{"title":"Specialised Infant Formulas: Overused, Overpriced and Obesogenic","authors":"Victoria L. Sibson, Susan Westland","doi":"10.1111/cea.14532","DOIUrl":"10.1111/cea.14532","url":null,"abstract":"<p>In Europe, North America and China, most infants are wholly or partially fed with a commercial milk formula during their first year despite consistent public health recommendations promoting breastfeeding. For some nonbreastfed babies, a standard first infant formula may not meet their nutritional needs, because of cows' milk allergy, an inherited metabolic condition, illness or prematurity. These infants may need ‘specialised’ infant formulas, which are classified by the World Health Organization and Food and Agriculture Organization Codex Alimentarius as Foods for Special Medical Purposes (FSMP) [<span>1</span>]. FSMP include low-allergy formulas such as soya formula, extensively hydrolysed formula and amino-acid formula, used for formula-fed infants with cows' milk allergy.</p><p>Legal definitions and regulatory requirements for FSMP are that they should be used under medical supervision and there should be scientific evidence that they are safe and meet the nutritional requirements of the intended target population. In Europe, there is also guidance on how to assess products against these requirements [<span>2</span>]. However, there is a lack of regulatory oversight for FSMP, and they are frequently used without medical supervision. Commercial milk formula companies are often able to choose whether to market a product as FSMP or as a standard infant formula. Thus, in the United Kingdom, antireflux and comfort milks are marketed as FSMP, despite the lack of evidence that comfort milks alleviate colic or constipation, whereas soya formula and lactose-free formula are not marketed as FSMP despite falling under the international definition of FSMP set by Codex. All four product types can be purchased over the counter in pharmacies, and in shops and supermarkets. In the United States, a comprehensive national survey found that almost 60% of formula purchased in stores had reduced or absent lactose [<span>3</span>]. Low-allergy formulas are also lactose-free or lactose-reduced, posing health risks above standard infant formulas because nonlactose carbohydrate sources such as maltodextrin and glucose syrup are associated with dental caries and early childhood obesity [<span>4</span>].</p><p>Other health risks associated with infant FSMP include increased risk of bacterial contamination due to the addition of probiotics, making proper sterilisation impossible, and potential adverse effects from components such as phyto-oestrogens in soya formula and thickeners in antireflux formula. In general, the health risks associated with FSMP are not clearly communicated to consumers through product labelling.</p><p>Infant FSMP not only carry health risks but also are more expensive than their brand-equivalent first infant formulas (Table 1). The record high prices of first infant formula in the current cost of living crisis are a concern for parents and carers, and high prices may lead to unsafe feeding practices [<span>5</span>]. This concern is exacerbat","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 7","pages":"452-454"},"PeriodicalIF":6.3,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14532","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sex Disparities in Asthma Related to Parental and Grandmaternal Smoking Habits—A Population-Based Register Study","authors":"Lennart Bråbäck, Shyamali Chandrika Dharmage, Caroline Lodge, Kadri Meister, Bertil Forsberg","doi":"10.1111/cea.14541","DOIUrl":"10.1111/cea.14541","url":null,"abstract":"<p>There is a mounting body of evidence that grandmaternal smoking increases the risk of asthma not only in their children but also in nonexposed grandchildren [<span>1</span>]. Effects of in utero exposure to tobacco smoke might be transmitted over generations via epigenetic modification of the foetal germ cells suggesting that the effects could be sex specific [<span>2</span>].</p><p>Using prospectively collected data over three generations from Swedish national registries, we have demonstrated that maternal [<span>3</span>] but not paternal [<span>4</span>] grandmother's smoking during pregnancy was related to an increased risk of grandchild asthma. We have now set up a much bigger registry-based cohort also comprising data on paternal smoking from the Swedish conscript registry. Our aim was to assess whether potential effects of grandmaternal and parental smoking were sex specific and whether paternal smoking affected the associations.</p><p>We have used dispensed prescriptions of leukotriene antagonists (Anatomic Therapeutic Chemical (ATC) code R03) and/or inhaled steroids (ATC codes R03AK06, R03AK07, R03AK08, R03AK11, R03BA) as a proxy for asthma. We have defined three phenotypes of asthma during the first 6 years of life as suggested by Martinez et al [<span>5</span>]:</p><p>Early transient asthma was defined as purchase of at least two prescriptions of asthma medication before 3 years of age and no or less than two purchases after 3 years of age, early persistent as at least two purchases also after 3 years of age and late onset as at least two prescriptions after 3 years of age but no or less than two before.</p><p>The study cohort comprised 28,723 children together with their parents and grandmothers. The prevalence of asthma was 7.8%. Grandchild asthma was almost twice as common in boys as in girls. Smoking during pregnancy has declined over the years, and maternal and grandmaternal smoking habits in early pregnancy were closely associated with maternal age. Additional information: https://zenodo.org/doi/10.5281/zenodo.12610766.</p><p>The effects of smoking variables on asthma risk were studied using multinomial logistic regression, with crude, adjusted and interaction models defined in Table 1.</p><p>In the final model with all adjustments allowing interaction between sex and smoking variables, the associations with maternal grandmother's smoking on late onset and early persistent asthma were statistically significantly larger in girls than in boys. Paternal grandmother's smoking had no association with grandchild asthma. However, paternal smoking increased early transient asthma and late-onset asthma in boys, with statistically significantly lower odds ratio (OR) in girls.</p><p>We have also assessed the outcome with a wider definition of asthma based on any asthma medication also including an inhaled beta<sub>2</sub>-agonist (ATC codes R03AC and R03AL). When this asthma definition was considered, maternal grandmother's smoking was a","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 12","pages":"1003-1005"},"PeriodicalIF":6.3,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rebecca C. Knibb, Eva L. Wooding, Heather Padley, Constantinos Petrides, Rosalynd Gourgey, Antony Aston, Louise J. Michaelis, Siân Ludman
{"title":"Psychology Provision for People With Food Allergy: A Survey of UK Healthcare Professionals and Psychologists","authors":"Rebecca C. Knibb, Eva L. Wooding, Heather Padley, Constantinos Petrides, Rosalynd Gourgey, Antony Aston, Louise J. Michaelis, Siân Ludman","doi":"10.1111/cea.14545","DOIUrl":"10.1111/cea.14545","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 11","pages":"933-935"},"PeriodicalIF":6.3,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141731048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sara Benedé, Leticia Pérez-Rodríguez, David Menchén-Martínez, Elena Molina, Rosina López-Fandiño
{"title":"Airway Exposure to House Dust Mite Promotes the Development of Allergy to Egg White in Mice","authors":"Sara Benedé, Leticia Pérez-Rodríguez, David Menchén-Martínez, Elena Molina, Rosina López-Fandiño","doi":"10.1111/cea.14543","DOIUrl":"10.1111/cea.14543","url":null,"abstract":"<p>Cases of adverse reactions to food in young children at their first known exposure have raised intriguing questions about food allergy development, leading to the hypothesis that sensitisation, at least to certain allergens such as peanut, may occur by contact through non-oral pathways like airway inhalation [<span>1</span>]. Interestingly, the biological activity of house dust mite (HDM) allergens stimulates bystander responses to other proteins, which implies that respiratory exposure to food allergens present in domestic dust, such as egg proteins could potentially lead to systemic sensitisation [<span>2</span>]. These findings suggest the possibility that prior sensitisation to egg proteins through the respiratory tract, facilitated by the adjuvant activity of accompanying HDM components, could lead to food allergies when egg is later ingested, in a way similar to that described for peanuts [<span>3, 4</span>]. To test this hypothesis, we used a murine model of sensitisation, without exogenous adjuvants, to investigate the immunostimulant properties of the proteolytically active and inactive forms of HDM in the development of allergy to egg white (EW) when administered either through inhalation or orally. Six-week-old female BALB/c mice received intranasally six doses of HDM, proteolytically inactive HDM (hereafter iHDM), or combinations of EW + HDM and EW + iHDM, followed by eight intragastric gavages with EW, before being intranasally challenged with EW. Materials and methods are provided in the open access repository OSF (https://doi.org/10.17605/OSF.IO/YCNPF).</p><p>Mice that received intranasally EW and its combinations with HDM or iHDM developed EW-specific IgE and IgG1 antibodies, while prior exposure to HDM or iHDM alone did not induce antibodies specific to EW after repeated oral EW administrations over 2 weeks (Figure 1a). Repeated oral administrations of EW did not elicit clinical signs or temperature changes, but, on Day 39, the jejunal concentration of MCP-1 was significantly elevated in mice that had received EW, EW + HDM and EW + iHDM intranasally (Figure 1b), indicating mast cell activation and degranulation in the intestinal mucosa of mice that had produced specific antibodies towards EW. Conversely, intranasal challenge with EW caused anaphylaxis symptoms in the mice that had previously received EW through the airways, particularly in the groups administered EW + HDM and EW + iHDM, which also experienced significant temperature drops, showing that both extracts had adjuvant activity that facilitated airway sensitisation to EW and anaphylaxis following intranasal challenge. Consistently, the concentration of MCP-1 in lung homogenates was significantly elevated in mice exposed to EW + HDM and EW + iHDM (Figure 1b). Mice receiving EW, EW + HDM and EW + iHDM exhibited significantly higher lung levels of IL-6 and IL-4, while the level of TNF-α was significantly higher in the mice exposed to EW + iHDM (Figure 1b). Analyses in t","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 10","pages":"777-780"},"PeriodicalIF":6.3,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14543","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicole L. Messina, Kaya Gardiner, Laure F. Pittet, Emily K. Forbes, Kate L. Francis, Bridget Freyne, Christel Zufferey, Veronica Abruzzo, Clare Morison, Hannah Turner, Katrina J. Allen, Katie L. Flanagan, Anne-Louise Ponsonby, Roy Robins-Browne, Frank Shann, Peter Vuillermin, Susan Donath, Dan Casalaz, Nigel Curtis, the Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) Group
{"title":"Neonatal BCG Vaccination for Prevention of Allergy in Infants: The MIS BAIR Randomised Controlled Trial","authors":"Nicole L. Messina, Kaya Gardiner, Laure F. Pittet, Emily K. Forbes, Kate L. Francis, Bridget Freyne, Christel Zufferey, Veronica Abruzzo, Clare Morison, Hannah Turner, Katrina J. Allen, Katie L. Flanagan, Anne-Louise Ponsonby, Roy Robins-Browne, Frank Shann, Peter Vuillermin, Susan Donath, Dan Casalaz, Nigel Curtis, the Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) Group","doi":"10.1111/cea.14537","DOIUrl":"10.1111/cea.14537","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The beneficial off-target effects of Bacille Calmette–Guérin (BCG) vaccination potentially include protection against allergy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>In the MIS BAIR trial, we aimed to determine whether neonatal BCG vaccination reduces atopic sensitisation and clinical food allergy in infants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this randomised controlled trial, 1272 neonates were allocated to BCG-Denmark vaccine (0.05 mL intradermal dose) or no BCG at birth. Randomisation was stratified by recruitment site, mode of delivery and plurality of birth. The primary outcome was the incidence of atopic sensitisation determined by skin prick test at 1 year of age. Food allergy was determined by 3-monthly online questionnaires and oral food challenges. Data were analysed by intention-to-treat using binary regression. Clinicaltrials.gov (NCT01906853).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Atopic sensitisation during the first year of life was 22.9% among infants in the BCG group and 18.9% in the control group (adjusted risk difference (aRD) 3.8% (95% CI −1.5 to 9.1) after multiple imputation). Clinical food allergy was similar between infants in the BCG and control groups (9.8% vs. 9.6%; aRD 0.2, 95% CI −3.4 to 3.8). An interaction was observed between the primary outcome and maternal history of BCG vaccination. No interaction was observed for the additional prespecified potential effect modifiers tested (sex, delivery mode, family history of any allergy, season of birth, hepatitis B vaccination at randomisation, BCG scar and age at BCG administration).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions and Clinical Relevance</h3>\u0000 \u0000 <p>Neonatal BCG-Denmark vaccination does not protect against atopic sensitisation or clinical food allergy in the first year of life.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 9","pages":"682-693"},"PeriodicalIF":6.3,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14537","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiakai Wu, Chiara Tontini, Ran Wang, Silvia Bulfone-Paus, Clare S. Murray, Angela Simpson
{"title":"Basophil Activating Factors in the Serum May Underlie the ‘Nonreleaser’ Basophil Status in the Basophil Activation Test","authors":"Jiakai Wu, Chiara Tontini, Ran Wang, Silvia Bulfone-Paus, Clare S. Murray, Angela Simpson","doi":"10.1111/cea.14542","DOIUrl":"10.1111/cea.14542","url":null,"abstract":"<p>Basophil activation test (BAT) has been increasingly used in allergy diagnosis. For certain food allergies, such as nut allergy, BAT has demonstrated high specificity and sensitivity in distinguishing allergic and tolerant subjects, which helps reduce the need for oral food challenges [<span>1</span>]. However, it has been reported that 10%–20% of subjects display ‘nonreleaser’ basophils due to spleen tyrosine kinase (Syk) deficiency [<span>2, 3</span>]. Although one study showed that ‘nonreleasers’ had a reduction in the incidence of allergic rhinitis [<span>3</span>], the status of ‘nonreleaser’ can change over time [<span>4</span>], and therefore, the clinical implications remain unknown.</p><p>The underlying cause of a ‘nonreleaser’ state remains unclear. The nonreleaser state is characterised as no response to IgE-mediated stimulation, via anti-FcεRI or anti-IgE engagement. In contrast, degranulation mediated by IgE-independent mechanisms remains intact, such as stimulation via G-protein–coupled fMLP receptors using fMLP [<span>5</span>]. The nonreleaser state is not a result of a genetic defect, as Syk is expressed normally in other granulocytes, such as eosinophils and neutrophils, and B cells, suggesting a separate regulation in basophils via mechanisms that remain largely unknown [<span>4</span>]. Although some researchers have speculated that it could be a protective mechanism for some individuals [<span>3</span>], a better explanation is needed as to why only basophils seem to be affected.</p><p>We hypothesise that a basophil-specific self-activating mechanism from the patient's own serum might be responsible for the observed ‘nonreleaser’ state. Loss of Syk in human basophils through IgE or non–IgE-dependent stimulation was reported previously [<span>6, 7</span>]. However, a clear link between nonreleaser basophils and basophil-specific self-activation mechanism was not established.</p><p>To investigate this hypothesis, we identified subjects most likely to carry basophils with impaired IgE-mediated degranulation function. To do this, we performed BAT using whole blood of subjects sensitised to at least one allergen (<i>n</i> = 30) and were not taking oral corticosteroids (Path 1 of Figure 1A). In parallel, subjects' sera were frozen, and batch tested using the progenitor cell derived basophils (PCB) [<span>8</span>]. This includes progenitor cell derived basophil activation test (PCBAT, Path 2 of Figure 1A) and serum-induced PCB activation test (Paths 3–4 of Figure 1A). Informed consent was obtained for all subjects (Rec reference: 20/NW/0302). Both BAT and PCBAT used 1 μg/mL anti-IgE as stimulant, and the percentage of degranulation was measured via CD63 expression compared with unstimulated control using flow cytometry.</p><p>While BAT results combine subject-dependent humoral and cellular factors, PCBAT only reflects the subjects' humoral responses via passive sensitisation of donor basophils using subjects' own sera (Figure 1A","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 10","pages":"774-776"},"PeriodicalIF":6.3,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14542","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Matteo Martini, Marina Mauro, Donatella Bignardi, Patrizia Bonadonna, Maria Chiara Braschi, Francesca Emiliani, Laura Guerra, Serena Liberati, Francesco Olivieri, Valerio Pravettoni, Donatella Preziosi, Erminia Ridolo, Federica Rivolta, Ilaria Baiardini, Maria Beatrice Bilò
{"title":"Quality of Life in Hymenoptera Venom Allergy: Minimal Clinically Important Difference for the Vespid Quality of Life Questionnaire","authors":"Matteo Martini, Marina Mauro, Donatella Bignardi, Patrizia Bonadonna, Maria Chiara Braschi, Francesca Emiliani, Laura Guerra, Serena Liberati, Francesco Olivieri, Valerio Pravettoni, Donatella Preziosi, Erminia Ridolo, Federica Rivolta, Ilaria Baiardini, Maria Beatrice Bilò","doi":"10.1111/cea.14540","DOIUrl":"10.1111/cea.14540","url":null,"abstract":"<p>Hymenoptera venom allergy (HVA) poses significant health concerns with implications for Health-Related Quality of Life (HRQoL) [<span>1</span>]. However, the Vespid Quality of Life Questionnaire (VQLQ), already validated in several languages to measure HRQoL in HVA [<span>2, 3</span>], lacks a formal minimal clinically important difference (MCID), limiting a comprehensive assessment of HRQoL. In fact, the commonly used 0.5 cut-off [<span>4</span>] is extrapolated from questionnaires with different characteristics that are used in different fields [<span>5</span>].</p><p>The objective of this multicenter, prospective, longitudinal, cohort study was to calculate a formal MCID for the VQLQ and to use it for a deeper multi-endpoint investigation of HRQoL, through the implementation of the MCID-event frequency and the time-to-MCID endpoints, in addition to the standard VQLQ score.</p><p>Seven Italian HVA-specialised allergy centers consecutively enrolled adult patients with HVA to Yellow Jacket, eligible to venom immunotherapy (VIT), and they were stratified into the following groups: pre-VIT, on-VIT (for <1 year, ≥1 to <3 years, ≥3 to ≤5 years) and post-VIT. The VQLQ, the Expectation of Outcome questionnaire (EoO), the Psychological General Well-Being Index (PGWBI) and the Global Rating Scale (GRS) were administered at baseline and after 1 year of follow-up. The correlation between VQLQ and the other questionnaires (Pearson's <i>r</i> correlation coefficient) was preliminary performed to test the external validity of VQLQ and to find the best anchor for the MCID analysis. The MCID was calculated with an anchor-based approach using the area under the curve (AUC) of the receiver operating curves (ROC) analysis to find the best VQLQ score difference, after follow-up, in detecting the MCID (whole cohort method) [<span>6</span>]. The global rating of change was measured using EoO, PGWBI and GRS, considering an improvement of at least +1 score, after 12 months of follow-up, as a standard reference for the ROC analysis. The best MCID was chosen according to the Youden method. Two additional sensitivity analyses for MCID calculation were performed, using anchor-based and distribution-based methods (additional information about study methods is available in the following repository: https://doi.org/10.5281/zenodo.11623493). A sample size of 140 patients was estimated to detect a 0.5 effect size (i.e. MCID used in previous studies [<span>4</span>]) of the mean VQLQ among the pre-planned VIT groups, in the cross-sectional analysis (one-way ANOVA, alpha = 5%, power = 80%). At least 33 patients were to be in the pre-VIT group, in order to obtain an effect size of 0.5 after 12 months of VIT, in the longitudinal analysis (paired <i>t</i>-test, alpha = 5%, power = 80%); the other patients were planned to be equally distributed over the other VIT groups. All the statistical analyses were performed with STATA v.18 (StataCorp LLC, Texas, USA). The study was ap","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 12","pages":"996-998"},"PeriodicalIF":6.3,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Didier G. Ebo, Michel Van Houdt, Michiel Beyens, Alessandro Toscano, Christel Mertens, Athina L. Van Gasse, Pierre Bruhns, Vito Sabato, Jessy Elst
{"title":"IgE-Mediated Mast Cell Responses to Rocuronium: A Matter of Protonation Status","authors":"Didier G. Ebo, Michel Van Houdt, Michiel Beyens, Alessandro Toscano, Christel Mertens, Athina L. Van Gasse, Pierre Bruhns, Vito Sabato, Jessy Elst","doi":"10.1111/cea.14536","DOIUrl":"10.1111/cea.14536","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 10","pages":"760-762"},"PeriodicalIF":6.3,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jasmijn A. Schrumpf, Dennis K. Ninaber, Christoph Müller, Bettina Rankl, Mikaela Tham, Erika von Mutius, Hermelijn H. Smits, Pieter S. Hiemstra
{"title":"Farm Dust Exposure Reduces Cytokine- and Rhinovirus-Induced IL-33 Expression in Bronchial Epithelial Cells","authors":"Jasmijn A. Schrumpf, Dennis K. Ninaber, Christoph Müller, Bettina Rankl, Mikaela Tham, Erika von Mutius, Hermelijn H. Smits, Pieter S. Hiemstra","doi":"10.1111/cea.14535","DOIUrl":"10.1111/cea.14535","url":null,"abstract":"<p>Pre-school wheeze, attributed to respiratory viral infections, with rhinovirus (RV) being the most important risk factor, may contribute to early-onset asthma development [<span>1, 2</span>]. In asthmatic children, the alarmin IL-33 is elevated in the airways and is involved in the development of T helper (Th)2 immunity and in Th2-driven immune responses to RV [<span>3, 4</span>]. Although IL-33 is constitutively expressed, IL-33 is also increased in response to pro-inflammatory cytokines like TNF-α and IFN-γ and after RV infections in airway epithelial cells [<span>5, 6</span>]. Children that grow up on traditional farms develop less wheezing, allergies and asthma [<span>7</span>]. This is partly caused by dust exposure from cow stables [<span>7</span>]. Furthermore, exposure to farm dust (FD) extract or its components protects against house dust mite (HDM)–induced allergic airway inflammation in mice [<span>7</span>] and enhances epithelial barrier function and RV clearance in primary bronchial epithelial cells (PBEC) [<span>7</span>]. Currently, the effects of FD on the alarmin IL-33 in human airway epithelial cells have not been investigated. The present study aims to investigate how exposure to FD affects the expression of IL-33 in PBEC. This article's Online Repository at Zenodo (https://zenodo.org/records/10417793) contains an extended version of this letter, including supporting data and a full description of methods.</p><p>To achieve our objective, submerged (S-) cultures of PBEC were pre-treated with FD for 24 h before being infected with RV-A1B for 48 h. Alternatively, cells were stimulated with TNF-α and INF-γ in the presence or absence of FD for 6 and 8 h. Changes in gene expression and protein levels were assessed using qPCR and HEK-Blue IL-33 reporter cells. We observed that FD pretreatment inhibited RV-mediated increase of <i>IL33</i> mRNA, without affecting viral RNA (vRNA) levels (Figure 1A). We furthermore showed that FD decreased the TNF-α-/IFN-γ-induced expression of <i>IL33</i> mRNA and protein in S-PBEC (Figure 1B). We further observed that FD reduced the TNF-α-/IFN-γ-induced expression levels of both IL-33 mRNA and protein in differentiated (ALI-)PBEC. However, effects of both TNF-α/IFN-γ-exposure and FD treatment were less prominent in ALI-PBEC, compared to S-PBEC (Online Repository).</p><p>We next explored the mechanism underlying the reduction of TNF-α-/IFN-γ-induced IL-33 by FD. We therefore pre-treated S-PBEC for 1 h with inhibitors of downstream IFN-γ signalling pathways or FD and stimulated with IFN-γ (a key driver of TNF-α-/IFN-γ-mediated IL-33 expression [<span>8</span>]) for 6 h to assess <i>IL33</i> mRNA expression and for 30 min for the analysis of phosphorylated (p-)STAT1, p-p38, p-EGFR and GAPDH. In addition to FD, inhibition of JAK–STAT, p38 MAPK and EGFR also decreased <i>IL33</i> expression in S-PBEC (Figure 1C). Western blot analysis showed that FD partially inhibited p-STAT1 (with a trend towards sign","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"54 10","pages":"766-769"},"PeriodicalIF":6.3,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.14535","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}