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Comparison of the cellular structure, function and immunity specialisations of the respiratory and gastrointestinal tracts Although the respiratory and gastrointestinal tracts have superficially similar structures, consisting of tracts lined with mucous membranes (an epithelium in contact with the lumen, a basement membrane, a lamina propria, smooth muscle layers and a submucosa) their functions are different. The respiratory tract's primary function is to facilitate gaseous exchange between air and the blood, and the gastrointestinal tract's primary function is to digest food and from it, absorb nutrients and water. This crucial dissimilarity results in many variances between the tracts; for example, airway epithelium is ciliated pseudostratified columnar, whereas gut epithelium is mainly simple columnar epithelium. Gut epithelial cells express many membrane proteins which the lung does not, such as SGLT1, a secondary active transporter which exchanges sodium for glucose from the intestinal lumen, and membrane-bound hydrolytic enzymes such as proteases. Intestinal epithelial cells are arranged in villi and have microvilli for increasing the surface area, enhancing absorption, whereas the respiratory epithelium increases surface area for gaseous exchange by forming multitudes of alveoli. Both the respiratory and gastrointestinal tract represents significant interfaces with the external environment, and are therefore exposed to a large number of antigens, some of which will be pathogens and require an immune response. These tracts are lined mainly with a single sheet of epithelium, so these barriers are specialised to provide innate immunity in what would otherwise be a vulnerable area. There exist several shared immunity mechanisms, such as IgA production, the actions of toll-like receptors (TLRs), goblet cell secretions, and the response of T cells, dendritic cells (DCs) and leukocytes. However, in the gastrointestinal tract there are additional cells which have a role in the immune response, including M cells, Paneth cells and follicle associated epithelium (FAE); this is specialised epithelium which covers the domed follicles over Peyer's patches. This illustrates another additional property of the gut compared to the lung, which is that in the gut there is anatomical separation of immune system tissue, e.g. the lymphoid tissue, with tissue of other functions. Although the airways do not have Peyer's patches and associated specialised cells, there are some cells interspersed in lung epithelium which are not present in the gastrointestinal tract, such as Clara cells, P1 cells and P2 cells. An interesting feature of the gut epithelium is that it requires non-pathogenic antigen activation of cells for homeostasis; this activation is due to the microbial flora which live commensally in the gut. Finally, there appears to be a complex system of 'homing' of immune cells to different mucosae, but this is more marked in the intestinal mucous membrane. Shared immunity mechanisms include IgA and defensin production, TLR expression, and the action of dendritic cells. Mucosal B cells, when activated, differentiate into mucosal plasma cells and release IgA7. IgA is indispensible in lumen as it has a higher resistance to proteases than other immunoglobulins, and so is not degraded on the mucosa surfaces 6. The actions of this antibody are varied and initiate many parts of the local immune response. IgA plays a role in M cell function; opsonisation of antigens; neutralisation of antigens on mucosal surfaces; and interacts with many immune cell types. Both GI and respiratory epithelial lining fluid contain defensins, which are microbicidal cationic substances able to kill potential pathogens, neutralised chemokines, and recruit dendritic and T cells; their presence increases in cystic fibrosis, COPD and bronchiolitis obliterans 3. TLRs are crucial components in detecting pathogens, able to bind to conserved microbial patterns in macromolecules such as lipopolysaccharides (LPS); LPS hyporesponsive mice have mutations in TLR44. Upon activation, the intracellular domains of TLRs initiate immune responses: TLR3 releases defensins, whilst TLR9 activation results in increased interleukin expression4. Numerous other roles mediated by specific TLR pathway responses are inducing
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