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The aim of this study was to create an overview on the COVID-associated burdens faced by the oral and maxillofacial surgery (OMS) workforce during 1 year of the pandemic. OMS hospitals and private practices nationwide were surveyed regarding health care worker (HCW) screening, infection status, pre-interventional testing, personal protective equipment (PPE), and economic impact. Participants were recruited via the German Society for Oral and Maxillofacial Surgery. A total of 11 hospitals (416 employees) and 55 private practices (744 employees) participated. The HCW infection rate was significantly higher in private practices than in clinics (4.7% vs. 1.4%, p0.01), although most infections in HCW occurred in private environment (hospitals 88.2%, private practice 66.7%). Pre-interventional testing was performed significantly less for outpatients in private practices than in hospitals (90.7% vs. 36.4%, p0.01). Polymerase chain reaction (PCR) was used significantly more for inpatients in hospitals than in private practices (100.0% vs. 27.3%, p0.01). FFP2/3 use rose significantly in hospitals (0% in second quarter vs. 46% in fourth quarter, p0.05) and private practices (15% in second quarter vs. 38% in fourth quarter, p0.01). The decrease in procedures (≤50%) was significantly higher in hospitals than in private practices (90.9% vs. 40.0%, p0.01). Despite higher infection rates in private practices, declining procedures and revenue affected hospitals more. Future COVID-related measures must adjust the infrastructure especially for hospitals to prevent further straining of staff and finances.

Ganoderma comprises a common bracket fungal genus that causes basal stem rot in deciduous and coniferous trees and palms, thus having a large economic impact on forestry production. We estimated pathogen abundance using long-term, daily spore concentration data collected in five biogeographic regions in Europe and SW Asia. We hypothesized that pathogen abundance in the air depends on the density of potential hosts (trees) in the surrounding area, and that its spores originate locally. We tested this hypothesis by (1) calculating tree cover density, (2) assessing the impact of local meteorological variables on spore concentration, (3) computing back trajectories, (4) developing random forest models predicting daily spore concentration. The area covered by trees was calculated based on Tree Density Datasets within a 30 km radius from sampling sites. Variations in daily and seasonal spore concentrations were cross-examined between sites using a selection of statistical tools including HYSPLIT and random forest models. Our results showed that spore concentrations were higher in Northern and Central Europe than in South Europe and SW Asia. High and unusually high spore concentrations (> 90th and > 98th percentile, respectively) were partially associated with long distance transported spores: at least 33% of Ganoderma spores recorded in Madeira during days with high concentrations originated from the Iberian Peninsula located >900 km away. Random forest models developed on local meteorological data performed better in sites where the contribution of long distance transported spores was lower. We found that high concentrations were recorded in sites with low host density (Leicester, Worcester), and low concentrations in Kastamonu with high host density. This suggests that south European and SW Asian forests may be less severely affected by Ganoderma. This study highlights the effectiveness of monitoring airborne Ganoderma spore concentrations as a tool for assessing local Ganoderma pathogen infection levels. (c) 2021 Elsevier B.V. All rights reserved.

Common ragweed (Ambrosia artemisiifolia L.) is a highly allergenic annual ruderal plant and native to Northern America, but now also spreading across Europe. Air pollution and climate change will not only affect plant growth, pollen production and duration of the whole pollen season, but also the amount of allergenic encoding transcripts and proteins of the pollen. The objective of this study was to get a better understanding of transcriptional changes in ragweed pollen upon NO2 and O3 fumigation. This will also contribute to a systems biology approach to understand the reaction of the allergenic pollen to air pollution and climate change. Ragweed plants were grown in climate chambers under controlled conditions and fumigated with enhanced levels of NO2 and O3. Illumina sequencing and de novo assembly revealed significant differentially expressed transcripts, belonging to different gene ontology (GO) terms that were grouped into biological process and molecular function. Transcript levels of the known Amb a ragweed encoding allergens were clearly up-regulated under elevated NO2, whereas the amount of allergen encoding transcripts was more variable under elevated O3 conditions. Moreover transcripts encoding allergen known from other plants could be identified. The transcriptional changes in ragweed pollen upon elevated NO2 fumigation indicates that air pollution will alter the transcriptome of the pollen. The changed levels of allergenic encoding transcripts may have an influence on the total allergenic potential of ragweed pollen.

Alnus pollen is one of the Northern Hemisphere's major aeroallergens. In Central Europe, the genus is represented by three species (Alnus glutinosa, Alnus incana, and Alnus viridis). The most common one, A. glutinosa (L.) Gaertn., is widespread in lowland riparian forests, swamps, and forest edges. However, to date is still unknown if all of them - in terms of pollen exposure - are clinically relevant for sensitized individuals. To investigate the associated pollen exposure, particularly also because of long-range transport of airborne pollen, we used backward air mass trajectories and tested this method for the year 2015, based on daily Alnus pollen concentrations at 26 sites in Bavaria, Germany. A. glutinosa's main pollen season extends from February to March, but a six-day, post-season episode was additionally identified in June. For this episode and all sites, 72-h backward trajectories were calculated at 3-h intervals using high spatial and temporal resolution ERA5 reanalysis data and the HYSPLIT (hybrid single-particle Lagrangian integrated trajectory) model. This backward trajectory method identified air masses from the alpine region in Switzerland and Austria, where relevant areas of A. viridis (Chaix) DC as potential pollen sources exist. These may explain the post-season episode in June, as additionally confirmed by its unique spatial distribution, by a considerably later flowering period, and by repeated long-range transport events as observed in a 23-year pollen time series.

BACKGROUND: A standardized human model to study early pathogenic events in patients with psoriasis is missing. Activation of Toll-like receptor 7/8 by means of topical application of imiquimod is the most commonly used mouse model of psoriasis. OBJECTIVE: We sought to investigate the potential of a human imiquimod patch test model to resemble human psoriasis. METHODS: Imiquimod (Aldara 5% cream; 3M Pharmaceuticals, St Paul, Minn) was applied twice a week to the backs of volunteers (n=18), and development of skin lesions was monitored over a period of 4weeks. Consecutive biopsy specimens were taken for whole-genome expression analysis, histology, and T-cell isolation. Plasmacytoid dendritic cells (pDCs) were isolated from whole blood, stimulated with Toll-like receptor 7 agonist, and analyzed by means of extracellular flux analysis and real-time PCR. RESULTS: We demonstrate that imiquimod induces a monomorphic and self-limited inflammatory response in healthy subjects, as well as patients with psoriasis or eczema. The clinical and histologic phenotype, as well as the transcriptome, of imiquimod-induced inflammation in human skin resembles acute contact dermatitis rather than psoriasis. Nevertheless, the imiquimod model mimics the hallmarks of psoriasis. In contrast to classical contact dermatitis, in which myeloid dendritic cells sense haptens, pDCs are primary sensors of imiquimod. They respond with production of proinflammatory and T17-skewing cytokines, resulting in a T17 immune response with IL-23 as a key driver. In a proof-of-concept setting systemic treatment with ustekinumab diminished imiquimod-induced inflammation. CONCLUSION: In human subjects imiquimod induces contact dermatitis with the distinctive feature that pDCs are the primary sensors, leading to an IL-23/T17 deviation. Despite these shortcomings, the human imiquimod model might be useful to investigate early pathogenic events and prove molecular concepts in patients with psoriasis.

Less vegetated mountainous areas may provide better conditions for allergy sufferers. However, atmospheric transport can result in medically relevant pollen loads in such regions. The majority of investigations has focused on the pollen load, expressed as daily averages of pollen per cubic meter of air (pollen grains/m³); however, the severity of allergic symptoms is also determined by the actual allergen content of this pollen, its pollen potency, which may differ between high and low altitudes. We analysed airborne birch and grass pollen concentrations along with allergen content (birch: Bet v 1, grass: Phl p 5) at two different altitudes (734 and 2650 m a.s.l.) in the Zugspitze region (2009–2010). Back-trajectories were calculated for the high altitude site and for specific days with abrupt increases in pollen potency. We observed several days with medically relevant pollen concentrations at the highest site. In addition, a few days with pollen were not associated with allergens and vice versa . The calculated seasonal mean allergen release per pollen grain was 1.8–3.3 pg Bet v 1 and 5.7 pg Phl p 5 in the valley and 1.1–3.7 pg Bet v 1 and 0.7–1.5 pg Phl p 5 at the high altitude site. Back-trajectories revealed that high pollen potency at the higher site was generally associated with south-westerly to south-easterly (birch), or northerly (grass) wind directions. By investigating days with sudden increases in pollen potency, however, it was difficult to draw definitive conclusions on long- or short-range transport. Our findings suggest that people allergic to pollen might suffer less at higher altitudes and further indicate that a risk assessment relying on the actual concentration of airborne pollen does not necessarily reflect the actual allergy exposure of individuals.

Pollution adversely affects vegetation; however, its impact on phenology and leaf morphology is not satisfactorily understood yet. We analyzed associations between pollutants and phenological data of birch, hazel and horse chestnut in Munich (2010) along with the suitability of leaf morphological parameters of birch for monitoring air pollution using two datasets: cumulated atmospheric concentrations of nitrogen dioxide and ozone derived from passive sampling (short-term exposure) and pollutant information derived from Land Use Regression models (long-term exposure). Partial correlations and stepwise regressions revealed that increased ozone (birch, horse chestnut), NO2, NOx and PM levels (hazel) were significantly related to delays in phenology. Correlations were especially high when rural sites were excluded suggesting a better estimation of long-term within-city pollution. In situ measurements of foliar characteristics of birch were not suitable for bio-monitoring pollution. Inconsistencies between long- and short-term exposure effects suggest some caution when interpreting short-term data collected within field studies.

Epithelial cells of both the respiratory tract and the skin form a tight barrier against environmental harm. They represent the site of first contact for airborne allergen carriers. Consequently, in this study, we analyzed the uptake of grass pollen allergens by epithelial cells: Phl p 1 was selected as a glycosylated allergen containing disulfide bridges whereas Phl p 6 lacks post-translational modifications. Allergen uptake by the respiratory epithelial cell line A549 reached a plateau at 2 hours, and both allergens were localized intracellularly in non-acidic vesicles. In addition, in A549 cells allergens were exocytosed, suggesting a transcytosis mechanism in the passage of allergens over the respiratory epithelial barrier. In contrast, allergens were predominately localized in lysosomes in keratinocytes, and allergen uptake did not reach a plateau up to 24 hours. Notably, keratinocytes from atopic patients showed a significantly increased uptake of Phl p 1 as compared with healthy donors. Preincubation of epithelial cells with IL-4 and/or IFN-gamma to simulate inflammatory status led to an increased allergen uptake only in keratinocytes. This higher engulfment of allergens by inflammatory-type keratinocytes suggests a higher susceptibility of inflamed skin for the uptake of allergens and consequently a potentially higher risk for sensitization under natural exposure conditions, such as chronic atopic eczema.

095 Koebnerisin (S100A15) signals via mTOR in keratinocytes to control epidermal maturation in psoriasis C Buerger, S Richert, V Lang, S Diehl, E Hattinger, R Kaufmann and R Wolf 1 Department of Dermatology, Clinic of the Goethe University, Frankfurt, Germany and 2 Department of Dermatology, Ludwig-Maximilian-University, Munich, Germany The mTOR (mechanistic target of rapamycin) pathway is a central regulator of cell growth and differentiation. In psoriasis, the mTOR kinase is activated throughout the whole epidermis, with particularly strong activation in the basal proliferating epidermal layer. To date, diseaseintrinsic factors which regulate epidermal mTOR activity are yet to be investigated. Koebnerisin (S100A15) is an innate anti-microbial and immune-modulatory peptide strongly upregulated in the psoriatic epidermis. Our data revealed that the localization of koebnerisin resembles the activation pattern of the mTOR kinase. We hypothesized a functional link and unveiled that koebnerisin was capable of activating mTOR signaling via the PI3-K/Akt cascade in keratinocytes. Functionally koebnerisin conferred a small effect on keratinocyte proliferation, which emphasizes previous results on the minor role of mTOR signaling in regulating epidermal proliferation. Further, koebnerisin induced mTOR activation interfered with the expression of differentiation markers mostly likely via post-transcriptional regulation. Data suggest a functional link between the innate anti-microbial peptide koebnerisin (S100A15) and mTOR signaling for epidermal maturation and emphasize the mTOR network as a therapeutic target in chronic inflammatory diseases in the skin and beyond. 096 Transcriptomic analysis of epidermal barrier molecules, cytokines and growth factors in atopic dermatitis lesions C Altunbulakli, A Neumann, F Castro Giner, N Garzorz-Stark, M Reiger, M Akdis, C Traidl-Hoffmann and CA Akdis 1 Swiss Institute for Allergy and Asthma Research, University of Zurich, Davos Platz, Switzerland, 2 Experimental Dermato-Immunology, Clinic and Polyclinic for Dermatology and Allergology at Biederstein, Munich, Germany, 3 Functional Genomics Center Zurich, ETH Zurich, Zurich, Switzerland and 4 Chair and Institute of Environmental Medicine, UNIKA-T, Technical University of Munich and Helmholtz Zentrum Munchen e German Research Center for Environmental Health (GmbH), Augsburg, Germany Atopic dermatitis (AD) is one of the most common inflammatory skin diseases in the general population. AD lesions are characterized by defective expression of skin tight junction (TJ) proteins, as well as changes in filaggrin and factors of the immunologic concert. However, regulation of the whole TJ family and cytokine expression during lesion formation remains to be elucidated to understand the key events behind AD lesion formation. Here, we performed RNA-sequencing and transcriptome analysis in punch biopsies from 11 atopic dermatitis patients and 7 healthy controls, comparing gene expression differences between healthy skin, AD lesional skin and AD non-lesional skin samples. Differentially expressed genes between three skin conditions were calculated, hierarchical clustering and principal component analysis of samples were performed, along with enrichment of the involved pathways and correlations between selected gene families. We found significant differential expression between AD patients and healthy donors, and between AD lesional and non-lesional skin samples. Gene expression of the TJ family and its adaptor molecules were downregulated in both AD lesional and non-lesional skin. FLG was found to be downregulated in lesional skin, and Loricrin was found to be downregulated in both lesional and non-lesional AD skin. Novel Inflammatory cytokines IL36A and IL36Gwere observed as upregulated in lesional skin. These results shed light on the functional pathways related to, and possibly leading to, AD formation, elucidating the complex interaction between the TJ system and the immune response.

Pollen monitoring is mostly performed manually. There is, however, a need for rapid reporting of pollen counts in addition to the alleviation of the workload of manual operation. We investigated the different steps needed for building an automatic pollen monitoring network in Bavaria, Germany. First, we tested the performance of the automatic pollen monitor BAA500, by comparing its data with data from a Hirst-type pollen trap at the same location. Next, during 2015, we built a new manual Bavarian pollen monitoring network with 27 Hirst-type pollen traps, including all closed but reopened operating traps from the German Polleninformation Network (PID). The selection of monitoring locations was based on: 1. Coverage of Bavarian land surface and population, but also 2. trying to represent the different environmental and climatic areas and 3. selecting the best positions to increase the predictability of pollen amounts based on forecasting models. Traps were located under optimal local monitoring conditions. The most informative locations were selected by applying redundancy and clustering analysis. Only 8 pollen traps are needed to cover most of variability in pollen dynamics. We found that three large groups of stations could be differentiated: 1. An extensive central cluster agglomerating most of the stations 2. a cluster agglomerating the stations located at the coldest areas of Bavaria and 3. a cluster of the Northern part of Bavaria. At the same time, we found the existence of eight sub-clusters related with different environmental conditions. We are now replacing these 8 manual stations by automatic pollen monitors and incorporating our network into local law to guarantee continuity.

Background Patients with atopic eczema (AE) regularly experience colonization with Staphylococcus aureus that is directly correlated with the severity of eczema. Recent studies show that an impaired IL-17 immune response results in diseases associated with chronic skin infections. Objective We sought to elucidate the effect of IL-17 on antimicrobial immune responses in AE skin. Methods T cells infiltrating atopy patch test (APT) reactions were characterized for IL-17 secretion to varying stimuli. IL-17–dependent induction of the antimicrobial peptide human β-defensin 2 (HBD-2) in keratinocytes was investigated. Results Approximately 10% of APT-infiltrating T cells secreted IL-17 after phorbol 12-myristate 13-acetate (PMA)/ionomycin stimulation. Among these, 33% belonged to the newly characterized subtype T H 2/IL-17. Despite the capacity to secrete IL-17, specific T-cell clones released only low amounts of IL-17 on cognate allergen stimulation, whereas IL-4, IFN-γ, or both were efficiently induced. IL-17 secretion was not enhanced by IL-23, IL-1β, or IL-6 but was enhanced by the S aureus –derived superantigen staphylococcal enterotoxin B. Both healthy and AE keratinocytes upregulated HBD-2 in response to IL-17, but coexpressed IL-4/IL-13 partially inhibited this effect. In vivo , additional application of staphylococcal enterotoxin B induced IL-17 in APT reactions, whereas IL-4, IFN-γ, and IL-10 were marginally regulated. Induced IL-17 upregulated HBD-2 in human keratinocytes in vivo . Conclusion IL-17–capable T cells, in particular T H 2/IL-17 cells, infiltrate acute AE reactions. Although IL-17 secretion by specific T cells is tightly regulated, it can be triggered by bacteria-derived superantigens. The ineffective IL-17–dependent upregulation of HBD-2 in patients with AE is due to a partial inhibition by the type 2 microenvironment, which could partially explain why patients with AE do not clear S aureus .