Immunological resilience and biodiversity for prevention of allergic diseases and asthma

Increase of allergic conditions has occurred at the same pace with the Great Acceleration, which stands for the rapid growth rate of human activities upon earth from 1950s. Changes of environment and lifestyle along with escalating urbanization are acknowledged as the main underlying causes. Secondary (tertiary) prevention for better disease control has advanced considerably with innovations for oral immunotherapy and effective treatment of inflammation with corticosteroids, calcineurin inhibitors, and biological medications. Patients are less disabled than before. However, primary prevention has remained a dilemma. Factors predicting allergy and asthma risk have proven complex: Risk factors increase the risk, while protective factors counteract them. Interaction of human body with environmental biodiversity with micro-organisms and biogenic compounds as well as the central role of epigenetic adaptation in immune homeostasis have given new insight. Allergic diseases are good indicators of the twisted relation to environment. In various non-communicable diseases, the protective mode of the immune system indicates low-grade inflammation without apparent cause. Giving microbes, pro- and prebiotics, has shown some promise in prevention and treatment. The real-world public health programme in Finland (2008-2018) emphasized nature relatedness and protective factors for immunological resilience, instead of avoidance. The nationwide action mitigated the allergy burden, but in the lack of controls, primary preventive effect remains to be proven. The first results of controlled biodiversity interventions are promising. In the fast urbanizing world, new approaches are called for allergy prevention, which also has a major cost saving potential.Peer reviewe

Host Specialization and Dispersal in Avian Haemosporidians

In order to be able to understand the ecological and evolutionary processes involved in the emergence of infectious diseases, one needs to comprehend how parasites arrive at new geographical areas and how they manage to maintain viable populations and even expand their ranges. We discuss host specificity in avian haemosporidians and how encounter and compatibility filters affect the dispersal of avian haemosporidians, and how these filters affect avian haemosporidian assemblages at different spatial and evolutionary scales. There are at least three important barriers to the dispersal of avian haemosporidians: (i) geographic barriers, (ii) environmental barriers, and (iii) interspecies barriers. In this chapter, we discuss the factors involved in these barriers and their effects on the structure of avian haemosporidian assemblages. Host specificity plays an important role in parasite dispersal, and in the case of avian haemosporidians that are vector-borne parasites, it needs to be evaluated both at the vector and bird host levels. Understanding the effects of these factors on host–vector–parasite dynamics is important to unravel the dispersal and diversification mechanisms of avian haemosporidians. We end this chapter reviewing host specialization in avian haemosporidians of tropical regions, discussing the mechanisms involved in the dispersal and specialization of these parasites and point out important research gaps that need attention

Resources, key traits and the size of fungal epidemics in Daphnia populations.

1. Parasites can profoundly affect host populations and ecological communities. Thus, it remains critical to identify mechanisms that drive variation in epidemics. Resource availability can drive epidemics via traits of hosts and parasites that govern disease spread. 2. Here, we map resource–trait–epidemic connections to explain variation in fungal outbreaks (Metschnikowia bicuspidata) in a zooplankton host (Daphnia dentifera) among lakes. We predicted epidemics would grow larger in lakes with more phytoplankton via three energetic mechanisms. First, resources should stimulate Daphnia reproduction, potentially elevating host density. Secondly, resources should boost body size of hosts, enhancing exposure to environmentally distributed propagules through size-dependent feeding. Thirdly, resources should fuel parasite reproduction within hosts. 3. To test these predictions, we sampled 12 natural epidemics and tracked edible algae, fungal infection prevalence, body size, fecundity and density of hosts, as well as within-host parasite loads. 4. Epidemics grew larger in lakes with more algal resources. Structural equation modelling revealed that resource availability stimulated all three traits (host fecundity, host size and parasite load). However, only parasite load connected resources to epidemic size. Epidemics grew larger in more dense Daphnia populations, but host density was unrelated to host fecundity (thus breaking its link to resources). 5. Thus, via energetic mechanisms, resource availability can stimulate key trait(s) governing epidemics in nature. A synthetic focus on resources and resource–trait links could yield powerful insights into epidemics

What is the evidence that ecosystem components or functions have an impact on infectious diseases? A systematic review protocol

Abstract Background Many infectious pathogens can be transmitted from animals to humans and vice versa, or by animals (especially arthropods) to humans. Such diseases are called zoonotic and/or vector-borne diseases. To control or prevent them, it is often recommended to target population reduction of host or vector species, through preventive culling or insecticide use for example. But these types of destructive interventions have shown several limits altering their efficiency, including acquired resistance of arthropods to insecticides, unpredicted change in the ecology of host populations, unexpected negative functional consequences on ecosystems, as well as economic embrittlement when livestock is concerned. An alternative pathway of action would be to rely on the functioning of ecosystems, and on their careful management, to regulate diseases and thus reduce their impact on human health. In this perspective, a thorough evaluation of the conditions that can potentially promote such a positive regulation of infectious pathogens by ecosystems, and their efficiency, is needed. Here, we present the protocol of a systematic review that will evaluate the scientific evidence existing on potential links between ecosystem components or functions and 14 vector-borne and zoonotic diseases impacting human health. Methods We will search for studies that tested the effect of changes in (i) biological communities, and (ii) habitats and landscapes, on diseases. Scientific literature from 5 publication databases will be screened in a 3-rounds process: title, abstract and full-text screening. At each stage, articles will be either rejected or kept for the next round, depending on whether they fall in the exclusion or inclusion criteria. We will present results in two parts: a systematic map and a systematic review. The systematic map will present, for the 14 diseases, the number of publications, their geographical distribution, the type of ecosystem component/function they studied, as well as the host(s) in which epidemiological measurements have been performed. From this systematic map, we will identify groups of articles that allow for critical appraisal, i.e. groups of articles that studied the effect of the same ecosystem component/function on the same disease. Only those articles will be included in the systematic review. The validity of these articles will be assessed by critical appraisal and presented as a narrative synthesis with confidence levels