Current Allergy and Asthma Reports最新文献

Purpose of review: This scoping review aimed to explore psychological and related biopsychosocial factors influencing adherence to biologic therapies among individuals with asthma. Despite the proven efficacy of biologics for severe type 2 inflammation, real-world adherence remains variable. The review sought to identify individual, clinical, and contextual determinants that facilitate or hinder adherence behaviors.

Recent findings: A systematic search of PubMed, Scopus, and APA PsycINFO identified 14 studies published between 2018 and 2025. Most were observational or retrospective and conducted in the United States. Adherence rates were generally moderate to high but varied across biologics. Systemic barriers included high out-of-pocket costs, complex insurance procedures, and limited access to specialist care. Clinically, patients with milder symptoms or low perceived treatment benefit were more likely to discontinue. Psychological barriers-such as fear of injections, illness denial, depression, and stigma-were recurrent yet understudied. Facilitators included perceived efficacy, emotional reassurance, shared decision-making, and supportive treatment settings. Adherence to biologic therapies in asthma reflects a multidimensional interplay between systemic, clinical, and psychological influences. Integrating psychological assessment, patient education, and system-level support is essential to sustain long-term engagement. Future research should address psychological mechanisms and develop tailored interventions to enhance adherence and improve clinical outcomes.

Purpose of review: Asthma represents a major global health burden, with incidence increasing substantially over the past 50 years. Epidemiologic studies have linked this rise in asthma to escalating air pollution; however, the biological mechanisms remain undefined. Recent evidence has highlighted a role for innate immune memory, or trained immunity, in asthma pathogenesis; however, the contribution of air pollution remains unclear. This review synthesizes emerging findings on how air pollution shapes trained immunity in asthma and related inflammatory lung diseases.

Recent findings: Air pollutants increase gene acetylation and methylation and disrupt innate immune cell metabolism. These immune mediated changes are consistent with features of trained immunity, a process that remains largely underexplored. Collectively, these data support the concept that air pollution imprints long-lasting epigenomic and immunometabolic changes on innate immune cells, thereby contributing to asthma susceptibility and severity. Future studies will focus on mechanistic investigations to further elucidate how pollutants dysregulate innate immune memory.

Purpose of review: This study employs bibliometric methods to analyze global research trends in managing comorbid allergic diseases (e.g., allergic rhinitis, asthma, eczema, food allergies), aiming to identify key contributors, frameworks, and research gaps.

Recent findings: Bibliometric analysis of Web of Science data using CiteSpace, Excel, and R revealed an increasing trend in research output, with the U.S., U.K., and China being the leading contributors. Key chronic disease frameworks like the Chronic Care Model, Self-Management Program, and Innovative Care Framework were highly cited. Research hotspots included management strategies, prevalence, risk factors, and quality of life, with increasing focus on management approaches over time. The findings highlight the rising importance of interdisciplinary collaboration in managing comorbid allergic diseases. Tailored management strategies are required to address the chronic and complex nature of these conditions. Future research should focus on improving treatment efficacy and enhancing patient quality of life, as significant gaps remain in optimizing long-term care for these conditions.

Purpose of review: Alpha-gal syndrome (AGS) is a novel allergic disease characterized by hypersensitivity responses following exposure to the glycan galactose-alpha-1,3-galactose (alpha-gal or α-Gal) attached to mammalian proteins and fats in food, supplements, and medications. Bites from hard-bodied ticks, including Amblyomma americanum (Aa or lone star tick) in the United States, have been identified as drivers of allergic sensitization to alpha-gal. Here, we review clinical presentation, epidemiology, diagnosis, and current understanding of the mechanistic drivers of AGS, with particular focus on the roles of allergic effector cells - mast cells (MCs) and basophils. We explore unique clinical characteristics of AGS through the lens of alpha-gal-specific IgE and MC activation in AGS. We propose potential explanations for delayed symptom onset, inconsistent symptom development, and persistence of allergic symptoms in some AGS patients despite removing all mammal products from the diet.

Recent findings: Current evidence implicate bites from hard-bodied ticks as the primary sensitizing agent in AGS. However, there is emerging evidence that other ecto- and endoparasites may also induce alpha-gal-specific IgE. Multiparameter flow and mass cytometry and RNA sequencing have demonstrated an enrichment of unique populations of T, B, invariant natural killer T (iNKT), natural killer B (NKB) and MC progenitor cells in human volunteers with AGS. Recently developed mouse models of AGS will support future studies to identify which cells are critical for the development of AGS. In vitro models of the allergic effector phase of AGS using human sera and novel human alpha-gal-specific IgE monoclonal antibodies in humanized rat allergic effector cell lines, human basophils, human MC lines, and primary human MC cultures, confirm alpha-gal-induced allergic effector cell activation. They also provide a system to study potential alpha-gal-antigen-independent drivers of MC activation in AGS. Efforts are ongoing to understand the epidemiology and immune mechanisms of AGS. Novel reagents (e.g. alpha-gal-specific monoclonal antibodies) and murine AGS models will facilitate deeper investigation of tick-driven, alpha-gal-specific IgE and allergic effector cell-induced pathology in AGS.

Purpose of review: Olfactory function is certainly associated with cognitive health, and the severity of loss of smell (LoS) has been associated with the rate of cognitive decline. In this review, we describe the relationship between olfactory dysfunction and cognitive decline, focusing on its relevance in type 2 and non-type 2 inflammatory upper respiratory diseases. We also highlight the relevant correlation between the alteration of the components of olfaction, such as odor identification, and the progression in cognitive decline leading to dementia.

Recent findings: A relevant number of studies suggest that olfactory identification impairment may predict the progression of cognitive decline from normal aging to mild cognitive impairment and dementia. In this review, we describe the association between olfactory dysfunction and cognitive decline, focusing in its relevance in type 2 and non-type 2 inflammatory upper respiratory diseases.

Purpose of this review: We review recent literature on impact of antibiotic allergy during pregnancy, and evidence for management in those self-reporting beta-lactam allergy.

Recent findings: Pregnant patients report a high-rate of antibiotic allergy, similar to the general public. Historically, antibiotic allergy evaluation has been reserved for non-pregnant patients, however, growing evidence supports safety and clinical utility for allergy evaluation during pregnancy. Recent studies have supported safety of outpatient skin testing with drug challenge in those with beta-lactam allergy, with most recent findings supportive of direct drug challenge in patients with low-risk allergy phenotypes. Evaluation of allergy label during pregnancy improves first-line antibiotic use of beta-lactam antibiotics. Allergy evaluation during pregnancy is a unique opportunity for allergists to impact clinical outcomes for both maternal and neonatal outcomes. Future studies should focus on standardization of evaluation protocols, improving access to allergy evaluation, and expand knowledge on neonatal clinical outcomes.

Purpose of review: Smell loss is among the most debilitating symptoms of chronic rhinosinusitis with nasal polyps (CRSwNP). We aimed to synthesize current evidence on the smell-restoring efficacy of biologics, focusing on outcomes measured by psychophysical tests.

Recent findings: Biologics mark a paradigm shift in the management of refractory CRSwNP, offering targeted, effective and safe treatment options. However, their relative impact on psychophysical smell outcomes remains uncertain. With several biologics now approved and real-world evidence emerging, a comprehensive evaluation is needed. This is a systematic review and meta-analysis of 8 RCTs (n = 2,024) and an additional review of 20 cohorts (n = 1,685). Among RCTs, biologic treatment produced a moderate to large pooled improvement in psychophysical smell scores (standardized mean difference, [SMD] = 0.72 (95% CI 0.32-1.13), p = 0.0004). The effect differed between drugs (χ² = 23.95, p < 0.0002). Dupilumab showed the largest improvements across four RCTs (SMD = 1.16, 95% CI = 0.35-1.97). In single RCTs, benralizumab showed large effect (1.03, 0.55-1.51), tezepelumab (0.56, 0.46-0.67), telikibart (0.35, 0.11-0.59), and omalizumab (0.27, 0.15-0.40) yielded modest but significant improvements. Mepolizumab showed no effect (0.1330 (95% CI -0.2490-0.5150). Blood-eosinophil level correlated with treatment response (p < 0.001). The cohort studies supported the findings (SMD = 1.20, 95% CI = 0.99-1.42), though most data were derived from studies of dupilumab. Overall, biologics substantially improve psychophysically measured olfactory function in CRSwNP. Future head-to-head trials are warranted to delineate comparative efficacy of smell recovery.

Purpose of review: The gut microbiota contributes to host homeostasis through the production of bioactive metabolites that regulate immune function. Some of these microbial metabolites, called short-chain fatty acids (SCFA), have been extensively associated with allergic diseases. However, this review aims to focus on other families of microbial metabolites that are also involved in regulating the immune and inflammatory responses. These include branched SCFA (BCFA), tryptophan and tyrosine (and their derivatives), secondary bile acids (BA), sphingolipids (SL), histamine, polyamines, and odd-chain fatty acid (OCFA)-containing metabolites.

Recent findings: In addition to the canonical SCFA, BCFA are also important regulators of innate and adaptive immunity. Specifically, they appear to participate in the mechanisms underlying allergic resolution and tolerance development. Furthermore, microbial derivatives of tryptophan, such as indole-3-acetic acid and indole-3-propionic acid, have been shown to regulate T helper 17 (Th17) and regulatory T cell populations, thereby reducing the allergic response. Products of the bacterial metabolism of other aromatic amino acids, such as tyrosine, are also associated with pro- and anti-inflammatory properties. Regarding secondary BA, isolithocholic acid has recently emerged as a key inhibitor of the Th17 response. Additionally, SL help maintain epithelial integrity and modulate the inflammatory response by regulating the levels of bioactive lipids, including ceramides and sphingosine-1-phosphate. Lastly, alterations in the bacterial metabolism of polyamines, including spermidine, and OCFA-containing metabolites, including lysophosphatidylcholines (LCP), have also been reported in allergic diseases. The microbiota metabolism modulates the immune response of its host and represents a potential target for the implementation of personalized therapeutic strategies in allergic patients.

Purpose of review: The optimal management of mucosal tissues during endoscopic sinus surgery (ESS) for chronic rhinosinusitis with nasal polyps (CRSwNP) remains controversial. This systematic review and network meta-analysis aimed to compare the efficacy and safety between mucosa-preserving surgical techniques, such as functional endoscopic sinus surgery (FESS) and extended endoscopic sinus surgery (EESS), and radical mucosa-resecting endoscopic sinus surgery (RESS) for the treatment of CRSwNP.

Recent findings: Nine studies involving 1,224 patients were included. RESS was associated with significantly lower recurrence rates compared to both FESS (relative risk [RR]: 2.37; 95% confidence interval [CI]: 1.64, 3.43) and EESS (RR: 2.22; 95% CI: 1.48, 3.36). EESS demonstrated a significantly lower revision surgery rate than FESS (RR: 2.95; 95% CI: 1.89, 4.82). Additionally, RESS showed greater improvement in overall symptom/severity visual analogue scale (VAS, 0-10 cm) scores compared to FESS (mean difference [MD]: -2.82, 95% CI: -3.02, -2.62) and EESS (MD: -2.64, 95% CI: -4.09, -1.21). No significant differences were observed in complication rates among these surgical techniques. Besides, no statistically significant differences were found in VAS-loss of smell score, Sino Nasal Outcome Test-22 score, or Lund-Kennedy endoscopic score. Mucosal resection during endoscopic sinus surgery is associated with reduced postoperative recurrence and improved overall symptom control in patients with CRSwNP compared to mucosal preservation techniques. The safety profiles of these surgical approaches are comparable.

Purpose of the review: The innate immune system plays a critical role in mediating many of the physiological consequences of high-fat diet consumption. Dietary lipids, and specifically saturated fatty acids like palmitate and stearate, directly activate innate immune cells and alter the composition of the gut microbiome. Moreover, long-term high-fat diet feeding can induce chronic inflammation, adipose expansion, and the development of obesity. High-fat diet consumption and obesity also worsen the risk for chronic diseases like asthma.

Recent findings: It is well known that high-fat diet feeding activates innate immune cells and alters the gut microbiome. However, emerging research provides new insight into the mechanisms by which high-fat diet feeding and obesity affect innate immunity and further disease development. These emerging mechanisms include the induction of lipid-associated macrophages (LAMs), innate immune memory, and innate-adaptive crosstalk leading to T cell exhaustion and granzyme K production. These novel mechanisms help us better understand the effect of high-fat diets on innate immunity, and future studies in these areas may help us better identify new therapeutic strategies for managing obesity and asthma.