Asthma is a complex inflammatory airway disease affecting a significant global population, spanning from childhood through adulthood. Despite advances in treatment modalities, a significant subset of patients, approximately 10%, grapple with severe asthma, characterized by increased healthcare utilization and diminished quality of life. Tezepelumab, a monoclonal antibody targeting thymic stromal lymphopoietin (TSLP), offers promising therapeutic potential. TSLP is a protein released by a variety of cells, with a predominance of epithelial cells, in reaction to plenty of stimuli, such examples as viruses, aeroallergens, and others. Its action is upstream and pertains to initiating numerous subsequent innate and adaptive immune reactions, contributing to the continuation of asthma pathophysiological processes. Tezepelumab’s unique efficacy spans diverse severe asthma phenotypes, significantly reducing exacerbation rates across eosinophilic and non-eosinophilic subtypes. Its favorable safety profile and clinically meaningful improvements in asthma control, accompanied by reductions in cytokine levels and baseline biomarkers, underscore its broad impact on asthma inflammation. Its efficacy, irrespective of type 2 (T2) endotype, reinforces the idea that TSLP blockade broadly inhibits pathways crucial to asthma pathophysiology, rather than narrowly focusing on individual downstream factors, as previous biological treatments have. This review discusses the rationale for TSLP blockade and the efficacy of tezepelumab in severe asthma using data from key trials.

Bronchiectasis is a heterogeneous chronic lung disease, characterised by irreversible dilatation of the airways and attributed to a wide spectrum of other underlying conditions, usually underdiagnosed and inadequately treated with a high burden for both the patients and the healthcare system. The way bronchiectasis is viewed by physicians has drastically changed over the last decades, with the topic of eosinophilia in the context of the disease being one of the substantially highlighted. Eosinophilia was traditionally considered as a means for distinguishing bronchiectasis from asthma, whereas bronchiectasis was primarily associated with neutrophilic inflammation. However, eosinophilic bronchiectasis is nowadays identified as a distinct disease endotype and is associated with a specific clinical course and response to treatment. Further research is needed to better characterise this endotype and improve its personalised investigation and management in daily clinical practice.

Asthma is a common chronic inflammatory disease of the airways that affects more than 330 million people globally. Severe asthma, despite being 5–10% of the total asthmatic population presents significant morbidity and high cost due to health care utilization. The management of severe asthma has dramatically changed with the use of biologics. However, biologics have been approved only for patients with severe asthma with type-2 mediated inflammation. Eosinophils are central in the T2 inflammatory process in asthma and this stands true for the severe form of the disease as well. In this review, we discuss basic insights into the pathogenesis of severe asthma related to eosinophilic inflammation and the pivotal role of T2 cytokines which have also become along with eosinophils the target of biologics. Novel biologics such as tezepelumab have demonstrated efficacy regardless of the blood eosinophil count and have shown promise for T2 low asthma, although to a lesser degree.

Eosinophilic gastrointestinal diseases (EGIDs) are a group of chronic conditions, characterized by an excessive accumulation of eosinophils in various areas of the mucosal of the gastrointestinal (GI) tract. EGIDs encompass a spectrum of diseases, including eosinophilic esophagitis (EoE), eosinophilic gastritis (EoG), eosinophilic enteritis (EoN), and eosinophilic colitis (EoC), each affecting different segments of the GI tract. The pathogenesis of EGIDs is multifaceted and involves an intricate interplay between genetic predisposition, environmental triggers, and dysregulated immune responses. Although the exact etiology behind EGIDs is not fully understood, it is clear that they are immune-mediated, with eosinophils having a central role in inflammation and tissue damage of GI mucosal. Clinical manifestations depend on the organ that is affected by the disease and on the depth of the eosinophil infiltration of the bowel wall. They range from mild discomfort to severe dysphagia, abdominal pain, malnutrition, and growth failure, particularly in pediatric cases. Regarding EGID management, it is a challenging issue to achieve clinical and histologic remission using pharmacotherapy and dietary elimination. Corticosteroids and proton pump inhibitors can be selected as an effective first-line treatment for certain patients and six-food elimination diet (6-FED) has been proven effective in inducing remission. Furthermore, biologic therapies have emerged as essential tools in controlling eosinophilic-driven inflammation. This review focuses on the complex pathogenesis and treatment of these inflammatory diseases, especially EoE.