Helminths in the hygiene hypothesis: sooner or later?

Abstract

SummaryThere is increasing recognition that exposures to infectious agents evoke fundamental effects on the development and behaviour of the immune system. Moreover, where infections (especially parasitic infections) have declined, immune responses appear to be increasingly prone to hyperactivity. For example, epidemiological studies of parasite-endemic areas indicate that prenatal or early-life experience of infections can imprint an individual’s immunological reactivity. However, the ability of helminths to dampen pathology in established inflammatory diseases implies that they can have therapeutic effects even if the immune system has developed in a low-infection setting. With recent investigations of how parasites are able to modulate host immune pathology at the level of individual parasite molecules and host cell populations, we are now able to dissect the nature of the host–parasite interaction at both the initiation and recall phases of the immune response. Thus the question remains – is the influence of parasites on immunity one that acts primarily in early life, and at initiation of the immune response, or in adulthood and when recall responses occur? In short, parasite immunosuppression – sooner or later?

Prevalence of intestinal parasites in Isfahan city, central Iran, 2014

“…During the last decades the good hygienic and sanitation status of human populations of some parts of the world is caused the intestinal parasitic infections to be decreased (Maizels et al 2014;Yazdanbakhsh et al 2002), which Iran is not an exception for this fact (Jafari et al 2014;Sayyari et al 2005). Intestinal parasitic infections were prevalent in most of the areas of Iran in the past (Arfaa and Ghadirian 1977;Fallah et al 2002), but nowadays reports shows that the incidence of these kinds of infections are dramatically decreased in the country during last decades (Jafari et al 2014).…”

Better with your parasites? Lessons for behavioural ecology from evolved dependence and conditionally helpful parasites

“…Whether or not an individual experiences autoimmune or allergic diseases in a hygienic environment is likely to depend on factors that include host genotype, the severity of infection (e.g. how many parasites an individual is infected with), interactions between the host microbiome and helminth parasites, interactions between multiple helminth species infecting the same host, and whether or not infection happens early or late in life (Maizels & Nussey, 2013;Maizels, McSorley, & Smyth, 2014;McKay, 2009;Zaiss et al, 2015). These complexities make studying the importance of evolved dependence of host behaviour on parasites a potentially daunting task, but unravelling this complexity will yield a more ecologically relevant understanding of host behaviour.…”

A Review of Autoimmune Disease Hypotheses with Introduction of the “Nucleolus” Hypothesis

“…As a result, similar AD mechanisms might have different effects depending on the tissue sites involved. [3,30] Hygiene Lack of early exposure in childhood to a broad range of agents and/or specific agents can leave a person susceptible to an immune reaction to those agents later in life since proper tolerance was not developed [34,37,127] Lymphocyte dysregulation Abnormal modifications (e.g., calcium dysregulation, kinase phosphorylation) can lead to aberrant leukocyte activity (e.g., hypersensitivity or hyperactivity). Mutations or overexpression of gene products, such as cell surface receptors that internalize extracellular signals or in intracellular signaling, could cause this dysregulation [39,40] Cytokine polarization Th1 cells fight pathogens and cancerous cells whereas Th2 cells stimulate antibody production.…”

“…The hygiene hypothesis can also involve the impact of nutrients and probiotics on the early development of the immune system [36]. With regards to helminths, chronic helminth infections with ongoing exposure of helminth antigens to the immune system can moderate the immune response to parasites by inducing a more regulated TH2 response [37]. This can allow the parasite to persist, restricting the actual pathological impact, and it can also dampen the overall immune response to autoantigens and allergens [38].…”