Where is the mucosal epithelium




















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Download references. You can also search for this author in PubMed Google Scholar. Correspondence to M A McGuckin. Reprints and Permissions. Mucins in the mucosal barrier to infection. Mucosal Immunol 1, — Download citation. Received : 27 November Accepted : 16 January Published : 05 March Issue Date : May Anyone you share the following link with will be able to read this content:.

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BMC Microbiology Gut Pathogens Nature Chemistry Nature Communications Scientific Reports Advanced search. Skip to main content Thank you for visiting nature. Download PDF. Abstract The mucosal tissues of the gastrointestinal, respiratory, reproductive, and urinary tracts, and the surface of the eye present an enormous surface area to the exterior environment. Mucins—an Integral Part of the Mucosal Barrier Mucosal epithelial tissues have evolved multiple mechanisms of defense in response to their vulnerability to microbial attack due to their exposure to the external environment.

Mucin Biosynthesis and Structure The tremendous energy investment by mucosal tissues in the production of mucins in the basal state, but particularly in response to infection, is testimony to the importance of these glycoproteins. Molecular structure of tight junctions and their role in epithelial transport.

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FEBS Lett. Coughlin SR, Camerer E. PARticipation in inflammation. J Clin Invest. Tissue factor- and factor X-dependent activation of protease-activated receptor 2 by factor VIIa. Trypsin IV, a novel agonist of protease-activated receptors 2 and 4. Protease-activated receptor 3 is a second thrombin receptor in humans. Nature —6. Cathepsin G activates protease-activated receptor-4 in human platelets. C Finally, epithelial cells recruit and regulate adaptive immune cells by expressing soluble and cell-surface molecules that alter the function of DCs and further modulate the adhesion, cytokine secretion, cytolytic activity, and differentiation of T cells in the late state of infection.

Furthermore, the differentiation and antibody secretion of B cells may also be modulated right. Among the three structural cell types epithelial cells, endothelial cells, and fibroblasts , epithelial cells constitute the external and internal surfaces of the body, creating physical barriers between our body and the external environment.

Notably, mucosal epithelia are large internal mucosal interfaces in the respiratory, gastrointestinal, and genital tracts that endow the mucosa with vital physiological functions.

In the context of infection, mucosal interfaces are often entry portals for many pathogens, especially viruses. Mucosal epithelial cells are usually the initial target cells for viral replication and the establishment of viral infections.

Thus, SARS-CoV-2 can efficiently infect upper respiratory epithelial cells and then spread to the submucosa and low respiratory tract. This cascade mechanism has been implicated in innate immune recognition and signaling, immune response and regulation, and immune pathology. A single-cell analysis of the small intestinal epithelium revealed that Salmonella-induced genes in all infected intestinal epithelial cells were enriched in pathways involved in the defense response to bacteria, including many genes that protect against Salmonella infection.

This process is especially important for the host response to primary viral infections in which no virus-specific immunity is available for host protection. Krausgruber et al. Surprisingly, structural cells expressed a variety of chemokines and cytokines in response to viral infection Fig.

This finding extends our view beyond typical immunological knowledge, in which the secretion of chemokines and especially cytokines has been thought to be mainly associated with immune cells. The results strongly suggested the presence of an interaction network between immune cells and structural cells and that the network could be altered during viral infection. LCMV is a well-studied virus that affects most organs, which allowed the authors to investigate global defense responses.

However, the systemic viral infection model is much different from mucosal-initiating viral infections. This notion also explains the notably high responses in fibroblasts and endothelial cells but not in epithelial cells in the liver, spleen, lungs, and large intestine after LCMV challenge. To evaluate the structural cell responses at the early stage of viral challenge, a mucosal viral infection model should be utilized.

The characteristics of early epithelial cell responses to mucosal viral infection could give us more concise and straightforward clues to understand the early viral trigger s and early activated genes in mucosal epithelial cells stimulated by natural mucosal viral infection. Furthermore, a mucosal viral infection model may provide an opportunity to perform longitudinal studies on the responses of epithelial cells, which would provide data on the early response of epithelial cells to infection at different time points.

This system would help to identify the early genes that play key roles in downstream immune regulation. In addition, to avoid overactivation or allergic reactions in the mucosa in response to the initial viral challenge, as well as to other stimuli from the external environment, it is hypothesized that genes with unrealized potential are activated under stringent regulation, such as more robust negative feedback in epithelial cells than in fibroblasts or endothelial cells.



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