Journal of Mucosal Immunology Research
Open Access

Airway Mucosal Immunity; Cytokines; Microbiome; Innate Lymphoid Cells; Dendritic Cells; Air Pollution; Respiratory Diseases; Asthma; Immune Response; Epithelial Cells

Introduction

Airway mucosal immunity is a complex system crucial for respiratory health. Epithelial cell-derived cytokines such as IL-25, IL-33, and TSLP initiate type 2 immune responses, promoting Th2 cell differentiation, allergic inflammation, and asthma[1].

The airway microbiome significantly modulates mucosal immunity; dysbiosis disrupts immune homeostasis and contributes to respiratory diseases[2].

Specific bacterial species can either promote or suppress inflammatory responses. Innate lymphoid cells (ILCs), especially ILC2s and ILC3s, are critical components of airway mucosal immunity[3].

They respond to epithelial-derived cytokines and contribute to both protective immunity and pathological inflammation in the lungs. Deficiencies in barrier function, due to viral infections or environmental pollutants, increase susceptibility to respiratory diseases[4].

Maintaining epithelial integrity prevents excessive immune activation. Dendritic Cells (DCs) in the airway mucosa sample antigens, migrate to lymph nodes, and present antigens to T cells, initiating adaptive immune responses[5].

DCs can promote either Th1 or Th2 immunity depending on the context. Emerging evidence highlights the importance of neuro-immune interactions in airway mucosal immunity[6].

Neuronal pathways can influence immune cell function and inflammatory responses in the lungs. Vitamin D modulates airway mucosal immunity; its deficiency increases susceptibility to respiratory infections and exacerbates asthma symptoms[7].

Airway epithelial cells actively participate in mucosal immunity, producing cytokines, chemokines, and antimicrobial peptides[8].

They also express pattern recognition receptors that detect pathogens and initiate immune responses. Long-term exposure to air pollution impairs airway mucosal immunity, increasing susceptibility to respiratory infections and chronic lung diseases[9].

Particulate matter and other pollutants disrupt epithelial barrier function and alter immune cell activity. Targeting specific immune pathways in the airway mucosa offers promise for novel therapies for respiratory diseases[10].

Approaches include blocking inflammatory cytokines, modulating ILC activity, and restoring epithelial barrier function.

Description

Airway mucosal immunity is a multifaceted defense system protecting the respiratory tract. Epithelial cells play a central role, releasing cytokines like IL-25, IL-33, and TSLP that trigger type 2 immune responses, driving allergic inflammation and asthma[1]. These cytokines activate innate immune cells and promote Th2 cell differentiation, leading to a cascade of events characteristic of allergic airway diseases. Disruption of this balance can lead to chronic inflammatory conditions. Understanding the precise mechanisms involved is crucial for developing targeted therapies.

The airway microbiome also profoundly influences mucosal immunity. Dysbiosis, or an imbalance in the microbial community, can compromise immune homeostasis and contribute to respiratory disease development[2]. The lung microbiome in healthy and diseased states demonstrates that specific bacterial species can either exacerbate or suppress inflammatory responses. This complex interplay between the microbiome and the host immune system is a key determinant of respiratory health. Further research is needed to identify the specific bacterial species that can be harnessed to promote beneficial immune responses.

Innate lymphoid cells (ILCs), particularly ILC2s and ILC3s, represent another critical component of airway mucosal immunity[3]. These cells respond to epithelial-derived cytokines and contribute to both protective immunity and pathological inflammation in the lungs. They can amplify or dampen inflammatory responses, depending on the context. Their role in allergic airway diseases such as asthma is particularly significant. Modulation of ILC activity is emerging as a promising therapeutic strategy. Deficiencies in barrier function, whether caused by viral infections or environmental pollutants, can lead to heightened susceptibility to respiratory diseases[4]. The integrity of the epithelial barrier is essential for preventing excessive immune activation.

Dendritic cells (DCs) in the airway mucosa initiate adaptive immune responses by sampling antigens, migrating to lymph nodes, and presenting these antigens to T cells[5]. Subsets of DCs can promote either Th1 or Th2 immunity, depending on the context. This fine-tuned regulation is essential for maintaining immune homeostasis. The role of DCs in asthma is particularly complex, as they can contribute to both disease exacerbation and resolution. Emerging evidence also points to the importance of neuro-immune interactions in airway mucosal immunity[6]. Neuronal pathways can influence immune cell function and inflammatory responses in the lungs.

Conclusion

Airway mucosal immunity is a complex system involving various components that protect the respiratory tract. Epithelial cells release cytokines that initiate type 2 immune responses, contributing to allergic inflammation and asthma. The airway microbiome modulates mucosal immunity, and imbalances can disrupt immune homeostasis and contribute to respiratory diseases. Innate lymphoid cells (ILCs) are crucial in airway mucosal immunity, responding to epithelial-derived cytokines and influencing inflammatory responses. Deficiencies in barrier function, caused by factors like viral infections or pollutants, increase susceptibility to respiratory diseases. Dendritic cells (DCs) initiate adaptive immune responses by sampling antigens and presenting them to T cells, influencing Th1 or Th2 immunity. Neuro-immune interactions are also important in airway mucosal immunity, with neuronal pathways affecting immune cell function and inflammatory responses. Vitamin D plays a modulatory role, and its deficiency can increase susceptibility to respiratory infections and exacerbate asthma symptoms. Airway epithelial cells actively participate in mucosal immunity by producing cytokines, chemokines, and antimicrobial peptides. Long-term exposure to air pollution can impair airway mucosal immunity, leading to increased susceptibility to respiratory infections and chronic lung diseases. Targeting specific immune pathways in the airway mucosa holds promise for developing novel therapies for respiratory diseases.

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