A four-part guide to lung immunology: Invasion, inflammation, immunity, and intervention

Abstract

Lungs are important respiratory organs primarily involved in gas exchange. Lungs interact directly with the environment and their primary function is affected by several inflammatory responses caused by allergens, inflammatory mediators, and pathogens, eventually leading to disease. The immune architecture of the lung consists of an extensive network of innate immune cells, which induce adaptive immune responses based on the nature of the pathogen(s). The balance of immune responses is critical for maintaining immune homeostasis in the lung. Infection by pathogens and physical or genetic dysregulation of immune homeostasis result in inflammatory diseases. These responses culminate in the production of a plethora of cytokines such as TSLP, IL-9, IL-25, and IL-33, which have been implicated in the pathogenesis of several inflammatory and autoimmune diseases. Shifting the balance of Th1, Th2, Th9, and Th17 responses have been the targets of therapeutic interventions in the treatment of these diseases. Here, we have briefly reviewed the innate and adaptive i3mmune responses in the lung. Genetic and environmental factors, and infection are the major causes of dysregulation of various functions of the lung. We have elaborated on the impact of inflammatory and infectious diseases, advances in therapies, and drug delivery devices on this critical organ. Finally, we have provided a comprehensive compilation of different inflammatory and infectious diseases of the lungs and commented on the pros and cons of different inhalation devices for the management of lung diseases. The review is intended to provide a summary of the immunology of the lung, with an emphasis on drug and device development.

Inflammation and Organic Cation Transporters Novel (OCTNs)

“…These features correlate well with the above-mentioned involvement of the OCTNs in inflammatory processes [36][37][38][39], characterized, among other factors, by excess ROS formation [40]. OCTN1 and OCTN2 also share localization in tissues such as the lungs, gut epithelia, and immune cells, directly or indirectly involved in inflammatory processes [5,6,21,[41][42][43][44][45]. Indeed, the frontier epithelia are exposed to microorganisms, inhaled drugs, cigarette smoke, and other pollutants that may give rise to inflammation [21,44,46].…”

Advances in the Immunology of the Host–Parasite Interactions in African Trypanosomosis, including Single-Cell Transcriptomics

“…The lung contains a varied community of tissue-resident innate and adaptive immune cells, cooperating to preserve tissue equilibrium and defend against recurring pathogen challenges. The immune cell architecture of the lungs comprises an extensive network of innate immune cells and an adaptive immune response that includes alveolar macrophages, dendritic cells, neutrophils, B cells, T cells, and antigen-presenting cells [ 171 , 172 ]. Specific populations of resident immune cells sustain immune homeostasis in various lung compartments.…”

Microbiota and Immunity during Respiratory Infections: Lung and Gut Affair

“…Pneumonias due to Gram-negative Haemophylus (H.) influenzae and Klebsiella (K.) pneumoniae spread among patients over 50 years with chronic obstructive lung disease or alcoholism, while pneumonias due to Gram-negative Mycoplasma pneumoniae and Chlamydophila pneumoniae are more diffuse in children. Viral pneumonias caused by respiratory syncytial virus (RSV) and adenoviruses are rare in the healthy population, whereas pneumonia caused by influenza viruses is still a cause of high mortality in old people and in patients with underlying diseases [42]. Ecologically, infections are characterized by an increased microbial burden and a reduction in community diversity, together with an increased host inflammation and tissue injury [43].…”