Mouse Lung epithelial cells are crucial for respiratory function. Located at the interface between the environment and the tissue, they act as protective shields. They also participate in fluid balance, immune response, surfactant synthesis, repair processes, particulate clearance, and disease pathogenesis. Due to the changes in the structure of the lungs during the respiratory cycle, they are exposed to mechanical stress. Due to their exposure to pathogens, they have become integral to research on understanding the pathophysiology of respiratory diseases, such as infections, chronic obstructive pulmonary diseases (COPD), asthma, idiopathic pulmonary fibrosis, non-small cell lung cancer (NSCLC), and infections such as COVID-19.
Types and Functions of Mouse Lung Epithelial Cells
The lung Epithelium consists of the airway and alveolar epithelium. The airway has a pseudostratified columnar epithelium. The  following are the most common cell type of the airway epithelium:
Basal cell: They are cuboidal and are responsible for regeneration of epithelium after injury and thus are the stem cells of airway epithelium. 
Goblet cell: They produce mucus containing antimicrobials, electrolytes, mucins, etc., that trap debris and pathogens.
Ciliated cell: The cilia on the cells move the mucus trapped debris upwards by a rhythmic wave movement for expulsion from the body.
Club or Clara cell: They are prominent in the epithelium of bronchioles. They can differentiate into other cells of the epithelium aiding in injury repair. 
Alveoil is lined by thin squamous epithelium for allowing gaseous exchange. It contains two primary cell types- type 1 pneumonocytes and type II pneumonocytes. Type 1 facilitates gas exchange, whereas type II pneumonocytes secrete surfactant that prevents the collapse of the lungs.
Mouse Lung Epithelial Cells in Injury Repair
Epithelium can be injured due to infections, allergies, xenobiotics (cigarette smoke), cancer, and inflammation. The injury recruits immune cells and initiates an inflammation cascade. It is a complex process that requires meticulous regulation by both indirect and direct mechanisms. The local progenitors migrate to the site of injury from the nearby region and peripheral blood, where they proliferate and differentiate to restore the structural integrity. While basal and club cells replenish the airway epithelium, type II pneumonocytes reestablish the alveolar epithelium by differentiating into type I pneumonocytes. Additionally, fibroblasts also proliferate and transform into myofibroblasts to produce extracellular matrix for structural support.
The cross-talk between epithelial and immune cells is crucial and any disruption might turn into a chronic condition. For example, IL-33 is damage associated molecular pattern (DAMP) which activates T cells, basophils, and eosinophils while transforming macrophages into pro-fibrotic M2 macrophages. The inflamed airways found in COPD and smoke damaged lungs, have high expression of IL-33.
Mouse Lung Epithelial Cells in Immune Response
These cells form the first line of defense against external pathogens. They secrete mucus containing mucin glycoproteins, lysozyme, immunoglobulin A, etc., to act against invading pathogens. Additionally, mucus also contains antimicrobial peptides belonging to the cathelicin and defensin families. 
The respiratory epithelium has pattern recognition receptors (PRRs), such as toll-like receptors (TLRs) and nucleotide oligomerization domain receptors (NOD), which detect damaged cells and pathogens. In response to pathogens, they secrete molecules that activate immune cells.  For example, pulmonary epithelial cells secrete IL-25 and IL-33 that activate eosinophils and basophils. Furthermore, the respiratory epithelium produces interferons and reactive oxygen species that modulate inflammation.
Epithelial Dysfunction
The value of lung epithelium is evident during diseases. The barrier function of the epithelium decreases while mucus production increases in asthma and COPD. The innate immune response and antioxidant activities of the epithelium also diminish. The resultant inflammation constricts the bronchioles, triggering epithelial remodeling. Cigarette smoke, a risk factor for COPD, increases the inflammatory mediators, resulting in reduced barrier function. COPD also demonstrates impaired cystic fibrosis transmembrane conductance receptor (CFTR) function. Cystic fibrosis also exhibits deficits in mucosal defense, impaired pathogen clearance, and airway remodeling.
Downregulation of Inflammation
Pulmonary epithelial cells also cause infection tolerance. It emphasises on restricting the ability of pathogens to inflict damage and abnormal activation of immune response. For instance, alveolar epithelium interacts with macrophages via connexin-based gap junctions to alleviate neutrophil recruitment and release of inflammatory cytokines. Another study also reported how mucin can regulate inflammation by TLR pathway.
Conclusion
The occurrence of COVID-19 has significantly exploded the research on pulmonary cells. Single-cell sequencing technology has been employed to identify the heterogeneous cell populations of lungs, especially the progenitors. Since the lung progenitors originate from epithelium, it has been subjected to extensive investigation. Additionally, their reentry from quiescent state into the cell cycle during an injury for proliferation and differentiation has also baffled scientists. Three-dimensional lung organoids and preliminary tissue models have facilitated the drug development process. The scope of pulmonary epithelium functions has notably expanded, encouraging further experimentation to pave the way for better therapeutic options and health outcomes. Kosheeka provides superior quality of primary mouse lung epithelial cells to assist in your investigational studies.