India bears one of the highest global burdens of tuberculosis (TB) and chronic respiratory diseases (CRDs), including chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis, and post-tuberculosis lung disease (PTLD). Traditionally, TB and chronic respiratory diseases have been managed through vertical and fragmented healthcare programmes, leading to inefficiencies, delayed diagnosis, and poor continuity of care. Increasing evidence demonstrates strong epidemiological, biological, environmental, and socioeconomic intersections between TB and other lung diseases. Shared risk factors such as tobacco smoking, biomass fuel exposure, ambient air pollution, occupational hazards, poverty, malnutrition, and overcrowding amplify the burden of respiratory illness in India. Recent WHO policy frameworks advocate a transition from disease-specific programmes toward integrated, people-centred lung health services. This review examines the rationale, evidence, opportunities, and challenges for integrating TB and lung disease services in India. It discusses the role of primary healthcare strengthening, diagnostic integration, pulmonary rehabilitation, digital health innovations, workforce development, and multisectoral interventions. Lessons from the Practical Approach to Lung Health (PAL) and Indian pilot initiatives are also explored. An integrated TB-lung health strategy offers a pragmatic pathway to improve respiratory outcomes, optimize healthcare resources, strengthen health systems, and accelerate progress toward universal health coverage in India.

This issue of the Biomedical Journal examines lumbar spinal loading and current approaches to its assessment using invasive measurements, biomechanical modeling, imaging, wearable technologies, and AI-assisted methods. Other contributions address coumarin derivatives as modulators of autophagy and PI3K/mTOR signaling in cancer and apply multi-omics approaches to uric acid metabolism and cardiometabolic disease. Further studies investigate molecular mechanisms linking mechanical irritation to oral squamous cell carcinoma progression, predictors of HBsAg seroclearance after antiviral treatment withdrawal, and age-dependent effects of exercise and losartan. Additional contributions explore PD-L1 signaling in allergic asthma, the antiviral activity of BPR2-D2 against chikungunya virus replication, and differences in objective tear function between patients with and without mental disorders.

Although in-home air cleaners are known to reduce particulate matter (PM) concentrations, their effects on PM chemical constituents and particle-bound radioactivity (PR) under real-world residential conditions remain poorly characterized. We evaluated the effects of a portable high-efficiency particulate air (HEPA) cleaner on particle mass, chemical composition, and particle-bound radioactivity in occupied homes. We collected 86 indoor samples from 19 homes in the Boston metropolitan area between June 2017 and March 2018. Measurements included size-resolved PM fractions (PM2.5, PM10-2.5, and > PM10), short-lived α activity (SLA) and long-lived α activity (LLA) associated with PM2.5, elemental composition, black carbon (BC), and a biomass-burning/cooking surrogate (DC). HEPA operation substantially reduced indoor particle concentrations, with mean decreases of 3.7, 1.0, and 0.5 µg/m3 for PM2.5, PM10-2.5, and >PM10, corresponding to removal efficiencies of approximately 60, 37, and 32%, respectively. LLA decreased by 0.68 mBq/m3, corresponding to a 63% removal efficiency (p < 0.001). SLA also decreased substantially, by 31.4 Bq/m3, or approximately 70%; however, this reduction was not statistically significant, likely because of the limited number of valid SLA measurements. Major and trace PM2.5 constituents -including sulfur, crustal elements, BC, and DC-also decreased significantly during HEPA operation. By jointly assessing PM mass, chemical composition, and particle-bound radioactivity across seasons (summer versus winter) and residential locations (family rooms versus basements), this study extends previous chamber-based and limited field investigations of air-cleaner performance. Overall, the findings indicate that portable HEPA cleaners can reduce indoor PM, chemically diverse PM2.5 constituents, and particle-bound radon decay products in occupied homes. HEPA filtration may therefore provide a practical supplemental strategy for reducing combined exposures to PM and particle-bound radioactivity. However, it does not remove gaseous radon and should not replace radon source-control or remediation measures.

Postmenopausal women are more susceptible to allergic asthma, likely due to estrogen deficiency-associated immune dysregulation, yet the effects of 17β-estradiol (E2) in postmenopausal allergic asthma remain incompletely defined. In this study, we investigated the effect of E2 in ovariectomized (Ovx) mice subjected to chronic house dust mite (HDM) challenge. Mice were assigned to Sham, Ovx, Sham+HDM, Ovx + HDM, Ovx + E2 and Ovx + HDM + E2 groups. Airway pathology, peripheral inflammatory cells, pulmonary cytokine transcripts, ERα, ERβ, and total NF-κB p65 protein levels, and untargeted lung-tissue metabolomics were assessed. HDM exposure exacerbated allergic airway responses, particularly in Ovx mice, whereas E2 treatment attenuated the reduction in body-weight gain, nasal rubbing, circulating eosinophil and basophil counts, lung inflammation, mucus production, and Il-4, Il-5, Il-13, and Ifn-γ mRNA expression. Moreover, HDM stimulation increased pulmonary ERα, ERβ, and total NF-κB p65 expression, particularly in Ovx mice, while E2 treatment reduced the levels of these proteins. Untargeted metabolomic profiling further revealed E2-associated shifts involving tryptophan-related, glycerophospholipid, sphingolipid, riboflavin, pyrimidine, and carbohydrate metabolism. These findings indicate that E2 attenuates HDM-induced allergic airway inflammation under estrogen-deficient conditions, accompanied by lower pulmonary ERα, ERβ, and total NF-κB p65 protein levels and partial modification of lung-tissue metabolic disturbances.

Work-related asthma (WRA) comprises asthma caused by chemicals in the workplace (occupational asthma, or OA) and preexisting asthma made worse by chemicals and conditions (work-exacerbated asthma, or WEA). Distinguishing these two mechanisms is extremely challenging but imperative for effective health management and regulation under global chemical regulations. The Specific Inhalation Challenge (SIC) test is considered by clinicians as the gold standard for identifying OA. However, an exposure reconstruction exercise based on the case study of methyl methacrylate, currently undergoing harmonized classification and labeling within Europe suggests that greater rigor may be needed when conducting these tests if false positive results, i.e., from nonspecific irritation are to be avoided. Accurate simulation of actual workplace conditions combined with direct measurement of peak exposure levels will likely improve test specificity.

Epithelial barriers represent the first line of defense against pathogens, yet their role in innate immunity is typically relegated to pathogen detection and immune cell recruitment. This perspective ignores a fundamental biological principle: Epithelia defended against pathogens long before complex immune systems evolved. Here, we demonstrate that human bronchial epithelium retains this ancestral capacity, autonomously clearing rhinovirus (RV) within 24 hours by selectively extruding infected cells, a process that we term virus-induced cell extrusion (VICE). VICE occurs in two waves: a rapid response occurring independently of complete virus entry, followed by a replication-dependent wave. Barrier-defective epithelia that cannot extrude do not eliminate RV. While VICE maintains barrier integrity and reduces local infection, it also expels virus-laden cells, which can infect fresh epithelia. Thus, VICE enables leukocyte-independent epithelial defense while inadvertently promoting viral spread, redefining epithelia as central to viral pathogenesis and host protection.

Biologics have revolutionized the treatment of severe allergic diseases in children that cannot be controlled by conventional treatments. These diseases are commonly driven by dysregulation of immune response, often driven by Type 2 pathways. By targeting them, biologics have the potential for treating one or more allergic diseases. Thus, a "treat to target" strategy is now prioritized, allowing treatment of allergic diseases in a personalized approach. The pioneer anti-IgE monoclonal antibody, omalizumab, was initially indicated for the treatment of moderate to severe allergic asthma and is now indicated for chronic spontaneous urticaria (CSU), chronic rhinosinusitis with nasal polyps (CRSwNP), and food allergy (FA), highlighting the ability of biologics to target multiple allergic diseases. Other biologics have been developed in asthma and other allergic diseases, including mepolizumab (anti-IL5), benralizumab (anti-IL5 receptor), dupilumab (anti-IL-4 receptor α), and more recently tezepelumab (anti-TSLP). Clinical trials in children and/or teenagers have demonstrated their efficacy and safety, confirmed by real-life studies, in asthma, atopic dermatitis (AD), CSU, and more recently in eosinophilic esophagitis (EoE) and FA. Beyond biologics, small molecules such as Janus kinase inhibitors target other key pathways and have already been approved in AD, with ongoing clinical trials in other allergic diseases. In the pediatric specific context, these treatments raise questions, particularly regarding the choice of biologics and the goals. In the long term, the sustained efficacy, safety and impact on the natural history of allergic diseases need to be further studied. The aim of this review is to discuss the most recent data in the use of biologics and small molecules in pediatric allergic diseases and to highlight the remaining gaps in knowledge.

Pulmonary drug delivery systems have gained increasing attention as an effective strategy for the treatment of both respiratory and systemic diseases by enabling targeted, noninvasive, and efficient drug administration through the lungs, with advantages including rapid onset of action, lower drug doses, and reduced systemic adverse effects. Despite these advances, challenges related to formulation stability, aerosol performance, lung clearance mechanisms, and regulatory approval remain. This review explores advanced pulmonary drug delivery systems, with emphasis on the anatomical, physiological, pharmaceutical, and device-related factors that influence aerosol deposition and therapeutic performance. The review examines key mechanisms of particle deposition such as inertial impaction, gravitational sedimentation, Brownian diffusion, interception, and electrostatic interactions, and advanced pulmonary drug carrier systems, including liposomes, nanoparticles, large porous particles, dendrimers, polymeric micelles, biodegradable polymers, and lactose-based dry powder platforms, which enhance drug stability, controlled release, lung retention, and site-specific targeting. The review further summarizes advances in particle engineering technologies and common and advanced inhalation devices, including pressurized metered-dose inhalers, dry powder inhalers, nebulizers, soft mist inhalers, and smart inhaler platforms. Clinical applications of pulmonary drug delivery extend beyond asthma and chronic obstructive pulmonary disease (COPD) to include cystic fibrosis, pulmonary infections, and pulmonary arterial hypertension, while emerging applications in tuberculosis, diabetes, vaccination, gene therapy, and cancer continue to be investigated. Future directions include personalized pulmonary medicine, inhaled biologics and mRNA therapeutics, environmentally sustainable inhaler technologies, artificial intelligence-assisted formulation and device optimization, and evolving regulatory frameworks. Advancements in pulmonary drug delivery technologies may focus on improving drug targeting, optimizing therapeutic performance, and broadening their application in modern clinical practice.