The Hygiene Hypothesis Revisited
Department of Pediatrics, University of Wisconsin-Madison, K4/910 CSC, 600 Highland Avenue, Madison, WI 53792-9988, USA. Immunology and Allergy Clinics of North America
(Impact Factor: 1.82).
06/2005; 25(2):247-62, v-vi. DOI: 10.1016/j.iac.2005.03.005
The original hygiene hypothesis proposed that reductions in family size and exposure to childhood infections were responsible for the rise in atopic diseases. Numerous epidemiologic and longitudinal studies have been performed to test this hypothesis, which has evolved in response to these findings and emerging concepts related to the innate immune response and immunoregulatory mechanisms. Collectively, these advances raise hope that the concepts espoused in original hygiene hypothesis may soon lead to new preventive approaches to atopic diseases.
Available from: Hossein Yousofi Darani
- "An inhibition of tumor cell proliferation has also been associated with certain types of parasites . These findings support the hygiene theory whereby a decrease in exposure to infectious agents early in life is predicted to increase susceptibility to allergies, and perhaps autoimmune diseases [9–11]. Protoscolices are small masses with four suckers and a double row of hooks and each is capable of developing into an adult worm in the intestine of the final host. "
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ABSTRACT: Both in vitro and in vivo models have demonstrated that some parasites can interfere with tumor cell growth. The present study investigates the anticancer activity of hydatid cyst protoscolices on WEHI-164 fibrosarcoma cells and baby hamster kidney (BHK) fibroblast cells in vitro. Those above two cell types were treated with live hydatid cyst protoscolices or left untreated for control groups. After 48 h, lactate dehydrogenase (LDH) and cell counts were assayed for both treated cells and control groups. Following treatment with hydatid cyst protoscolices, cell proliferation of both cell types was inhibited, and lysis of fibrosarcoma cells increased. Based on these results, it appears that hydatid cyst protoscolices have strong anticancer activity, and additional studies are needed to further clarify the mechanisms of this activity.
Available from: Zak Callaway
- "Early childhood exposure to certain pathogens may actually be protective against atopy and/or asthma, termed the "hygiene hypothesis" . This highly controversial idea was borne from early observations showing the risk of developing allergy and/or asthma was inversely related to the number of children in the family . "
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ABSTRACT: There is a growing list of viruses and bacteria associated with wheezing illness and asthma. It is well known that a few of these pathogens are strongly associated with wheezing illness and asthma exacerbations. What is not known is if early childhood infections with these pathogens cause asthma, and, if so, exactly what are the pathophysiologic mechanisms behind its development. The current consensus is respiratory infection works together with allergy to produce the immune and physiologic conditions necessary for asthma diasthesis. One link between respiratory infection and asthma may be the eosinophil, a cell that plays prominently in asthma and allergy, but can also be found in the body in response to infection. In turn, the eosinophil and its associated products may be novel therapeutic targets, or at the very least used to elucidate the complex pathophysiologic pathways of asthma and other respiratory illnesses. Together or separately, they can also be used for diagnosis, treatment and monitoring. The optimal care of a patient must take into consideration not only symptoms, but also the underlying disease mechanisms.
Available from: Staci D Bilbo
- "Our data in particular also suggest that the consequences of early-life immune challenge should be considered within a cost/ benefi t perspective, in which outcomes in adulthood may be differentially protected or impaired (which may indeed be a consequence of distinct functions depending on different brain regions as suggested above). This idea is not without precedence—the " hygiene hypothesis " was proposed nearly 20 years ago as a way to explain the increased incidence of asthma/allergy and other autoimmune disorders in developed countries, and the idea that " too-sterile " environments do not provide suffi cient early training for the immune system, with resulting over-reactions in later life (Bufford and Gern, 2005; Strachan, 1989). Another elegant example of this concept comes from the fi eld of metabolism in which the " fetal origins of adult disease " was fi rst characterized – Dr. "
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ABSTRACT: The immune system is well characterized for its critical role in host defense. Far beyond this limited role however, there is mounting evidence for the vital role the immune system plays within the brain, in both normal, "homeostatic" processes (e.g., sleep, metabolism, memory), as well as in pathology, when the dysregulation of immune molecules may occur. This recognition is especially critical in the area of brain development. Microglia and astrocytes, the primary immunocompetent cells of the CNS, are involved in every major aspect of brain development and function, including synaptogenesis, apoptosis, and angiogenesis. Cytokines such as tumor necrosis factor (TNF)alpha, interleukin [IL]-1beta, and IL-6 are produced by glia within the CNS, and are implicated in synaptic formation and scaling, long-term potentiation, and neurogenesis. Importantly, cytokines are involved in both injury and repair, and the conditions underlying these distinct outcomes are under intense investigation and debate. Evidence from both animal and human studies implicates the immune system in a number of disorders with known or suspected developmental origins, including schizophrenia, anxiety/depression, and cognitive dysfunction. We review the evidence that infection during the perinatal period of life acts as a vulnerability factor for later-life alterations in cytokine production, and marked changes in cognitive and affective behaviors throughout the remainder of the lifespan. We also discuss the hypothesis that long-term changes in brain glial cell function underlie this vulnerability.
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