*Inhalation of Ascorbic Acid Modulates Sinonasal Immune System DOI: http://dx.doi.org/10.5772/intechopen.110891*

Nasal epithelial cells have the function as physical barrier and to eliminate pathogens through the generation of enzymes (lysozyme, peroxidases, phospholipases), complement components, protease inhibitors [Secretory Leukocyte Proteinase Inhibitor (SLPI) and elafin], permeabilizing peptides [β-defensins, cathelicidins, Bacterial Permeability Increasing protein (BPI) and Palate, Lung, and Nasal Epithelium Clone (PLUNC)], collectins (such as SP-A, SP-D, and MBL), binding/neutralizing proteins [mucins, Serum Amyloid A (SAA), and lactoferrin], pentraxins (PTX- 3 and CRP), small oxygen-reactive molecules (reactive oxygen species/ROS and nitric oxide), whose production is regulated by the engagement of Pathogen-Recognition Receptors (PRRs), such as Toll-Like Receptors (TLRs), and NOD-Like Family Receptors (NLR) [1–4]. In addition to their direct antimicrobial activity, epithelial-derived β-defensins and collectins (such as SP-A, SP-D) can also function as "Damage-Associated Molecular Patterns" (DAMPs). In particular, β-defensin 2 activates dendritic cells (DCs) upon binding to TLR-4, and β-defensin 3 to TLR-1 and TLR-2, while SP-A and SP-D act through the modulation and/or direct binding of TLR-2 and TLR-4 [3].

Exogenous antigens are transported by specialized intraepithelial M cells to antigen-presenting cells, such as macrophages, which in turn proceed and provide antigens to CD4+ T lymphocytes, which polarize in TH2 cells, generating Interleukin (IL)-4, IL-5 and IL-6, which trigger an Ig A-committed B-cell development, associated to the formation of the intrafollicular Germinal Centers (GC) [1–4]. Human M cells in adenoidal tissues are recognized by cytokeratin 20 (Ck20), and irregular microvilli as well as pocket-like structures, observed by Scanning Electron Microscopy (SEM) (**Figure 1**) [3, 6].
