Mucosal immunity and trained innate immunity of the gut play a pivotal role in maintaining intestinal homeostasis and defending against microbial pathogens. This review provides an overview of the mechanisms underlying mucosal immunity and the concept of trained innate immunity in the gut. We discuss the interaction between gut microbiota and the host immune system, highlighting the role of epithelial cells, dendritic cells, and innate lymphoid cells, as well as the novel concept of trained innate immunity and its role in perpetuating or attenuating gut inflammation. We also comment on the current models for investigating mucosal immunity, their limitations, and how they can be overcome. Additionally, we explore the potential therapeutic implications of modulating mucosal immunity and trained innate immunity in gastrointestinal diseases. Only by elucidating the mechanisms underlying mucosal immunity and the concept of trained innate immunity, innovative approaches to modulate immune responses and restore intestinal homeostasis in the context of gastrointestinal disorders could be implemented.

Inflammation of the upper respiratory tract in patients with allergic rhinitis (AR) may contribute to lower respiratory airways’ inflammation. T-helper 17 (Th17) cells and related cytokines are also involved in the immunological mechanism of AR along with the classical Th2 cells. It is hypothesized that upon Th2 pressure, the inflammatory response in the lungs may lead to Th17-induced neutrophilic inflammation. However, the findings for interleukin-17 (IL-17) are bidirectional. Furthermore, the role of Th17 cells and their counterpart—T regulatory cells—remains unclear in AR patients. It was also shown that a regulator of inflammation might be the individual circulating specific non-coding microRNAs (miRNAs), which were distinctively expressed in AR and bronchial asthma (BA) patients. However, although several circulating miRNAs have been related to upper and lower respiratory tract diseases, their function and clinical value are far from being clarified. Still, they can serve as noninvasive biomarkers for diagnosing, characterizing, and providing therapeutic targets for anti-inflammatory treatment along with the confirmed contributors to the pathogenesis—Th17 cells and related cytokines. The narrow pathogenetic relationship between the nose and the bronchi, e.g., upper and lower respiratory tracts, confirms the concept of unified airway diseases. Thus, there is no doubt that AR and BA should be diagnosed, managed, and treated in an integrated manner.

Although the cough reflex is one of the essential protective mechanisms in the respiratory tract, it is considered a considerable health problem in adults and children when it becomes chronic and hypersensitive. However, the need for biomarkers for chronic cough in children and adults is critical. The problem with cough is also a severe symptom in hypersensitivity children. Respiratory infections are a considerable challenge for pediatricians, especially in allergic children. The term cough hypersensitivity syndrome, although introduced in adults, was questioned for children. Eosinophil cationic protein (ECP) is a promising marker for chronic cough but still needs to be validated and proved in clinical settings. In this review article, we aimed to discuss the possible role of ECP in connection to IgE for chronic cough in children.

Allergic rhinitis (AR) is a major public health problem with a growing global prevalence, currently affecting approximately 30% of the world population. There remains limited understanding of how local cytokine production patterns following nasal allergen challenge relate to clinical symptoms, particularly in the context of the late-phase allergic response. Interleukin-13 (IL-13) has emerged as a significant contributor to the development of allergic inflammation in recent years. It shares many functional features with interleukin-4 (IL-4) due to the presence of a common receptor subunit. Although findings in the literature remain conflicting, they consistently support the role of IL-13 as a primary cause of allergic inflammation. The IL13 gene is expressed at higher levels in the nasal mucosa of both humans and mouse models with allergic rhinitis; however, the exact role of IL-13 in AR pathogenesis remains unclear. The present study aimed to investigate IL-13 expression levels in patients with clinically confirmed allergic rhinitis and demonstrate that increased expression levels of IL-13 gene products (protein and mRNA) play a critical role in disease development and immune activation, potentially serving as a diagnostic and therapeutic biomarker. In recent years, IL-13 has emerged as a key mediator in the pathology of allergic inflammation. It shares numerous functional properties with IL-4, owing to their use of a common receptor subunit. While literature findings vary, they consistently support the role of IL-13 as a key driver of allergic inflammation.

The research presented in this article determined the systemic (blood plasma) and local (nasal lavage fluid) levels of interleukin-17 (IL-17) and interleukin-33 (IL-33) in healthy volunteers, patients with allergic rhinitis (AR), and patients with both allergic rhinitis and recently diagnosed bronchial asthma (AR+BA). IL-17 and IL-33 levels were consistent between AR and AR+BA patients but diverged when comparing either patient group or the combined group of all patients with healthy volunteers. These results indicate that AR and AR+BA patients represent a homogeneous group and suggest a role for IL-17 and/or IL-33 in the progression of AR to AR+BA. In conclusion, our data show that patients with AR only and those who progress to AR+BA from AR alone have elevated IL-17 levels in both nasal lavage fluid (NLF) and serum. This finding is consistent with recent studies and identifies a novel population of AR+BA patients with elevated IL-17 levels. The possibility of novel IL-33 regulatory mechanisms in these patients warrants further research.