According to Tantisira &Weiss(2006), an estimated 300 million individuals are affected with asthma(Tantisira & Weiss, 2006). Asthma is a clinical disease characterized by the inflammation, reversible airway obstruction, and bronchial hyper responsiveness(Tantisira &Weiss, 2006), the intermittent contraction of these bronchial muscles is as a result of abundant production of immunoglobulin E antibodies in the body of the sufferer (Johnson, 2010). Umetsu &Dekruyff(2006) added that asthma was an immunological disease and that it has increased dramatically in its prevalence over the past two decades. They stated that the statistics is common in the United States and other Westernized nations. With one in five to ten individuals affected, they posited that asthma has reach an epidemic proportion, and that current healthcare expenditures for asthma in industrialized nations is huge (Umetsu&Dekruyff, 2006).
Umetsu & Dekruyff (2006) stated that asthma and allergy are inflammatory diseases caused by the dysregulated immune responses in the respiratory mucosa, thie is suggestive that asthma originates from overzealous T-helper 2(Th2)- driven responses giving rise to asthma development(Umetsu &Dekruyff, 2006). In accordance with their findings, they showed that it was CD+4 Tcells producing Th2 cytokines that plays the prominent role in the lungs of asthma sufferers, due to interleukin-4(IL-4) and IL-13 enhance immunologlobulin E(IgE) production, while IL-4, and IL-10, enhances mast growth cell, likewise IL-5 enhancing eosinophil accumulation. This demonstrated that both IL-9 and IL-13 were direct precursors for mucus hypersecretion and airway hyperactivity (AHR) (Umetsu &Dekruyff, 2006). Allergen tolerance is the medium that confers the preventive properties of these responses, but the actual imuunological 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. But because asthma is a complex disease, there is no single gene responsible for it, instead, it is likely a result from the influence of multiple genetic, environmental, and developmental factors(Tantisira &Weiss, 2006). This is further supported by Yeatts et al (2006) that environmental factors and genetic contributions largely has increased the prevalence of this disease(Yeatts, 2006).
According to Han et al(2008), the hygiene hypothesis suggests that infections of microbial origin or substance may modify host's immune system, hence regulating the progression of allergic diseases (Han et al., 2008). They demonstrated that intracellular bacterial infection or its products are capable of inhibiting airway eosinophilic inflammation, mucus overproduction, allergen- specific IgE production, airway hyperresponsiveness and remodeling ( Han et al., 2008). This hypothesis was earlier demonstrated by (Tantisira &Weiss, 2006; Umetsu & Dekruyff, 2006).
Intermittent manifestations of asthma is accompanied by bronchoconstriction, wheezing, cough, and over production of sputum due to allergens taken up by the body. Han et al (2008) found out that the modification of cytokine design and the induction of immunosuppressive or regulatory T cell appear to be an important precursor for infection-mediated inhibition of allergy(Han et al., 2008). This findings is consistent with the mechanism of protection observed by Umetsu & Dekkruyff (2006) that because Th1 cells dross regulate Th2 cells in certain systems, allergen-specific Th1 cells are thought to be responsible for the regulation of allergic diseases and asthma (Umetsu &Dekruyff, 2006). According to these researchers, T-helper 1cells inhibit the advancement and production of Th2 cells, and IgE proliferation was complimentarily modulated by IL-4 and inferno-?(IFN-?), inferring that immunity from allergy was as a result of the development of inhibitory allergen-specific Th1 cell(Umetsu &Dekruyff, 2006).
Han et al(2008) carried out a study on the role of NK cells in hygiene hypothesis. They conducted this study by assessing the function of chlamydial infection and the development of allergic response induced by ovalbumin. The effect of this response was observed by using a mouse with airway inflammation (Han et al., 2008). They mentioned that inhibition of airway eosinophilic inflammation and mucus secretion induced by allergen stimulation and exposure was implicated by the prior infection with Chlamydia( Han et al., 2008). The researchers demonstrated that blockage of the allergic activity was synonymous with the altering of cytokine - producing network of the T cells. This therefore implies that T cell is implicated in the progression of hyperactivity of the airways, a typical manifestation of asthma and allergic response (Han et al., 2008). While carrying out this research, they observed that transferred NK cells that were isolated from mice infected with Chlamydia showed a large inhibitory change on response to allergen (Han et al., 2008). One limitation of this result was its consistent with earlier studies done by Briode et al (2001) that decrease of natural killer cells during allergen challenge phase has no immunosuppressant genetic sequence to block airway inflammation and hyperreactivity (Briode et al., 2001). Han's and colleagues proved that Natural Killer cell has an important role to play in allergic response.
Heaton et al(2003) conducted another study on the existence of Staph. aureus on the skin of persons with severe form of eczema (atopic eczema/dermatitis syndrome) (AEDS). They aimed at elucidating the regulatory effect of Sag Staphylococcal enterotoxin B(SEB) on the production of cytokines in peripheral blood mononuclear cells(PBMC) from patients with AEDS. Cells used for this study was cultured for 24 to 96 hours with house dust mite(HDM), SEB and phytohaemagluttinin were assayed for cytokine levels(Heaton et al., 2003). Their resuls indicated that SEB sparingly stimulates IL-5 intereleukin production in people with AEDS and not nonatopics. This study correlates with previous findings by Umetsu &Dekruyff (2006) that IL-5 enhances eosinophilic accumulation (Umetsu & Dekruyff, 2006).
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 Staph antigens. One limitation of this study is the restrictive partten of the stimulatory effects of SEB on IL-5, which is different from what is obtainable on IL-4 and IFN production present only in persons with current atopic disease ( Heaton et al., 2003).
Public Health Application
About 300 million people around the world are plagued with asthma, 17 million of these persons exist in North America, this has substantially resulted in high morbidity, mortality and strain on the healthcare delivery system ( Johnson 2010; Tantisira &Weiss, 2006). The two studies presented above has demonstrated that microorganisms( Staph. and Chlamydia) in this context plays a significant role in triggering responses against asthma and allergic diseases. This is in alignment with the hygiene hypothesis theory which proposes that there is a decrease of/or altered exposure of microorganism in the environment which may be as a direct result of improved sanitation, hygiene or childhood immunization in a way confers immunity on the individual against asthma and allegic diseases (Umetsu & Dekruyff, 2006). The activities of Tcells and Natural Killer cells has shedded more light in the understanding of airway inflammation and hyperactivity and subsequence responses in the individual's immune system. These studies may open more doors to research opportunities for enactment of public health policies, medications and therapy for affected persons.
In conclusion, therefore, I would recommend further research into these models presented by these authors, because what is not very certain about their findings would be the effect of prolonged exposure of Th1 allergen-specific reaction in people.