Browsing by Subject "ALLERGIC SENSITIZATION"

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  • DIABIMMUNE Study Grp; Schmidt, Felicitas; Hose, Alexander J.; Siljander, Heli; Knip, Mikael; Ege, Markus J. (2019)
    Background: The prevalence of atopy is associated with a Western lifestyle, as shown by studies comparing neighboring regions with different socioeconomic backgrounds. Atopy might reflect various conditions differing in their susceptibility to environmental factors. Objective: We sought to define phenotypes of atopic sensitization in early childhood and examine their association with allergic diseases and hereditary background in Finland and Estonia. Methods: The analysis included 1603 Finnish and 1657 Estonian children from the DIABIMMUNE multicenter young children cohort. Specific IgE levels were measured at age 3, 4, and 5 years, respectively, and categorized into 3 CAP classes. Latent class analysis was performed with the statistical software package poLCA in R software. Results: Both populations differed in terms of socioeconomic status and environmental determinants, such as pet ownership, farm-related exposure, time spent playing outdoors, and prevalence of allergic diseases (all P Conclusion: Despite profound differences in environmental exposures, there might exist genuine patterns of atopic sensitization. The distribution of these patterns might determine the contribution of atopic sensitization to disease onset.
  • Hurme, Pekka; Homil, Kiara; Lehtinen, Pasi; Turunen, Riitta; Vahlberg, Tero; Vuorinen, Tytti; Camargo, Carlos A. Jr Jr; Gern, James E.; Jartti, Tuomas (2021)
    Background Acute rhinovirus-induced wheezing is common in young children and may respond to systemic corticosteroid. There are no trials on the efficacy of inhaled beta(2)-agonist in this clinical scenario. Objective To study post hoc the short-term (up to 2 months) efficacy of inhaled beta(2)-agonist with and without oral corticosteroid in the first acute rhinovirus-induced severe wheezing episode in young hospitalized children. Methods The study population came from two randomized controlled trials comparing oral prednisolone (2 mg/kg/d for 3 days) to placebo: Vinku (n = 35, NCT00494624) used high-dose regular nebulized salbutamol (0.15 mg/kg 2-4 h intervals) and Vinku2 (n = 60, NCT00731575, EudraCT 2006-007100-42) used inhaled salbutamol on-demand. Both studies used identical detailed follow-up assessments. The primary outcome of the former was the duration of hospitalization and of the latter the occurrence of and the time to a new physician-confirmed wheezing episode within 2 months after discharge. Treatment groups included salbutamol high-dose vs. salbutamol on-demand while adjusting for prednisolone status and acknowledging for interactions with exception of the duration of hospitalization in which prednisolone groups could not be fully used due to protocol differences. Results Median age of subjects was 13 months, 32% were sensitized and 22% had doctor-diagnosed eczema. In the duration of hospitalization, salbutamol high-dose/placebo versus salbutamol on-demand/placebo groups did not differ (p = .12). In the occurrence of and time to relapse within 2 months, a significant group x treatment interaction was observed (both p = .02), such that high-dose group had less and longer time to relapses than on-demand group in prednisolone arm (both p < .05), but no difference was detected in placebo arm (both p > .26). Conclusions In young, hospitalized children with first episode of rhinovirus-induced wheezing, high-dose inhaled salbutamol may interact with oral prednisolone. However, further trials are warranted.
  • Korhonen, Laura; Seiskari, Tapio; Lehtonen, Jussi; Puustinen, Leena; Surcel, Heljä-Marja; Haapala, Anna-Maija; Niemelä, Onni; Virtanen, Suvi M.; Honkanen, Hanna; Karjalainen, Mira; Ilonen, Jorma; Veijola, Riitta; Knip, Mikael; Lönnrot, Maria; Hyöty, Heikki (2018)
    Background: Prenatal environment has been shown to influence child's risk of atopic diseases. Laboratory-confirmed data about the role of maternal infections during pregnancy is scarce. Objective: The aim of this study was to determine the associations between serologically confirmed maternal infections during pregnancy and atopic disease in the offspring. Methods: This was a nested case-control study within a prospective birth cohort study. Altogether 202 atopic case children and 333 matched non-atopic control children were included. Atopic outcome was defined as having an atopic disease and IgE sensitization by the age of 5 years. We analysed serologically acute enterovirus (EV), influenza virus A (IAV) and Mycoplasma pneumoniae (M. pneumoniae) infections during pregnancy, and mother's seropositivity against human cytomegalovirus (CMV) and Helicobacter pylori. Results: Maternal EV infection during pregnancy was inversely associated with atopic outcome in the offspring (odds ratio 0.43; 95% confidence interval: 0.23-0.80, P = 0.008). Acute IAV or M. pneumoniae infections or seropositivity against CMV or Helicobacter pylori were not associated with the atopic outcome. Conclusions and Clinical Relevance: Our results suggest that maternal EV infections during pregnancy are inversely associated with atopic disease in the offspring. Our finding provides further support to the previous studies suggesting an important role of the in utero environment in the development of atopic diseases.
  • Ruokolainen, L.; von Hertzen, L.; Fyhrquist, N.; Laatikainen, T.; Lehtomaki, J.; Auvinen, P.; Karvonen, A. M.; Hyvarinen, A.; Tillmann, V.; Niemela, O.; Knip, M.; Haahtela, T.; Pekkanen, J.; Hanski, I. (2015)
  • Andersen, Heidi; Ilmarinen, Pinja; Honkamäki, Jasmin; Tuomisto, E. Leena; Hisinger-Mölkänen, Hanna; Backman, Helena; Lundbäck, Bo; Rönmark, Eva; Lehtimäki, Lauri; Sovijärvi, Anssi; Piirilä, Päivi; Kankaanranta, Hannu (2021)
    Purpose: Asthma is a heterogeneous disease, and factors associated with different asthma phenotypes are poorly understood. Given the higher prevalence of farming exposure and late diagnosis of asthma in more rural Western Finland as compared with the capital of Helsinki, we investigated the relationship between childhood farming environment and age at asthma diagnosis. Methods: A cross-sectional population-based study was carried out with subjects aged 2069 years in Western Finland. The response rate was 52.5%. We included 3864 participants, 416 of whom had physician-diagnosed asthma at a known age and with data on the childhood environment. The main finding was confirmed in a similar sample from Helsinki. Participants were classified as follows with respect to asthma diagnosis: early diagnosis (011 years), intermediate diagnosis (12-39 years), and late diagnosis (40-69 years). Results: The prevalence of asthma was similar both without and with childhood exposure to a farming environment (11.7% vs 11.3%). Allergic rhinitis, family history of asthma, exsmoker, occupational exposure, and BMI >= 30 kg/m(2) were associated with a higher likelihood of asthma. Childhood exposure to a farming environment did not increase the odds of having asthma (aOR, 1.10; 95% CI, 0.87-1.40). It did increase the odds of late diagnosis (aOR, 2.30; 95% CI, 1.12-4.69), but the odds were lower for early (aOR, 0.49; 95% CI, 0.30-0.80) and intermediate diagnosis of asthma (aOR, 0.75; 95% CI, 0.47-1.18). Conclusion: Odds were lower for early diagnosis of asthma and higher for late diagnosis of asthma in a childhood farming environment. This suggests a new hypothesis concerning the etiology of asthma when it is diagnosed late.
  • Skaaby, Tea; Taylor, Amy E.; Jacobsen, Rikke K.; Paternoster, Lavinia; Thuesen, Betina H.; Ahluwalia, Tarunveer S.; Larsen, Sofus C.; Zhou, Ang; Wong, Andrew; Gabrielsen, Maiken E.; Bjorngaard, Johan H.; Flexeder, Claudia; Mannisto, Satu; Hardy, Rebecca; Kuh, Diana; Barry, Sarah J.; Mollehave, Line Tang; Cerqueira, Charlotte; Friedrich, Nele; Bonten, Tobias N.; Noordam, Raymond; Mook-Kanamori, Dennis O.; Taube, Christian; Jessen, Leon E.; McConnachie, Alex; Sattar, Naveed; Upton, Mark N.; McSharry, Charles; Bonnelykke, Klaus; Bisgaard, Hans; Schulz, Holger; Strauch, Konstantin; Meitinger, Thomas; Peters, Annette; Grallert, Harald; Nohr, Ellen A.; Kivimaki, Mika; Kumari, Meena; Voelker, Uwe; Nauck, Matthias; Voeizke, Henry; Power, Chris; Hypponen, Elina; Hansen, Torben; Jorgensen, Torben; Pedersen, Oluf; Salomaa, Veikko; Grarup, Niels; Langhammer, Arnulf; Romundstad, Pal R.; Skorpen, Frank; Kaprio, Jaakko; Munafo, Marcus R.; Linneberg, Allan (2017)
    Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0.68, 95% confidence interval (CI): 0.61, 0.76; P <0.001) and allergic sensitization (OR = 0.74, 95% CI: 0.64, 0.86; P <0.001), but similar asthma risk (OR = 1.00, 95% CI: 0.91, 1.09; P = 0.967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0.958, 95% CI: 0.920, 0.998; P = 0.041), a lower risk of allergic sensitization (OR = 0.92, 95% CI: 0.84, 1.02; P = 0.117), but higher risk of asthma (OR = 1.06, 95% CI: 1.01, 1.11; P = 0.020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.
  • Brick, Tabea; Schober, Yvonne; Boecking, Christian; Pekkanen, Juha; Genuneit, Jon; Loss, Georg; Dalphin, Jean-Charles; Riedler, Josef; Lauener, Roger; Nockher, Wolfgang Andreas; Renz, Harald; Vaarala, Outi; Braun-Fahrlander, Charlotte; von Mutius, Erika; Ege, Markus Johannes; Pfefferle, Petra Ina; PASTURE Study Grp (2016)
    Background: Living on a farm has repeatedly been shown to protect children from asthma and allergies. A major factor involved in this effect is consumption of unprocessed cow's milk obtained directly from a farm. However, this phenomenon has never been shown in a longitudinal design, and the responsible milk components are still unknown. Objectives: We sought to assess the asthma-protective effect of unprocessed cow's milk consumption in a birth cohort and to determine whether the differences in the fatty acid (FA) composition of unprocessed farm milk and industrially processed milk contributed to this effect. Methods: The Protection Against Allergy-Study in Rural Environments (PASTURE) study followed 1133 children living in rural areas in 5 European countries from birth to age 6 years. In 934 children milk consumption was assessed by using yearly questionnaires, and samples of the ``usually'' consumed milk and serum samples of the children were collected at age 4 years. Doctor-diagnosed asthma was parent reported at age 6 years. In a nested case-control study of 35 asthmatic and 49 nonasthmatic children, 42 FAs were quantified in milk samples. Results: The risk of asthma at 6 years of age was reduced by previous consumption of unprocessed farm milk compared with shop milk (adjusted odds ratio for consumption at 4 years, 0.26; 95% CI,0.10-0.67). Part of the effect was explained by the higher fat content of farm milk, particularly the higher levels of omega-3 polyunsaturated FAs (adjusted odds ratio, 0.29; 95% CI,0.11-0.81). Conclusion: Continuous farm milk consumption in childhood protects against asthma at school age partially by means of higher intake of omega-3 polyunsaturated FAs, which are precursors of anti-inflammatory mediators.
  • DIABIMMUNE Study Grp; Korhonen, Laura; Oikarinen, Sami; Lehtonen, Jussi; Mustonen, Neea; Tyni, Iiris; Niemelä, Onni; Honkanen, Hanna; Huhtala, Heini; Ilonen, Jorma; Hämäläinen, Anu-Maaria; Peet, Aleksandr; Tillmann, Vallo; Siljander, Heli; Knip, Mikael; Lönnrot, Maria; Hyöty, Heikki; Härkönen, Taina; Ryhänen, Samppa; Koski, Katriina; Kiviniemi, Minna; Ahlfors, Helena; Kallionpää, Henna; Laajala, Essi; Lahesmaa, Riitta; Lähdesmäki, Harri; Moulder, Robert; Nieminen, Janne; Ruohtula, Terhi; Vaarala, Outi; Alahuhta, Kirsi; Virtanen, Suvi M.; Kondrashova, Anita (2019)
    Previous data about the role of viruses in the development of allergic immunoglobulin E (IgE) sensitization are contradictory. The aim of this study was to determine the possible associations between exposure to different viruses (rhinovirus, enterovirus, norovirus, and parechovirus) during the first year of life and IgE sensitization. Viruses were analyzed from stool samples collected monthly from infants participating in a prospective birth cohort study. From that study, 244 IgE sensitized case children and 244 nonsensitized control children were identified based on their allergen-specific IgE antibody levels at the age of 6, 18, and 36 months. Stool samples (n = 4576) from the case and control children were screened for the presence of rhinovirus, enterovirus, norovirus, and parechovirus RNA by reverse transcription quantitative polymerase chain reaction. The study showed that rhinovirus was the most prevalent virus detected, present in 921 (20%) samples. None of the viruses were associated with IgE sensitization in the full cohort but after stratifying by sex, the number of rhinovirus positive samples was inversely associated with IgE sensitization in boys (odds ratio [OR]: 0.81; 95% confidence interval [CI]: 0.69-0.94; P = 0.006). There was also a temporal relation between rhinoviruses and IgE sensitization, as rhinovirus exposure during the first 6 months of life was associated with a reduced risk of subsequent IgE sensitization in boys (OR: 0.76; 95% CI: 0.6-0.94; P = 0.016). In conclusion, early exposure to rhinoviruses was inversely associated with IgE sensitization but this protective association was restricted to boys.
  • Flandroy, Lucette; Poutahidis, Theofilos; Berg, Gabriele; Clarke, Gerard; Dao, Maria-Carlota; Decaestecker, Ellen; Furman, Eeva; Haahtela, Tari; Massart, Sebastien; Plovier, Hubert; Sanz, Yolanda; Rook, Graham (2018)
    Plants, animals and humans, are colonized by microorganisms (microbiota) and transiently exposed to countless others. The microbiota affects the development and function of essentially all organ systems, and contributes to adaptation and evolution, while protecting against pathogenic microorganisms and toxins. Genetics and lifestyle factors, including diet, antibiotics and other drugs, and exposure to the natural environment, affect the composition of the microbiota, which influences host health through modulation of interrelated physiological systems. These include immune system development and regulation, metabolic and endocrine pathways, brain function and epigenetic modification of the genome. Importantly, parental microbiotas have transgenerational impacts on the health of progeny. Humans, animals and plants share similar relationships with microbes. Research paradigms from humans and other mammals, amphibians, insects, planktonic crustaceans and plants demonstrate the influence of environmental microbial ecosystems on the microbiota and health of organisms, and indicate links between environmental and internal microbial diversity and good health. Therefore, overlapping compositions, and interconnected roles of microbes in human, animal and plant health should be considered within the broader context of terrestrial and aquatic microbial ecosystems that are challenged by the human lifestyle and by agricultural and industrial activities. Here, we propose research priorities and organizational, educational and administrative measures that will help to identify safe microbe-associated health-promoting modalities and practices. In the spirit of an expanding version of "One health" that includes environmental health and its relation to human cultures and habits (EcoHealth), we urge that the lifestyle-microbiota-human health nexus be taken into account in societal decision making. (C) 2018 The Authors. Published by Elsevier B.V.