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Objective Anxiety is among the major psychological concerns for children living with food allergy (FA). Yet research exploring the variables driving anxiety symptoms in FA remains sparse, and most studies still utilize homogeneous samples to assess anxiety symptoms. The current study seeks to evaluate the rates of clinically significant anxiety symptoms among a diverse sample of youth with FA and examine whether a heightened risk perception of FA outcomes and FA burden (vs. FA medical history) is associated with anxiety in youth. Methods 94 youth ages 10–14 and their parents were recruited from FA clinics at a mid-Atlantic children's hospital. Both youth and parents completed demographic and FA medical history questionnaires, the Screen for Child Anxiety Related Emotional Disorders, and the Food Allergy Independent Measure as part of a longitudinal study about FA adjustment and adherence. Results Over a third (37%) of youth scored above clinical cut-offs for overall anxiety symptoms. At least 25% of youth reported clinically significant scores on panic disorder, generalized anxiety, social anxiety, separation anxiety, and school avoidance subscales. Perception of risk of adverse FA outcomes and burden—but not FA medical history–were associated with total anxiety, generalized anxiety, panic disorder, and school avoidance symptoms, but not social anxiety and separation anxiety. Having more FAs was associated with higher social anxiety scores but not with other anxiety subscales. Conclusions Youth with FA might benefit from psychosocial interventions that address FA risk perception management and promote appropriate FA vigilance to cope with anxiety symptoms. [ABSTRACT FROM AUTHOR]

Asthma, a prevalent chronic respiratory condition affecting millions of children globally, presents a significant health challenge. This review critically examines the developmental pathways of asthma in children, focusing on genetic, environmental, and early-life determinants. Specifically, we explore the impact of prenatal and postnatal factors such as maternal smoking, nutrition, respiratory infections, and allergen exposure on asthma development. Our analysis highlights the intricate interplay of these influences and their contribution to childhood asthma. Moreover, we emphasize targeted strategies and interventions to mitigate its burden, including genetic counseling for at-risk families, environmental modifications to reduce triggers, and early-life immunomodulation. By delving into these preventive measures and interventions, our review aims to provide actionable insights for healthcare professionals in developing tailored strategies to address the complexities of childhood asthma. In summary, this article offers a detailed examination of asthma development in children, aiming to enhance understanding and inform efforts to reduce its burden through targeted interventions. [ABSTRACT FROM AUTHOR]

Background: Allergic rhinitis (AR) is a typical type 2 inflammatory disease and eosinophils play a critical role of cardinal effectors in type 2 inflammation. However, the distribution of eosinophils in patients with different subtypes of rhinitis and the effect of allergen exposure on them remain understudied. The aim of this study was to investigate the characteristics and factors influencing the distribution of systemic and local eosinophils in patients with non-AR (NAR), perennial AR (PAR), and seasonal AR (SAR), as well as the effect of seasonal allergen exposure levels on eosinophils. Methods: This was a population-based, cross-sectional observational study of consecutive chronic rhinitis (CR) outpatients who volunteered to participate in the survey during the spring pollen season and non-pollen season of 2023 in Beijing. All participants underwent serum allergen testing, blood routine examination, and nasal secretion smear cytology, and completed questionnaires mainly involving basic information, history review, and symptom assessment. Spring pollen dispersal concentration were considered. Results: A total of 558 CR patients eligible for enrollment were collected, including 198 NAR, 204 PAR, and 156 SAR patients. PAR had the highest blood eosinophil levels and the most severe overall nasal and ocular symptoms of SAR. Compared with subjects with blood eosinophil counts

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BackgroundRegulatory T cells (Tregs) contribute to the maintenance of immunological tolerance. There is evidence of impaired function of these cells in people with asthma and allergy. In this study, we evaluated and compared the function of Tregs in allergic asthmatic and allergic non-asthmatic patients, both before and after low-dose allergen challenges.MethodsThree groups of subjects were recruited for a baseline evaluation: healthy controls without allergy or asthma, allergic asthmatic subjects, and allergic non-asthmatic subjects. All of them were subjected to expiratory flow measurements, sputum induction, and blood sampling. In addition, both groups of allergic subjects underwent low-dose allergen challenges. Tregs were isolated from whole blood using CD4+CD25high and CD127low staining. The suppression function was measured by flow cytometry. The levels of IL-10, IFN-γ, IgG4, IgA, and TGF-β were measured using ELISA, and sputum Foxp3 was evaluated using qRT-PCR.ResultsThe suppressive function of Tregs in healthy controls was significantly higher than in allergic asthmatic or allergic non-asthmatic subjects. Repeated exposure to low doses of allergen increased the suppressor function of Tregs in allergic non-asthmatic subjects but decreased it in allergic asthmatic subjects. Foxp3 gene expression was increased in induced sputum in allergic non-asthmatic subjects, whereas it did not change in asthmatic subjects. Serum IL-10 level was decreased in allergic asthmatic subjects after allergen challenge but not in allergic non-asthmatic subjects. IFN-γ level increased upon allergen challenge in allergic non-asthmatic subjects. IgG4 level was higher in allergic non-asthmatic subjects than in allergic asthmatic subjects.ConclusionsLow-dose allergen challenges stimulate the suppressor function of Tregs in non-asthmatic allergic subjects but not in allergic asthmatic subjects.

Abstract Background The typical clinical symptoms of allergic rhinitis (AR) are known to be associated with allergen exposure; however, the underlying mechanisms are not fully understood. We wanted to gain a comprehensive view of the molecular mechanisms related to allergen exposure in a well-controlled mouse model of AR. Methods An OVA-induced AR model was developed. Two hours and 4 weeks after the last OVA challenge, AR symptoms and local immune responses were assessed. At the same time, differentially expressed genes (DEG) in nasal mucosa were identified by gene expression microarray and further analyzed by bioinformatics methods. Verification of DEG was done by quantitative RT-PCR and immunohistochemistry. Results The number of nasal rubbings and sneezes, serum OVA-specific IgE concentrations, and the number of neutrophils and eosinophils in the nasal mucosa were significantly increased at 2 h and decreased at 4 weeks after the last allergen challenge compared to controls. A total of 2119 DEG were identified, and their expression dynamics were clustered into 8 profiles. Enriched functions in Profile 5, which had a similar trend to clinical features, were mainly related to inflammatory and immune response to environmental factors, eosinophils and neutrophils chemotaxis, and cell migration. Gene co-expression Network for genes from profile 5 identified BCL3, NFKB2, SOCS3, and CD53 having a higher degree. Profile 6 showed persistence of inflammatory and immune response at 4 weeks after the last allergen challenge. Olfactory and coagulation functions were enriched mainly in profiles with downward trends. Conclusions A wide range of genes with sequential cooperative action were identified to be associated with allergen exposure in AR. BCL3 may be the most vital in symptoms manifestation. Moreover, some inflammatory responses persisted for a period after allergen exposure, supporting a new treatment strategy of targeting inflammation out of season. This study may contribute to a better understanding of AR pathogenesis and provide potential therapeutic targets for AR patients.

Background: The typical clinical symptoms of allergic rhinitis (AR) are known to be associated with allergen exposure; however, the underlying mechanisms are not fully understood. We wanted to gain a comprehensive view of the molecular mechanisms related to allergen exposure in a well-controlled mouse model of AR. Methods: An OVA-induced AR model was developed. Two hours and 4 weeks after the last OVA challenge, AR symptoms and local immune responses were assessed. At the same time, differentially expressed genes (DEG) in nasal mucosa were identified by gene expression microarray and further analyzed by bioinformatics methods. Verification of DEG was done by quantitative RT-PCR and immunohistochemistry. Results: The number of nasal rubbings and sneezes, serum OVA-specific IgE concentrations, and the number of neutrophils and eosinophils in the nasal mucosa were significantly increased at 2 h and decreased at 4 weeks after the last allergen challenge compared to controls. A total of 2119 DEG were identified, and their expression dynamics were clustered into 8 profiles. Enriched functions in Profile 5, which had a similar trend to clinical features, were mainly related to inflammatory and immune response to environmental factors, eosinophils and neutrophils chemotaxis, and cell migration. Gene co-expression Network for genes from profile 5 identified BCL3, NFKB2, SOCS3, and CD53 having a higher degree. Profile 6 showed persistence of inflammatory and immune response at 4 weeks after the last allergen challenge. Olfactory and coagulation functions were enriched mainly in profiles with downward trends. Conclusions: A wide range of genes with sequential cooperative action were identified to be associated with allergen exposure in AR. BCL3 may be the most vital in symptoms manifestation. Moreover, some inflammatory responses persisted for a period after allergen exposure, supporting a new treatment strategy of targeting inflammation out of season. This study may contribute to a better understanding of AR pathogenesis and provide potential therapeutic targets for AR patients. [ABSTRACT FROM AUTHOR]

Severe asthma (SA) is categorized into multiple overlapping phenotypes and clinical characteristics driven by complex mechanistic inflammatory pathways. Mepolizumab is a human monoclonal antibody effectively targeting interleukin-5 in severe eosinophilic asthma. However, the eligibility of biologics in coincident SA phenotypes is still unclear. We assessed the efficacy and safety of mepolizumab in real-life patients with the overlapping T2-high SA endotype. This was a phase IV, single-centre observational cohort study including patients with severe refractory T2-high asthma in treatment with mepolizumab. After 12 months of treatment with mepolizumab, significant improvements (p < 0.0001) in asthma control and lung function were recorded. Rates of clinically significant annual asthma exacerbation were also decreased by 71.22% after 52-week therapy with mepolizumab (p < 0.001) associated with a reduction in the mean daily dose of oral corticosteroids. Two patients (3.27%) had to discontinue mepolizumab due to musculoskeletal disorders with no severe safety issues reported. The use of mepolizumab as an add-on therapy in routine clinical practice was safely associated with significant clinical and functional in the overlapping eosinophilic-and-allergic SA phenotype. The current data should support clinical and therapeutic decision-making in this T2-high SA endotype. [ABSTRACT FROM AUTHOR]

The links between allergen exposure and sensitization are complex and depend not only on the type of allergen but on various genetic and environmental factors. This review discusses the link between allergen exposure and atopic sensitization for different types of allergens and the factors that mediate or affect this link. For the purposes of this review search of PubMed was undertaken to identify English language articles using the terms 'sensitization' and 'allergen exposure' and 'children/or adolescents.' Regarding food sensitization, the available data for peanuts and eggs suggest that there is a window period between 4 and 6 months of age when the introduction of these foods may limit sensitization and clinically overt allergy to the respective foods. As far as it concerns aeroallergens, it seems that there is a complex and variable relationship between mite exposure and specific sensitization especially if the exposure occurs early in life. Early exposure to dog allergens does not seem to be associated with specific sensitization; regarding cats, the results are still inconsistent. Several factors may mediate the relationship between early exposure to allergens and the development of sensitization or clinical allergy. [ABSTRACT FROM AUTHOR]

Storage mites (SM) may induce allergic respiratory symptoms in sensitized individuals, in both rural and urban settings. The relationship among specific IgE reactions to determined groups of SM allergens in the coincident asthma pheno-endotypes has not yet been investigated. We aimed to study a Precision Allergy Molecular Diagnosis (PAMD@) model to depict the SM molecular profile in individuals presenting with Type-2 inflammation, in two different (moderate and severe) asthma phenotypes. A customized PAMD@ panel, including SM allergens and their concurrent protein allergenic characterization was investigated. Mite group 2 allergens were most frequently recognized, including Lep d 2 (83.45%), followed by Gly d 2 (69.17%) and Tyr p 2 (47,37%), in 133/164 asthmatic subjects. Blo t 5 and Blo t 21 exhibited significant higher titres in both asthma groups. Although relevant mite group 2 allergens cross-reactivity is suggested, individualized sensitization patterns were relevantly identified. The present PAMD@ panel confirmed the dominance of mite group 2 allergens in moderate-to-severe T2 asthmatics. A broadly heterogeneous molecular repertoire of SM allergens was found in all subjects, regardless of their asthma severity. Blomia tropicalis deserves special attention in certain territories, as diagnostic and/or therapeutic approaches merely based on Pyroglyphidae mites may be insufficient. [ABSTRACT FROM AUTHOR]

BackgroundProtease resistance is considered a risk factor for allergenicity of proteins, although the correlation is low. It is nonetheless a part of the weight-of-evidence approach, proposed by Codex, for assessing the allergenicity risk of novel food proteins. Susceptibility of proteins to pepsin is commonly tested with purified protein in solution.ObjectiveFood proteins are rarely consumed in purified form. Our aim was to evaluate the impact of experimental and endogenous food matrices on protease susceptibility of homologous protein pairs with different degrees of allergenicity.MethodsPorcine and shrimp tropomyosin (ST) were subjected to sequential exposure to amylase, pepsin, and pancreatin in their respective endogenous matrix (pork tenderloin/boiled shrimp) and in three different experimental matrices (dessert mousse [DM], soy milk [SM], and chocolate bar [CB]). Digestion was monitored by immunoblotting using tropomyosin-specific antibodies. Recombinant peach and strawberry lipid transfer protein were biotinylated, spiked into both peach and strawberry fruit pulp, and subjected to the same sequential digestion protocol. Digestion was monitored by immunoblotting using streptavidin for detection.ResultsChocolate bar, and to a lesser extent SM, had a clear protective effect against pepsin digestion of porcine tropomyosin (PT) and to a lesser extent of ST. Increased resistance was associated with increased protein content. Spiking experiments with bovine serum albumin (BSA) confirmed the protective effect of a protein-rich matrix. The two tropomyosins were both highly resistant to pepsin in their protein-rich and lean native food matrix. Pancreatin digestion remained rapid and complete, independent of the matrix. The fat-rich environment did not transfer protection against pepsin digestion. Spiking of recombinant peach and strawberry lipid transfer proteins into peach and strawberry pulp did not reveal any differential protective effect that could explain differences in allergenicity of both fruits.ConclusionsProtein-rich food matrices delay pepsin digestion by saturating the protease. This effect is most apparent for proteins that are highly pepsin susceptible in solution. The inclusion of food matrices does not help in understanding why some proteins are strong primary sensitizers while homologs are very poor allergens. Although for induction of symptoms in food allergic patients (elicitation), a protein-rich food matrix that may contribute to increased risk, our results indicate that the inclusion of food matrices in the weight-of-evidence approach for estimating the potential risks of novel proteins to become allergens (sensitization), is most likely of very limited value.

Rationale: Environmental exposures have been associated with adverse outcomes in chronic obstructive pulmonary disease (COPD). Approximately one-third of individuals with COPD have allergic sensitization, but it is unknown whether exposure to allergens in the home is associated with outcomes. Objectives: To determine the prevalence and associations of allergen sensitization with exposure to common indoor allergens with symptoms and exacerbation risk in COPD. Methods: Allergen sensitization to five common indoor allergens was assessed in former smokers with COPD. Home settled dust was assessed for presence of corresponding allergens. Sensitization and exposure status was determined and associations evaluated in adjusted models with longitudinal outcomes including symptoms, lung function, and exacerbations. Interactions were assessed between sensitization/exposure status and lung function. Measurements and Main Results: One hundred eighty-three individuals studied were on average 67.3 years of age (SD, 8.22) with average FEV1 of 53.2% (SD, 17.6%). Seventy-seven percent of participants were exposed to at least one tested allergen, and 17% had sensitization with corresponding allergen exposure. After adjustment, sensitization with exposure was associated with lower lung function (β, -8.29; 95% confidence interval [CI], -14.80 to -1.77), higher St. George's Respiratory Questionnaire Total Score (β, 6.71; 95% CI, 0.17 to 13.25), and higher exacerbation risk (odds ratio, 2.31; 95% CI, 1.11 to 4.79). Associations appeared to be more pronounced among individuals with lower lung function. Conclusions: Allergen exposures are common in COPD and associated with adverse outcomes among those with concomitant allergen sensitization. This study establishes allergens as an important home exposure that potentially could be addressed with comprehensive home environmental modification strategies to improve COPD outcomes. [ABSTRACT FROM AUTHOR]

Severe asthma (SA) is categorized into multiple overlapping phenotypes and clinical characteristics driven by complex mechanistic inflammatory pathways. Mepolizumab is a human monoclonal antibody effectively targeting interleukin-5 in severe eosinophilic asthma. However, the eligibility of biologics in coincident SA phenotypes is still unclear. We assessed the efficacy and safety of mepolizumab in real-life patients with the overlapping T2-high SA endotype. This was a phase IV, single-centre observational cohort study including patients with severe refractory T2-high asthma in treatment with mepolizumab. After 12 months of treatment with mepolizumab, significant improvements (p < 0.0001) in asthma control and lung function were recorded. Rates of clinically significant annual asthma exacerbation were also decreased by 71.22% after 52-week therapy with mepolizumab (p < 0.001) associated with a reduction in the mean daily dose of oral corticosteroids. Two patients (3.27%) had to discontinue mepolizumab due to musculoskeletal disorders with no severe safety issues reported. The use of mepolizumab as an add-on therapy in routine clinical practice was safely associated with significant clinical and functional in the overlapping eosinophilic-and-allergic SA phenotype. The current data should support clinical and therapeutic decision-making in this T2-high SA endotype.

The consequences of climate change, the increasing frequency, duration and intensity of extreme events such as excessive drought, heat waves, large-scale forest fires, heavy rainfall and associated flooding also affect workers' conditions in the workplace in many ways. Allergic diseases of the respiratory tract and skin due to workplace exposure can also arise or be influenced by direct and indirect consequences of climate change. This affects outdoor workers not only through increased exposure to pollen allergens, but also through climate-related increases in typical workplace allergens. As an indirect effect of climate change, manufacturing processes and exposure at workplaces are changing, which can also cause new sensitization and allergies. Lifestyle changes, which are primarily intended to contribute to climate protection and sustainability, can also lead to new or changed products and thus to changed manufacturing processes and exposures in the workplace, so this should also be considered an indirect effect of climate change on the health of workers. The emergence of new occupational sources of sensitization due to new or changed allergen exposures must be considered in the context of occupational health and safety and requires proactive measures to protect workers., (© 2023. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Background: Regulatory T cells (Tregs) contribute to the maintenance of immunological tolerance. There is evidence of impaired function of these cells in people with asthma and allergy. In this study, we evaluated and compared the function of Tregs in allergic asthmatic and allergic non-asthmatic patients, both before and after low-dose allergen challenges., Methods: Three groups of subjects were recruited for a baseline evaluation: healthy controls without allergy or asthma, allergic asthmatic subjects, and allergic non-asthmatic subjects. All of them were subjected to expiratory flow measurements, sputum induction, and blood sampling. In addition, both groups of allergic subjects underwent low-dose allergen challenges. Tregs were isolated from whole blood using CD4 + CD25 high and CD127 low staining. The suppression function was measured by flow cytometry. The levels of IL-10, IFN-γ, IgG4, IgA, and TGF-β were measured using ELISA, and sputum Foxp3 was evaluated using qRT-PCR., Results: The suppressive function of Tregs in healthy controls was significantly higher than in allergic asthmatic or allergic non-asthmatic subjects. Repeated exposure to low doses of allergen increased the suppressor function of Tregs in allergic non-asthmatic subjects but decreased it in allergic asthmatic subjects. Foxp3 gene expression was increased in induced sputum in allergic non-asthmatic subjects, whereas it did not change in asthmatic subjects. Serum IL-10 level was decreased in allergic asthmatic subjects after allergen challenge but not in allergic non-asthmatic subjects. IFN-γ level increased upon allergen challenge in allergic non-asthmatic subjects. IgG4 level was higher in allergic non-asthmatic subjects than in allergic asthmatic subjects., Conclusions: Low-dose allergen challenges stimulate the suppressor function of Tregs in non-asthmatic allergic subjects but not in allergic asthmatic subjects., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Klein, Plante, Boulay, Boulet and Chakir.)

The school is a microenvironment well-known to host many indoor allergens and pollutants, with a strong association between school allergen exposure and childhood asthma morbidity. Despite advances in therapies, asthma continues to be one of the most common chronic conditions among children, associated with significant morbidity, health care utilization, and productivity loss. Asthma prevalence is also disproportionately high among children in minority communities. This review will focus on environmental exposures associated with asthma morbidity (cockroach, mouse, cat and dog, dust mite, fungus, air pollution). This review will also discuss recent school-based interventions to improve allergy morbidity among school-aged children. Understanding the multifaceted environmental factors which may contribute to asthma pathogenesis is necessary to help guide potential school-based interventions., Competing Interests: Acknowledgments Grant IDs:1. 5K24AI106822 2. 5U01AI126614 3. 5R01HL137192 4. 5UO1AI1103975. Co-Author Tina Banzon also has a NIH T32 grant which should be placed on the cover: NIH T32 AI7512-35. Disclosure All authors do not have any financial and personal relationships with other people or organizations that could influence (bias) their work. The authors have no disclosures of any affiliation with any organization with a financial interest, direct or indirect, in the subject matter or materials discussed in the article (such as consultancies, employment, paid expert testimony, honoraria, speaker’s bureaus, retainers, stock options or ownership, patents or patent applications or travel grants) that may affect the conduct or reporting of the work submitted., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Protease resistance is considered a risk factor for allergenicity of proteins, although the correlation is low. It is nonetheless a part of the weight-of-evidence approach, proposed by Codex, for assessing the allergenicity risk of novel food proteins. Susceptibility of proteins to pepsin is commonly tested with purified protein in solution., Objective: Food proteins are rarely consumed in purified form. Our aim was to evaluate the impact of experimental and endogenous food matrices on protease susceptibility of homologous protein pairs with different degrees of allergenicity., Methods: Porcine and shrimp tropomyosin (ST) were subjected to sequential exposure to amylase, pepsin, and pancreatin in their respective endogenous matrix (pork tenderloin/boiled shrimp) and in three different experimental matrices (dessert mousse [DM], soy milk [SM], and chocolate bar [CB]). Digestion was monitored by immunoblotting using tropomyosin-specific antibodies. Recombinant peach and strawberry lipid transfer protein were biotinylated, spiked into both peach and strawberry fruit pulp, and subjected to the same sequential digestion protocol. Digestion was monitored by immunoblotting using streptavidin for detection., Results: Chocolate bar, and to a lesser extent SM, had a clear protective effect against pepsin digestion of porcine tropomyosin (PT) and to a lesser extent of ST. Increased resistance was associated with increased protein content. Spiking experiments with bovine serum albumin (BSA) confirmed the protective effect of a protein-rich matrix. The two tropomyosins were both highly resistant to pepsin in their protein-rich and lean native food matrix. Pancreatin digestion remained rapid and complete, independent of the matrix. The fat-rich environment did not transfer protection against pepsin digestion. Spiking of recombinant peach and strawberry lipid transfer proteins into peach and strawberry pulp did not reveal any differential protective effect that could explain differences in allergenicity of both fruits., Conclusions: Protein-rich food matrices delay pepsin digestion by saturating the protease. This effect is most apparent for proteins that are highly pepsin susceptible in solution. The inclusion of food matrices does not help in understanding why some proteins are strong primary sensitizers while homologs are very poor allergens. Although for induction of symptoms in food allergic patients (elicitation), a protein-rich food matrix that may contribute to increased risk, our results indicate that the inclusion of food matrices in the weight-of-evidence approach for estimating the potential risks of novel proteins to become allergens (sensitization), is most likely of very limited value., Competing Interests: EI was employed by BASF Corporation. GL was employed by Dupont Nutrition and Biosciences. SM was employed by SAS Institute. AS was employed by Bayer U.S. Crop Science. RR was reported consultancy for HAL Allergy, Citeq, Angany, Reacta Healthcare, Mission MightyMe, AB Enzymes. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Akkerdaas, Cianferoni, Islamovic, Kough, Ladics, McClain, Poulsen, Silvanovich, Pereira Mouriès and van Ree.)

Summary: Anaphylaxis is the most severe systemic hypersensitivity reaction, it can be caused by a number of well identified triggers such as foods, drugs, stinging insects and facilitated by predisposing clinical conditions. However, sometimes anaphylaxis shows up with uncommon or peculiar characteristics which could delay diagnosis and therapeutic treatment. In this report we aimed to describe less accounted / difficult-to-approach shapes of anaphylaxis to facilitate clinicians to suspect these severe reactions even in uncommon conditions. We choose to present data on anaphylaxis regarding simulation, mode of exposure to sensitizing agents, pregnancy, exposure to animals, intimate behaviour, psychological stress and other situations.

Background: Whether concomitant home exposures modify the effectiveness of mouse allergen reduction among mouse-sensitized children with asthma is unknown., Objective: To determine whether a lower baseline home mouse allergen level, lower particulate matter 10 μ or less (PM 10 ), and the absence of sensitization and exposure to other indoor allergens are associated with greater improvements in asthma associated with mouse allergen reduction., Methods: A secondary analysis of a randomized clinical trial of a home mouse allergen intervention was performed to examine the effect of 3 indoor factors on the relationship between mouse allergen reduction and a range of asthma outcomes., Results: Participants (N = 297) were predominantly minority (78% African American, 22% Hispanic) and publicly insured (88%). Higher baseline mouse allergen levels were associated with a greater response to mouse allergen reduction for several symptom and exacerbation outcomes. Lower indoor PM 10 levels were associated with a greater response to mouse allergen reduction for several symptom outcomes, but not exacerbation outcomes. Overall, sensitization and exposure to other indoor allergens did not appear to modify the effect of mouse allergen reduction., Conclusions: In this population of predominantly low-income children with persistent asthma and mouse sensitization, mouse allergen reduction was associated with improvements in asthma, especially among those with high baseline mouse allergen exposure. Lower indoor PM 10 was associated with greater improvements in asthma symptoms., (Copyright © 2021 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)