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The World Allergy Organization Journal Feb 2021Tobacco smoke has been described as causing increased prevalence of rhinitis symptoms and decreased atopy. Furthermore, these nasal symptoms and quality of life in...
BACKGROUND
Tobacco smoke has been described as causing increased prevalence of rhinitis symptoms and decreased atopy. Furthermore, these nasal symptoms and quality of life in smokers with Allergic Rhinitis (AR) were not significantly different to non-smokers. As a result of this duality, a comparison study between the quality of life and inflammatory markers of atopy among active smokers and non-smokers having AR was put forward.
MATERIAL AND METHODS
Cross-sectional study in adult smokers and non-smokers, with a clinical diagnosis of AR and positive Skin Prick Test (SPT). Smoking status was confirmed by salivary cotinine measurements. Functional respiratory evaluation was performed, and quality of life between groups was compared using Mini-RQLQ questionnaire. Immunological markers in serum and nasal washes (IgE, IL-4, IL 5, IL 13, IL 17, IL 33) were evaluated, while samples from a third group of passive smokers was incorporated for serological comparison exclusively. The statistical analysis included Student T test, x2, Mann Whitney U (Anova 2-way), and Kruskal Wallis for 3 groups analysis. Values of P < 0.05 were considered significant.
RESULTS
Twenty-two patients per group with similar demographics and allergen sensitivity were studied. Regarding inflammatory markers, a reduction of IL 33 in the serum of smokers (P < 0.001) was the only statistically significant different parameter revealed, showing a remarkable trend in nasal lavage. Salivary cotinine levels were absolutely different (P < 0.0001), but pulmonary function evaluations were not statistically significant after multiple adjusting. There were no significant differences in quality of life parameters.
CONCLUSIONS
In our study of AR, active smokers do not demonstrate impaired nasal related quality of life or impact on atopic inflammatory parameters, compared to non-smokers. Reduced levels of IL33 could explain a lack of symptoms alerting smokers of the harmful consequences of smoking.
PubMed: 33510834
DOI: 10.1016/j.waojou.2020.100504 -
The Journal of Allergy and Clinical... Nov 2021Black, Latinx, and Indigenous people in the United States experience a disproportionate burden of asthma and atopic dermatitis. The study of these disease disparities... (Review)
Review
Black, Latinx, and Indigenous people in the United States experience a disproportionate burden of asthma and atopic dermatitis. The study of these disease disparities has focused on proximal socioenvironmental exposures and on the biomechanistic (including genetic) differences between racial and ethnic groups. Although biomedical research in allergy and immunology stands to benefit from the inclusion of diverse study populations, the narrow focus on biologic mechanisms disregards the complexity of interactions across biologic and structural factors, including the effects of structural racism. Structural racism is the totality of ways in which society fosters discrimination by creating and reinforcing inequitable systems through intentional policies and practices sanctioned by government and institutions. It is embedded across multiple levels, including the economic, educational, health care, and judicial systems, which are manifested in inequity in the physical and social environment. In this review, we present a conceptual framework and pull from the literature to demonstrate how structural racism is a root cause of atopic disease disparities by way of residential segregation, socioeconomic position, and mass incarceration, which may lead to aberrations in the innate and adaptive immune response and the augmentation of physiologic stress responses, contributing to a disproportionate disease burden for racial and ethnic populations.
Topics: Asthma; Dermatitis, Atopic; Ethnicity; Health Status Disparities; Healthcare Disparities; Humans; Racism; United States
PubMed: 34743832
DOI: 10.1016/j.jaci.2021.09.020 -
Journal of Clinical Medicine Aug 2023Among preterm infants, the risk of developing asthma is a matter of debate. This review discusses the state of the art of poorly understood prematurity-associated... (Review)
Review
Among preterm infants, the risk of developing asthma is a matter of debate. This review discusses the state of the art of poorly understood prematurity-associated asthma. Impaired pulmonary function is common in children born prematurely. Preterm infants are prone to developing viral respiratory tract infections, bronchiolitis in the first year of life, and recurrent viral wheezing in preschool age. All of these conditions may precede asthma development. We also discuss the role of both atopic sensitization and intestinal microbiome and, consequently, immune maturation. Diet and pollution have been considered to better understand how prematurity could be associated with asthma. Understanding the effect of factors involved in asthma onset may pave the way to improve the prediction of this asthma phenotype.
PubMed: 37629440
DOI: 10.3390/jcm12165400 -
Microorganisms Sep 2021Dysbiosis refers to a reduction in microbial diversity, combined with a loss of beneficial taxa, and an increase in pathogenic microorganisms. Dysbiosis of the... (Review)
Review
Dysbiosis refers to a reduction in microbial diversity, combined with a loss of beneficial taxa, and an increase in pathogenic microorganisms. Dysbiosis of the intestinal microbiota can have a substantial effect on the nervous and immune systems, contributing to the onset of several inflammatory diseases. Epidemiological studies provided insight in how changes in the living environment have contributed to an overall loss of diversity and key taxa in the gut microbiome, coinciding with increased reports of atopy and allergic diseases. The gut microbiome begins development at birth, with major transition periods occurring around the commencement of breastfeeding, and the introduction of solid foods. As such, the development of the gut microbiome remains highly plastic and easily influenced by environmental factors until around three years of age. Developing a diverse and rich gut microbiome during this sensitive period is crucial to setting up a stable gut microbiome into adulthood and to prevent gut dysbiosis. Currently, the delivery route, antibiotic exposure, and diet are the best studied drivers of gut microbiome development, as well as risk factors of gut dysbiosis during infancy. This review focuses on recent evidence regarding key environmental factors that contribute to promoting gut dysbiosis.
PubMed: 34683389
DOI: 10.3390/microorganisms9102066 -
Clinical and Experimental Immunology Apr 2023IKAROS/IKZF1 plays a pivotal role in lymphocyte differentiation and development. Germline mutations in IKZF1, which have been shown to be associated with primary... (Review)
Review
IKAROS/IKZF1 plays a pivotal role in lymphocyte differentiation and development. Germline mutations in IKZF1, which have been shown to be associated with primary immunodeficiency, can be classified through four different mechanisms of action depending on the protein expression and its functional defects: haploinsufficiency, dimerization defective, dominant negative, and gain of function. These different mechanisms are associated with variable degrees of susceptibility to infectious diseases, autoimmune disorders, allergic diseases, and malignancies. To date, more than 30 heterozygous IKZF1 germline variants have been reported in patients with primary immunodeficiency. Here we review recent discoveries and clinical/immunological characterization of IKAROS-associated diseases that are linked to different mechanisms of action in IKAROS function.
Topics: Humans; Autoimmune Diseases; Ikaros Transcription Factor; Neoplasms; Transcription Factors
PubMed: 36433803
DOI: 10.1093/cei/uxac109 -
Frontiers in Medicine 2022SARS-CoV-2 enters lung cells angiotensin-converting enzyme 2 (ACE2) receptor. Several studies suggest that interleukin-13, an important cytokine involved in T2...
BACKGROUND
SARS-CoV-2 enters lung cells angiotensin-converting enzyme 2 (ACE2) receptor. Several studies suggest that interleukin-13, an important cytokine involved in T2 inflammation, reduces ACE2 expression, and therefore, asthma would not be a significant risk factor for the development of severe COVID-19. However, several asthma-related risk factors should be valued during the concurrent occurrence of asthma and COVID-19. The purpose of this study was to compare the evolution of asthma in patients who had COVID-19 with those who did not have the disease.
METHODS
This was an observational and retrospective study involving asthmatic patients followed up at a tertiary center. Patients were assessed for severity of asthma, atopy, comorbidities, and COVID-19. Worsening of asthma was considered when, during the period of Sept 2020 to Oct 2021, patients referred an increasing of asthma symptoms and a need to increment their maintenance therapy.
RESULTS
This study included 208 asthmatic patients, the mean age was 52.75 years, 79.81% were atopic asthmatics, and 59 (28.37%) had laboratory-confirmed coronavirus disease. Of all patients infected with the SARS-CoV-2, eleven (18.64%) needed hospitalization and required oxygen supply with an O2 mask. Comparing the worsening of asthma between patients who had COVID-19 and those who had not the disease, there was a statistically significant difference, 33.90 vs. 11.41%, respectively ( < 0.001). There was no statistical significance regarding asthma comorbidities.
CONCLUSION
This study assessed a group of asthmatic patients that had COVID-19, and that although the respiratory symptoms related to COVID-19 were mild to moderate, a subgroup of these asthmatic patients evolved with a chronic worsening of their asthma requiring an increment in asthma medication to control the disease.
PubMed: 36186769
DOI: 10.3389/fmed.2022.882665 -
Frontiers in Allergy 2023Transcription factors (TFs) are critical components involved in regulating immune system development, maintenance, and function. Monogenic defects in certain TFs can... (Review)
Review
Transcription factors (TFs) are critical components involved in regulating immune system development, maintenance, and function. Monogenic defects in certain TFs can therefore give rise to inborn errors of immunity (IEIs) with profound clinical implications ranging from infections, malignancy, and in some cases severe allergic inflammation. This review examines TF defects underlying IEIs with severe atopy as a defining clinical phenotype, including STAT3 loss-of-function, STAT6 gain-of-function, FOXP3 deficiency, and T-bet deficiency. These disorders offer valuable insights into the pathophysiology of allergic inflammation, expanding our understanding of both rare monogenic and common polygenic allergic diseases. Advances in genetic testing will likely uncover new IEIs associated with atopy, enriching our understanding of molecular pathways involved in allergic inflammation. Identification of monogenic disorders profoundly influences patient prognosis, treatment planning, and genetic counseling. Hence, the consideration of IEIs is essential for patients with severe, early-onset atopy. This review highlights the need for continued investigation into TF defects to enhance our understanding and management of allergic diseases.
PubMed: 37727514
DOI: 10.3389/falgy.2023.1237852 -
Journal of Clinical Medicine Nov 2022Inhaled bronchodilators are frequently used among patients with primary ciliary dyskinesia (PCD), although neither the effectiveness nor the prevalence of their use is...
BACKGROUND
Inhaled bronchodilators are frequently used among patients with primary ciliary dyskinesia (PCD), although neither the effectiveness nor the prevalence of their use is known, due to the paucity of relevant studies.
METHODS
This is a retrospective analysis of pre- and post-bronchodilator spirometry results, of patients with PCD from two centers. Correlations were examined of bronchodilator response, with asthma and atopy markers.
RESULTS
Of 115 patients, 46 (40%) completed spirometry pre- and post-bronchodilation. Of these, 26 (56.5%) demonstrated reversible airway obstruction (increase in %FEV predicted ≥ 10%). Obstruction reversibility was not found to be associated with a family history of asthma, blood eosinophil level, elevated IgE, or atopy symptoms. Of the 46 patients who completed bronchodilator spirometry, 29 (63%) were regularly using bronchodilators and inhaled corticosteroids.
CONCLUSIONS
More than half of patients with PCD presented with reversible airway obstruction, without any correlation to markers of personal or familial atopy. Inhaled bronchodilators and corticosteroid therapies are commonly used for treating PCD. Evaluating bronchodilator response should be considered, and its effectiveness should be further studied.
PubMed: 36431268
DOI: 10.3390/jcm11226791 -
Frontiers in Immunology 2022Atopic disorders, including atopic dermatitis, food and environmental allergies, and asthma, are increasingly prevalent diseases. Atopic disorders are often associated... (Review)
Review
Atopic disorders, including atopic dermatitis, food and environmental allergies, and asthma, are increasingly prevalent diseases. Atopic disorders are often associated with eosinophilia, driven by T helper type 2 (Th2) immune responses, and triggered by disrupted barrier function leading to abnormal immune priming in a susceptible host. Immune deficiencies, in contrast, occur with a significantly lower incidence, but are associated with greater morbidity and mortality. A subset of atopic disorders with eosinophilia and elevated IgE are associated with monogenic inborn errors of immunity (IEI). In this review, we discuss current knowledge of IEI that are associated with atopy and the lessons these immunologic disorders provide regarding the fundamental mechanisms that regulate type 2 immunity in humans. We also discuss further mechanistic insights provided by animal models.
Topics: Animals; Dermatitis, Atopic; Disease Susceptibility; Eosinophilia; Immune System; Immunologic Deficiency Syndromes
PubMed: 35572516
DOI: 10.3389/fimmu.2022.860821