RESUMEN
Global warming has direct and indirect effects, as well as short- and long-term impacts on the respiratory and skin barriers. Extreme temperature directly affects the airway epithelial barrier by disrupting the structural proteins and by triggering airway inflammation and hyperreactivity. It enhances tidal volume and respiratory rate by affecting the thermoregulatory system, causing specific airway resistance and reflex bronchoconstriction via activation of bronchopulmonary vagal C fibers and upregulation of transient receptor potential vanilloid (TRPV) 1 and TRPV4. Heat shock proteins are activated under heat stress and contribute to both epithelial barrier dysfunction and airway inflammation. Accordingly, the frequency and severity of allergic rhinitis and asthma have been increasing. Heat activates TRPV3 in keratinocytes, causing the secretion of inflammatory mediators and eventually pruritus. Exposure to air pollutants alters the expression of genes that control skin barrier integrity and triggers an immune response, increasing the incidence and prevalence of atopic dermatitis. There is evidence that extreme temperature, heavy rains and floods, air pollution, and wildfires increase atopic dermatitis flares. In this narrative review, focused on the last 3 years of literature, we explore the effects of global warming on respiratory and skin barrier and their clinical consequences.
Asunto(s)
Dermatitis Atópica , Rinitis Alérgica , Humanos , Calentamiento Global , Frecuencia Respiratoria , InflamaciónRESUMEN
BACKGROUND: Sunflower seeds are a popular allergen-free peanut alternative. OBJECTIVE: To describe sunflower seed allergy incidence and characteristics. METHODS: We conducted a retrospective cohort study of patients with sunflower seed allergy from 1995 to 2021 in a pediatric allergy clinic. We described demographics, testing results, atopic comorbidities, and reaction histories of patients with sunflower seed allergy, and calculated the annual cumulative incidence of the allergy. Logistic regression was used to estimate the increase in odds of sunflower seed allergy diagnosis for each year from 1995 to 2021. RESULTS: From 1995 to 2021, we identified 235 patients with sunflower seed allergy. Among patients with sunflower seed allergy, the median age at diagnosis was 3.9 years. Over three quarters of patients had another atopic condition. Half of reactions consisted of mild urticaria or rash, and a quarter met criteria for anaphylaxis. The cumulative incidence ranged from 0% (1995-1999, 2001-2004 and 2006) to 0.38% (2021). From 1995 to 2021, the odds of sunflower seed allergy diagnosis increased annually by 21% (OR 1.21, 95% CI: 1.17-1.25). CONCLUSION: In our single-center cohort of children with sunflower seed allergy, most children were diagnosed in early childhood, had high rates of comorbid atopic conditions, and had high rates of cutaneous reactions to sunflower seed products. Moreover, in our cohort, incidence of sunflower seed allergy increased.
RESUMEN
STAT2 is a transcription factor activated by type I and III IFNs. We report 23 patients with loss-of-function variants causing autosomal recessive (AR) complete STAT2 deficiency. Both cells transfected with mutant STAT2 alleles and the patients' cells displayed impaired expression of IFN-stimulated genes and impaired control of in vitro viral infections. Clinical manifestations from early childhood onward included severe adverse reaction to live attenuated viral vaccines (LAV) and severe viral infections, particularly critical influenza pneumonia, critical COVID-19 pneumonia, and herpes simplex virus type 1 (HSV-1) encephalitis. The patients displayed various types of hyperinflammation, often triggered by viral infection or after LAV administration, which probably attested to unresolved viral infection in the absence of STAT2-dependent types I and III IFN immunity. Transcriptomic analysis revealed that circulating monocytes, neutrophils, and CD8+ memory T cells contributed to this inflammation. Several patients died from viral infection or heart failure during a febrile illness with no identified etiology. Notably, the highest mortality occurred during early childhood. These findings show that AR complete STAT2 deficiency underlay severe viral diseases and substantially impacts survival.