006) carried out a study to determine that NK Cells contribute to intracellular bacterial infection-mediated inhibition of Allergic responses. To experimentally examine the hygiene hypothesis, the author studied the effect of chlamydial infection on the development of allergic responses induced by ovalbumin (OVA) and the involvement of NK cells in this process using a mouse model of airway inflammation. The result of their findings was that prior Chlamydial infection can inhibit airway eosinophilic inflammation and mucus production induced by allergen sensitization and challenge. In this laboratory study, Han et al(2008) demonstrated that the inhibition was correlated 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, the adoptive transfer of NK cells that were isolated from infected mice showed a significant inhibitory effect on allergic responses, similar to that they observed 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 elucidated 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 inhibit airway allergic responses. This is consistent with a study done by Broide et al( 2001) who demonstrated that the depletion of NK cells during the allergen challenge stage did not affect the ability of immunostimulatory DNA sequences to inhibit allergic eosinophilic inflammation and airway hyperreactivity (Broide et al., 2001) .
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Heaton et al (2003), conducted another on the incidence of Staphylococcus aureus (S. aureus) colonization on the skin of patients with atopic eczema/dermatitis syndrome (AEDS) to elucidate the role of staphylococcal enterotoxin B (SEB) in atopic disease.The researchers 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 that PBMC were isolated from normal nonatopic adults, 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 selectively stimulates the production of interleukin (IL)-5 in AEDS sufferers but not in asymptomatic atopics. These researchers equally observed relative susceptibility to the IL-5- stimulatory effects 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 theprogression 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
Owing to the need to bring up the significance of the public health problem again (incidence, prevalence, morbidity, mortality, that sort of thing). Then, bring up the findings from the above studies and discuss how the information we gain from studies like this are used to increase knowledge, promote evidence based policy and practice, educate, reduce the impact of this problem, etc. Be sure to cite the studies as you bring them up. Try to avoid focusing only on pure clinical treatment, which is medicine rather than public health. But, you can talk about how this sort of research helps us to devise better treatments, prevention, screening, education, etc. End with some recommendation, perhaps something that would help fill the gap of what we don't know, or something that could be improved upon.
A page break follows, for your reference page. Use APA format and hanging indent style. Review your manual for the details, especially for more than two authors. Check to make sure your paper is about five pages long without the title and references. Do not resort to squashed margins to try to make your paper longer and try not to go more than one or two pages over the limit if you are very "into" the topic. Give the appropriate scholarly depth, but be concise and focused. The research section should be the longest, and if you follow the instructions to discuss at least three research studies in some depth, plus the introduction material, and the application of the findings, you should not have trouble getting five pages and the minimum number of primary sources. Proof read for spelling, grammar, punctuation, capitalization and other errors before submitting. Check to make sure you have not copied passages of material, even if you cited it, because copy and paste of source material leads to plagiarism if you have not also provided quotes to show that the words were not yours. Check for excessive quoting, which does not show your understanding, and replace it with proper paraphrasing and original writing. Check to make sure all facts are cited, and all citations appear in the reference list. Do not use figures unless you have permission from the source (generally, figures are discouraged for this paper-it is your writing that I want to see). If you don't have at least three recent research studies in your reference list, plus other scholarly supporting sources, do not expect to get full credit.