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Journal articleZheng Y, Li Y, Zeyneloglu C, et al., 2026, , Allergy, Vol: 81, Pages: 1397-1432
The post-COVID pandemic era has witnessed a concerning resurgence of respiratory viruses, driving a global increase in acute respiratory infections. This trend may stem from relaxed non-pharmaceutical interventions, waning herd immunity, immunological imprinting limiting heterosubtypic protection, or viral antigenic evolution. This review aims to identify and characterize risk and protective factors associated with infection, hospitalization, severe illness, and mortality, while elucidating the drivers of the rising incidence of respiratory virus infections post-pandemic. Evidence on SARS-CoV-2 sublineages, influenza, respiratory syncytial virus, rhinovirus, adenovirus, human metapneumovirus, human parainfluenza virus, human coronaviruses, and cytomegalovirus has been collected and identified. Identified risk factors include demographic characteristics such as pediatrics and older age, male sex, race (Black, Hispanic, American Indian or Alaska native), preterm birth, and HLA-DQA1, IFNAR2, ST6GAL, and B3GALT5 genetic susceptibility. Behavioral, socioeconomic (low socioeconomic status, crowded living conditions), environmental influences (cold seasons, pollution), smoking, obesity and malnutrition could also exacerbate the risk of infection and adverse outcomes. Comorbidities, such as chronic conditions and immunocompromised states, significantly increase the risk of severe disease and hospitalization. Laboratory indices linked to severe disease outcomes include neutrophilia or neutropenia, lymphopenia, eosinopenia, and elevated C-reactive protein. Viral subtypes, viral load kinetics, vaccination status, and antiviral therapies further delineate risk profiles. Epithelial barrier impairment and underlying chronic airway diseases characterized by type 2 immunity also play a detrimental role in the development and severity of respiratory viral infections. Our findings highlight the need for stratified prevention strategies, which combine universal measures targeting shar
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Journal articleWallace DV, Hossny EM, Levin M, et al., 2026, , Immunol Allergy Clin North Am, Vol: 46, Pages: 233-256
This article compares 12 national and international anaphylaxis guidelines published between 2006 and 2025, highlighting evolving methodological frameworks, diagnostic criteria, and treatment approaches. While consensus supports prompt epinephrine use, differences remain in definitions, risk stratification, and post-acute care. Gaps in education, early childhood care protocols, and global harmonization continue to exist. The analysis emphasizes the shift from crisis-based to proactive anaphylaxis management and underscores the need for equity-focused, evidence-based interventions.
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Journal articleBush A, 2026, , Allergol Int
The areas covered represent a personal selection in the field. Asthma is defined in this manuscript as a clinical syndrome of wheeze, breathlessness and chest tightness, sometimes with excess cough. No assumptions are made about underlying pathology, and asthma thus becomes a clinical description, not a diagnosis. The areas covered include the need never to forget the importance of getting the basics right, including correct diagnosis and appropriate management; most children with asthma do not need biologics. Recent advances in preschool wheeze are covered next, especially the beginnings of phenotype-driven treatment, and the difficult issue of understanding non-eosinophilic wheezing. It is becoming clearer that infection likely plays a big role, but management is very difficult with no evidence base. We are now coming to realize the importance of phenotyping acute asthma attacks; one size does not fit all, but whereas many are eosinophilic, some are infection driven and are non-eosinophilic, especially in the preschool years. A phenotypic approach may allow us to reduce the burden of repeated oral corticosteroid bursts. Furthermore, we need to move beyond mere cell counting to assessing functional status. We are increasingly appreciating the importance of replacing short-acting β-2 agonist reliever therapy with combined inhaled corticosteroid and a fast acting short- and especially long-acting β-2 agonists. Finally, the use of biologicals in severe asthma is discussed. The possibility that early use of biologics may induce remission or even cure asthma.
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Journal articleKlimek L, Mullol J, Reitsma S, et al., 2026, , Allergy
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Journal articleSafavi S, Smith S, Jahnke N, et al., 2026, , Cochrane Database Syst Rev, Vol: 4
RATIONALE: Cystic fibrosis (CF) is an inherited multi-organ disorder. People with CF (pwCF) experience recurrent and chronic lung infections and a progressive loss of lung function. PwCF with poor and rapidly declining lung function may be considered for lung transplantation (LTx), which may improve their quality of life and survival. Nontuberculous mycobacteria (NTM) can cause pulmonary disease in pwCF, and NTM infection is a poor prognostic factor in LTx. Guidelines recommend NTM infection should not automatically preclude LTx. It is important to evaluate the evidence base for LTx in pwCF and NTM pulmonary disease. OBJECTIVES: To evaluate clinical outcomes in pwCF and with NTM infection (NTM infection alone or with NTM pulmonary disease) who undergo LTx by comparing: 1. pwCF with current NTM lung infection who undergo LTx versus those with NTM infection who do not undergo LTX; 2. pwCF with current NTM lung infection who undergo LTx versus those without NTM undergoing LTx. SEARCH METHODS: We searched the Cochrane Cystic Fibrosis Trials Register, CENTRAL, MEDLINE, Embase, and PubMed as well as two ongoing trials registries. We checked references. The latest search date was 17 February 2026. ELIGIBILITY CRITERIA: We considered non-randomised studies of pwCF (any age) with or without NTM lung infection or disease being considered for LTx as well as studies of pwCF and NTM who either did or did not undergo LTx. OUTCOMES: Our critical outcomes were mortality, disseminated NTM infection post-LTx, time to chronic lung allograft dysfunction (CLAD), and quality of life at any time points reported. We additionally planned to report lung function, hospitalisations for pulmonary exacerbations, and nutritional parameters in the review. RISK OF BIAS: We assessed the risk of bias in three studies using ROBINS-I and in one study using the Joanna Briggs Institute checklist for case series. SYNTHESIS METHODS: We could only report results narratively. We used GRADE to assess the cert
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Journal articleScheire S, Lourijsen E, Blauwblomme M, et al., 2026, , Allergy
Systemic glucocorticosteroids (sGCS) are widely used in the treatment of chronic inflammatory airway diseases such as rhinitis, rhinosinusitis and asthma. It is well-known that systemic use is linked to multiple adverse effects (AEs) both in the short- and the long-term. However, less is known about the safety of multiple short courses of sGCS. Currently there is no established agreement on the acceptable cumulative exposure to sGCS, considering the potential for various AEs. This systematic review and meta-analysis evaluated sGCS-related AEs in both upper and lower inflammatory airway disease, with a particular focus on short- and long-term risks. We further evaluated whether a dose-response relationship existed between the daily and cumulative dosages of sGCS and the occurrence of those AEs. Our meta-analysis confirmed that cumulative dosages between 500 mg and 1 g prednisolone-equivalent significantly increase the risk of most AEs, with risks increasing with incremental dose. These findings underscore the importance of: (a) judicious sGCS prescription and need for steroid stewardship, due to their potential for short- and long-term complications, occurring even with repeated short courses, and (b) prioritization of steroid-sparing approaches (e.g., biologicals) to avoid reaching a cumulative dose of 500 mg.
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Journal articleJenkins RG, 2026, , Nat Immunol
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Journal articleMakuyana N, Seldeslachts L, Michiels L, et al., 2026, , Sci Immunol, Vol: 11
Respiratory infections that result in severe and life-threatening immune-mediated respiratory decline are a major public health issue. Controlling local respiratory immune reactions without the use of systemic immunosuppressants remains an unmet clinical challenge. We developed a gene delivery system to express anti-inflammatory cytokines in the lung, which reestablishes local immune homeostasis without triggering systemic effects. Using an adeno-associated vector cargo system (AAV6.2-CC10), we induced production of interleukin-2 (IL-2), IL-1 receptor antagonist (IL-1RA), and IL-10 in situ in the lung microenvironment, with no detectable expression or immunological deviation in the peripheral immune system. We demonstrate the effective potential of IL-2, IL-1RA, and IL-10 as immunomodulatory cargos in severe infectious challenge, which reduced respiratory pathology after influenza-associated pulmonary aspergillosis. Thus, the AAV6.2-CC10 platform enables targeted delivery of biologics to the lung, modulates the lung environment, and improves pathology without inducing systemic immune reactions.
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Journal articleMohammed Abdul Wajid L, Saglani S, Nagakumar P, et al., 2026, , Arch Dis Child, Vol: 111, Pages: 444-448
OBJECTIVE: This study aimed to explore health professionals' perspectives on the management of preschool wheeze, including their views on using tests to guide treatment for children with recurrent wheeze. DESIGN: Purposive and snowball sampling were used in this qualitative study to recruit health professionals with experience of managing children with pre-school wheeze from primary and secondary care settings across England. Semi-structured interviews were conducted via Microsoft Teams. Transcripts were analysed thematically, supported by the use of NVivo software, to identify key themes. RESULTS: 14 health professionals participated: four general practitioners, four general paediatricians, four hospital asthma nurses, one tertiary respiratory paediatrician and one primary care nurse. Participants agreed that preschool wheeze remains a significant disease. Thematic analysis identified four key themes: (1) challenges with diagnostic terminology, where a lack of consistent terminology was considered to impact communication and management; (2) diagnostic uncertainty, where the absence of objective tests for early asthma diagnosis negatively contributed to management plans; (3) current practice of investigating children with preschool wheeze, where participants described a lack of infrastructure and approach to performing tests in primary and secondary care; and (4) treatment considerations in which parents' medication beliefs were thought to influence adherence to prescribed treatments. There were differences in the views regarding the management of preschool wheeze between primary and secondary care professionals. CONCLUSION: Health professionals' views highlight inconsistent use of diagnostic terminology for preschool wheeze, contributing to variation in management. Integrated care pathways and infrastructure are urgently needed to improve outcomes for children with preschool wheeze.
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Journal articleCanizales J, Schofield S, Shamji MH, et al., 2026, , Clin Exp Allergy
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Journal articlePeter J, Jindal A, Del Giacco S, et al., 2026, , Allergy
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Journal articleKaenmuang P, Barnett JL, Maher TM, et al., 2026,
Association of bronchoalveolar lavage cellular analysis and radiological findings in fibrotic interstitial lung diseases
, BMJ Open Respiratory 91桃色, ISSN: 2052-4439Background and aims: Inflammation may play a role in driving interstitial lung diseases (ILD). Radiological ground-glass opacity (GGO) may not reliably distinguish fine intralobular fibrosis from inflammatory processes in fibrotic ILD. We therefore investigated the relationship between GGO, fibrosis and leukocytes in bronchoalveolar lavage (BAL).Methods: We recruited patients with fibrotic ILD at a single centre between May 2014 and February 2018. The extent of GGO and fibrosis were evaluated by two radiologists. Linear regression examined the association between leukocyte numbers in BAL obtained from the right middle lobe (RML) and GGO/fibrosis extent in whole lung, adjusting for age, sex, and smoking. Z-test was used to compare the association between BAL and GGO/fibrosis.Results: 316 patients were included. Adjusting analyses for covariates, only BAL eosinophil and eosinophil-to-macrophage ratio were positively associated with GGO involvement (0.23 [95%CI 0.03 to 0.42] p = 0.023 and 11.21[1.33, 21.08] p = 0.026). Lymphocyte percentages (fibrosis -0.17 vs. GGO -0.02 p = 0.046); neutrophil percentages (fibrosis 0.38 vs. GGO 0.06 p 0.002); neutrophil-to-lymphocyte ratio (fibrosis 0.63 vs. GGO -0.05 p 0.027); neutrophil-to-macrophage ratio (Fibrosis 14.08 vs. GGO 2.57 p = 0.015), and neutrophilia (fibrosis 6.81 vs. GGO -0.31 p = 0.002) all demonstrated a significantly stronger associations with fibrosis than GGO. Conclusions: Lack of relationships between radiological GGO and BAL leukocyte counts in fibrotic lung disease indicates that GGO may not always be inflammatory in nature. Higher levels of neutrophil were associated with more extensive fibrosis.
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Journal articleWu Z, Yazbeck L, Smith DJF, et al., 2026, , Chest
BACKGROUND: Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease (ILD) driven by repeated antigen exposure in susceptible individuals. Cough is a prominent but poorly characterised symptom, especially in relation to objective measures and treatment response. RESEARCH QUESTION: What are the clinical predictors of cough severity in HP, and how does cough respond to corticosteroid therapy based on subjective and objective assessments? STUDY DESIGN AND METHODS: A prospective cohort of patients with fibrotic HP diagnosed per ATS/JRS/ALAT guidelines was recruited. Baseline assessments included cough visual analogue (VAS) and the Leicester cough Questionnaire (LCQ). Cough frequency was assessed using the VitaloJAK cough monitor in a subset of patients. Multivariable models evaluated predictors of cough severity, and in incident cases, changes in cough outcomes were evaluated after three months of corticosteroid therapy. RESULTS: A total of 101 patients were recruited (41 male; mean age 65 years). The median cough VAS was 35 mm (IQR 14-50 mm) and the median LCQ was 15.2 (IQR 13.2-17.4). The median cough count was 8.7/hr (range 0.2-32.1/hr, n=28). Subjective cough scores correlated with objective cough frequency (cough VAS ρ = 0.69, P < 0.001 and LCQ ρ=-0.555, P = 0.002). Female sex, reduced forced vital capacity (FVC), and higher bronchoalveolar lavage (BAL) lymphocyte fractions were independent predictors of worse cough severity, as measured by cough VAS. Corticosteroids significantly improved cough subjectively (cough VAS -13.7 mm, P = 0.002 and LCQ +1.9, P < 0.001; n = 44) but did not significantly reduce objective cough frequency (n=16). Lung function remained unchanged at three months. INTERPRETATION: Cough is a major symptom for patients with HP. While corticosteroids improved subjective cough, there was no impact on objective cough count. Randomised controlled trials are required to validate these findings and provide eviden
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Journal articleCustovic D, Custovic A, Gern J, et al., 2026, , J Allergy Clin Immunol
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Journal articleBonner KL, Fontanella S, Gore M, et al., 2026, , Am J Respir Crit Care Med, Vol: 212, Pages: 733-745
RATIONALE: Recurrent preschool wheeze accounts for most childhood hospitalizations for asthma and often responds poorly to inhaled corticosteroids (ICSs). OBJECTIVE: To relate lower airway immune cell composition in children with recurrent severe wheeze (RSW) to infection, allergic sensitization, and prescribed treatments. METHODS: Children with RSW aged 1 to 5 years underwent clinical phenotyping, bronchoscopy, multiparameter flow cytometry of blood and bronchoalveolar lavage (BAL) to characterize leukocytes, and assessments of lower airway bacterial and viral infection. An unsupervised analysis was undertaken to uncover clusters of airway inflammation. MEASUREMENTS AND MAIN RESULTS: Of 106 children (median age 36.5 months), 32% had allergic sensitization. Lower airway immune cells were similar in type and abundance in sensitized and nonsensitized children. However, significantly more nonsensitized wheezers had positive BAL bacterial culture. Bacterial infection was associated with neutrophils with low CD62L and CXCR2 expression. Children without airway bacterial infection also had up to 50% neutrophils but with high CD62L and CXCR2 expression. The data-driven analysis revealed 3 clusters: cluster 1, airway infection predominant with CD62Llo neutrophils; cluster 2, eosinophil/lymphocyte rich with CD62Lhi neutrophils; and cluster 3, low infection rate with CD62Lhi neutrophils. The clusters were independent of clinical features, prescribed ICSs, antibiotics, and allergic sensitization. CONCLUSIONS: Airway inflammation in RSW is heterogeneous. A subgroup had airway neutrophilia but with distinct neutrophil subtypes. Those with bacterial infection had CD62Llo neutrophils (cluster 1). Others had CD62Lhi neutrophils (clusters 2 and 3). Intervention trials stratifying using these clusters may provide a novel management approach.
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Journal articleAnanth S, Aerts J, Chotirmall SH, et al., 2026, , Breathe (Sheff), Vol: 22, ISSN: 1810-6838
The ERS "My Career Path" series provides an excellent insight into different subspecialties in respiratory medicine. All episodes can be found on the ERS Respiratory Channel. https://bit.ly/4sADqiS.
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Journal articleSousa-Pinto B, Bousquet J, Vieira RJ, et al., 2026, , Allergy, Vol: 81, Pages: 954-976
BACKGROUND: Allergic rhinitis (AR) impacts quality of life, work and school productivity. Over the last years, an important body of evidence resulting from mHealth data has led to a better understanding of AR. Such advances have motivated an EAACI-endorsed update of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines (ARIA 2024-2025). This manuscript presents the ARIA 2024-2025 recommendations for intranasal treatments, one of the mainstays for AR management. METHODS: The ARIA 2024-2025 guideline panel issued recommendations following the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) evidence-to-decision framework. Several sources of evidence were used to inform panel judgments and recommendations, including systematic reviews, evaluation of mHealth and pharmacovigilance data, as well as a survey of experts on costs. RESULTS: Eleven guideline questions concerning intranasal treatments for AR were prioritized, leading to recommendations. Overall, these questions concern the choice between different classes of intranasal medications-most notably, intranasal corticosteroids (INCS), antihistamines (INAH), fixed combinations of INAH+INCS and decongestants-or between different individual medications within each class. Four questions had not been evaluated in previous ARIA guidelines, while for the other three there was a change in the strength or directionality of recommendations. Overall, recommendations point to the suggested use of INAH+INCS over INAH or INCS and INCS over INAH. CONCLUSION: This ARIA 2024-2025 article supports patients, their caregivers, and healthcare professionals in choosing an intranasal treatment. However, decisions on AR treatment should consider the clinical variability of the disease, patients' values, and the affordability of medications.
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Journal articleKarp T, Merid SK, Kermani NZ, et al., 2026, , J Allergy Clin Immunol, Vol: 157, Pages: 879-889
BACKGROUND: Type 2 (T2)-low asthma is defined by low levels of T2 inflammation and is associated with resistance to inhaled corticosteroids. Its molecular mechanisms are mostly unknown, and treatment options are limited. We previously showed that nasal brush transcriptomes differ between asthma and controls, reflecting disease-relevant biology. OBJECTIVE: We explored nasal gene expression related to T2-low asthma in the ATLANTIS cohort. METHODS: We compared nasal brush RNA sequencing data between 82 T2-low and 63 T2-high asthma patients and 57 controls. T2-low asthma was defined as blood eosinophil counts < 0.15 × 109/L and Feno < 25 ppb and T2-high as blood eosinophil counts > 0.3 × 109/L and Feno > 25 ppb. Weighted gene coexpression network analysis (WGCNA) was applied to identify gene modules associated with T2-low asthma. The BAMSE and U-BIOPRED cohorts were used for replication analyses. RESULTS: Although differentially expressed genes were found in patients with T2-high asthma across all 3 cohorts, no differentially expressed genes were observed in individuals with T2-low disease compared to controls in ATLANTIS, nor consistently across other cohorts. Our assessment of molecular heterogeneity could not attribute this result to greater intersample variability within the T2-low group. WGCNA in ATLANTIS identified "black" and "purple" gene modules linked to T2-low asthma, with genes enriched in T-cell immunity and ribosomal RNA biology pathways, respectively. The "black" module was replicated in U-BIOPRED and showed the same direction in BAMSE. CONCLUSION: T2-high asthma shows a distinct nasal gene expression signature compared to healthy controls, while patients with T2-low asthma exhibit no consistent changes. Future studies should explore T-cell immunity in T2-low asthma and integrate lower airway multiomics data.
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Journal articleFreeman A, Rink S, Bansal AT, et al., 2026, , Lancet Reg Health Eur, Vol: 63
BACKGROUND: The phenotypic nature of multimorbidity in severe asthma is poorly understood. Our aims in this study were to define multimorbidity phenotypes and their characteristics in severe asthma across Europe by identifying and characterising co-aggregation of comorbidities. METHODS: Cross-sectional patient data were analysed from the pan-European Severe Heterogenous Asthma 91桃色 Collaboration: Patient Centred (SHARP) Central database of national severe asthma registries. Patients were grouped by four European regions (North, South, East, and West). Hierarchical clustering of comorbidities was applied to characterise the correlation structure of the ten commonest comorbidities within these geographical regions. Subsequent multimorbidity phenotypes (MMP) and their clinical features were then defined. FINDINGS: Data were available for 2690 severe asthma patients and 23 comorbidities from 11 countries. Three comorbidity clusters were consistently seen across the four European regions: 1) osteoporosis plus steroid-induced weight gain, 2) eczema plus rhinitis, and 3) chronic sinusitis plus nasal polyps. Four further comorbidities (obesity, bronchiectasis, gastro-oesophageal reflux disease, psychological factors) showed variable clustering. Multimorbidity was ubiquitous. Patients were assigned multimorbidity phenotypes (MMP) according to comorbidity cluster alignment. MMP sn (sinonasal-associated) and MMP u (no specific cluster alignment) were commonest. MMP ster (steroid-associated multimorbidity) had highest maintenance oral steroid (m-OCS) use, and Body Mass Index, plus worst lung function, asthma control, and asthma exacerbation frequency. MMP max (maximal multimorbidity) showed high prevalence of variably assigned comorbidities, higher m-OCS and biologic treatment needs. INTERPRETATION: Multimorbidity is common in severe asthma and can be classified into replicable novel phenotypes with characteristic clinical traits and outcomes. Recognising these phenotypes c
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Journal articleBush A, 2026, , Pediatr Pulmonol, Vol: 61
The association of early life adverse events with worse adult outcomes was first proposed by David Barker, the Developmental Origins of Health and Disease (DOHaD). Subsequently we have learned that adverse exposures are not merely important during pregnancy, but also exert transgenerational effects. Most of our knowledge derives from studies of nicotine and tobacco exposure. Adverse intrauterine exposures lead to low birth weight and premature delivery; altered airway and parenchymal structure; altered immune function; sensitization to later adverse exposures; and premature aging manifest by premature telomere shortening. Impaired spirometry for most tracks from birth to late middle age, and especially a low forced vital capacity, is associated with premature respiratory and all cause morbidity and mortality. Childhood exposure to passive smoking exacerbates antenatal effects on lung function, as does pollution. Pollution also increases the risk of early life respiratory infection which are a cause of impaired lung function in at least some studies, and also are associated with premature mortality. Diseases traditionally thought of as arising in adult life, including late-onset and occupational asthma, chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis all have their roots in early life adverse exposures, especially childhood onset smoking. Smoking provides proof of concept that prevention of adult disease must start earlier than adult life if it is to be effective. It is also likely that other early adverse exposures contribute to adult disease. Political action is needed to counteract the view that children "just grow out of it". They do not.
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