Climate change and allergies

The climate crisis poses a major challenge to human health as well as the healthcare system and threatens to jeopardize the medical progress made in recent decades. However, addressing climate change may also be the greatest opportunity for global health in the 21st century. The climate crisis and its consequences, such as rising temperatures, forest fires, floods, droughts, and changes in the quality and quantity of food and water, directly and indirectly affect human physical and mental health. More intense and frequent heat waves and declining air quality have been shown to increase all-cause mortality, especially among the most vulnerable. Climate warming alters existing ecosystems and favors biological invasions by species that better tolerate heat and drought. Pathogen profiles are changing, and the transmission and spread of vector-borne diseases are increasing. The spread of neophytes in Europe, such as ragweed, is creating new pollen sources that increase allergen exposure for allergy sufferers. In addition, the overall milder weather, especially in combination with air pollution and increased CO(2) levels, is changing the production and allergenicity of pollen. The phenomenon of thunderstorm asthma is also occurring more frequently. In view of the increasing prevalence of allergic diseases due to climate change, early causal immunomodulatory therapy is therefore all the more important. During a climate consultation, patients can receive individual advice on climate adaptation and resilience and the benefits of CO(2) reduction—for their own and the planet’s health. Almost 5% of all greenhouse gas emissions in Europe come from the healthcare sector. It thus has a central responsibility for a climate-neutral and sustainable transformation

Birch pollen induces toll-like receptor 4-dependent dendritic cell activation favoring t cell responses

Seasonal exposure to birch pollen (BP) is a major cause of pollinosis. The specific role of Toll-like receptor 4 (TLR4) in BP-induced allergic inflammation and the identification of key factors in birch pollen extracts (BPE) initiating this process remain to be explored. This study aimed to examine (i) the importance of TLR4 for dendritic cell (DC) activation by BPE, (ii) the extent of the contribution of BPE-derived lipopolysaccharide (LPS) and other potential TLR4 adjuvant(s) in BPE, and (iii) the relevance of the TLR4-dependent activation of BPE-stimulated DCs in the initiation of an adaptive immune response. In vitro, activation of murine bone marrow-derived DCs (BMDCs) and human monocyte-derived DCs by BPE or the equivalent LPS (nLPS) was analyzed by flow cytometry. Polymyxin B (PMB), a TLR4 antagonist and TLR4-deficient BMDCs were used to investigate the TLR4 signaling in DC activation. The immunostimulatory activity of BPE was compared to protein-/lipid-depleted BPE-fractions. In co-cultures of BPE-pulsed BMDCs and Bet v 1-specific hybridoma T cells, the influence of the TLR4-dependent DC activation on T cell activation was analyzed. In vivo immunization of IL-4 reporter mice was conducted to study BPE-induced Th2 polarization upon PMB pre-treatment. Murine and human DC activation induced by either BPE or nLPS was inhibited by the TLR4 antagonist or by PMB, and abrogated in TLR4-deficient BMDCs compared to wild-type BMDCs. The lipid-free but not the protein-free fraction showed a reduced capacity to activate the TLR4 signaling and murine DCs. In human DCs, nLPS only partially reproduced the BPE-induced activation intensity. BPE-primed BMDCs efficiently stimulated T cell activation, which was repressed by the TLR4 antagonist or PMB, and the addition of nLPS to Bet v 1 did not reproduce the effect of BPE. In vivo, immunization with BPE induced a significant Th2 polarization, whereas administration of BPE pre-incubated with PMB showed a decreased tendency. These findings suggest that TLR4 is a major pathway by which BPE triggers DC activation that is involved in the initiation of adaptive immune responses. Further characterization of these BP-derived TLR4 adjuvants could provide new candidates for therapeutic strategies targeting specific mechanisms in BP-induced allergic inflammation

Earth observation for exposome mapping of Germany: analyzing environmental factors relevant to non-communicable diseases

Non-communicable diseases - NCDs - (e.g., asthma, cancer, or diabetes) are a major concern for society and medicine. According to the World Health Organization, NCDs are responsible for > 70 % of global premature deaths. Apart from increasing mortality, these diseases strain one’s immune system which leads to higher susceptibility to transmittable diseases. NCD-susceptibility depends on the genome (genetic predisposition), behavior (lifestyle), and exposome of a person. The exposome is a composition of environmental parameters such as exposure to air pollution, noise, extreme temperatures, or surrounding greenness. Using Earth Observation data, the majority of factors making up the exposome can be monitored over long periods of time at high resolution and with nearly global coverage. Still, exposome maps and products communicating NCD risk are not widely available. In this study, we utilize eight land surface datasets (distance to green spaces, distance to blue spaces, temperature, noise from industry, as well as road, rail, and air traffic, and light pollution) as well as two air pollution datasets (PM2.5 and NO2) to map health-relevant environmental exposure. We use an established cumulative approach and incorporate exposure-response relationships from scientific literature to map environments that impact public health for the complete area of Germany. We present results communicating exposure relevant to myocardial infarction risk. The methodology is transferable to other NCDs and other areas of interest. In the context of the global health burden from NCDs and ongoing global change, this approach supplies findings for communicating health-relevant exposure

Pollen grains induce a rapid and biphasic eczematous immune response in atopic eczema patients

Introduction: Eczematous reactions to type I allergy-inducing antigens are documented in a subgroup of patients with atopic eczema. Yet, the underlying immunological mechanisms are not well understood. Material and Methods: To delineate the effect of native pollen grains on human skin of healthy and atopic individuals we performed patch tests (atopy patch test with native pollen grains, PPT). Nickel patch tests (NPT) served as an established model of contact dermatitis. Skin site biopsies were taken 6 - 96 h after allergen application and investigated immunohistochemically. Results: Histology of positive patch tests showed an influx of mononuclear cells (predominantly CD4+, CD25+, CD45RO+). This influx was detected earlier in the PPT reaction than in the immune response to nickel. A biphasic cytokine response could be detected in the PPT: IL-5 dominated in the early, IFN-gamma in the late phase. The NPT was continuously dominated by IFN-gamma. Dendritic cell subpopulations imitated the earlier kinetics of the mononuclear infiltrate. Discussion: Thus, pollen grains induce eczematous reactions in susceptible individuals. This reaction appears clinically and immunohistochemically similar to the contact hypersensitivity reaction to nickel but follows a faster kinetic and a biphasic course: Th2 and IgE in the early (24 h) and Th1 predominance in the late (96 h) phase. Copyright (c) 2007 S. Karger AG, Basel