xRead - Nasal Obstruction (September 2024) Full Articles

20426984, 2021, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/alr.22741 by Stanford University, Wiley Online Library on [01/07/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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International consensus statement on rhinosinusitis

during primary ESS in order to reduce the risk of persistent or recurrent CRS. 799

control patients. Trefoil factor family (TFF) proteins are also involved in epithelial protection and repair. 805,806 On the contrary, 1 study showed decreased innate pep tide activity in CRSsNP, although in a different family of proteins. Richer et al. 807 found that S100A7, A8, and A9 mRNA levels were significantly decreased in CRSsNP when compared with controls. Pattern Recognition Receptors (PRRs) and Bitter Taste Receptors. The specific patterns of microbial components are recognized by PRRs, which are components of the innate immune system in mammals. The TLRs represent the primary PRRs, playing an important role in recogniz ing specific microbial components and triggering a signal ing cascade that directly activates the immune cells. 808 The TLR family consists of at least 13 members. For example, TLR4 was identified as a receptor that responds to gram negative bacteria lipopolysaccharide (LPS). The MyD88 dependent pathway and TRIF-dependent pathway were predominant TLR-mediated signaling pathways that have been identified. 809 These pathways subsequently induce profound inflammatory cytokine genes. More recently, the evidence demonstrates that activation of TLR4 by inhaled pathogens results in a doubling of basal exosome secretion and subsequent induce a 4-fold increase in NO production. 810 A number of investigations have demonstrated altered activity of PRRs in CRSsNP. Van Crombruggen et al. exam ined the receptor for glycation end products (RAGE) in CRSsNP and controls. They found sinus mucosal pro tein levels of the soluble form of RAGE to be elevated in CRS while the membrane form was decreased. 811 Zhang et al. 812 showed that TLR4 and TLR7 mRNAs and pro teins levels were significantly lower in the sinonasal tis sue of CRSsNP compared to that of CRSwNP and controls. Similarly, Detwiller et al. 813 revealed that patients with CRSsNP showed lower mean expression of TLR2 mRNA in mucosal biopsy specimens compared to controls. Con versely, Hirschberg et al. 806 showed the tissue TLR2 mRNA level in patients with CRSsNP was significantly higher compared to healthy controls. However, 2 studies found that there were no significant differences between CRSsNP patients and controls in terms of the level of tissue TLR9 protein or mRNA. 813,814 These studies suggest that altered PRR responses, especially TLR2, 4, and 7, may play a role inCRSsNP. Taste receptor family 2 (T2R) bitter taste receptors were originally identified and named based on their role in type 2 taste cells of the tongue. The function of T2R is to detect the presence of potentially harmful ingested chemicals. 815 One T2R isoform, taste receptor family 2 isoform 38 pro tein (T2R38) has recently been linked with sinonasal innate immunity, upper airway infection. The activation of T2R38 by bacteria increases NO production, ciliary beat

Septal Deviation as a Contributing Factor for CRS Aggregate Grade of Evidence: C (Level 2: 1 study; level 3: 1 study, Level 4: 1 study; Table IX-12).

IX.C.11 Contributing Factors for CRSsNP: Innate immunity Multiple innate immune mechanisms exist at the sinonasal mucosal surface to defend the host against envi ronmental organisms and pathogens. Innate immunity includes nonspecific innate immune mucosal defense and pathogen-specific innate mechanisms that are directed against shared microbial patterns. Nonspecific innate immune mucosal defense includes, but is not limited to, sinonasal MCC, secreted antimicrobials, and com plements. One example of a pathogen-specific innate immune mechanism is pattern recognition receptors (PRRs). The 2 best-characterized classes of PRRs are the TLR family and the nucleotide-binding oligomer ization domain-like receptors (NLR) family. 800 It has been hypothesized that dysregulation of PRR pathways and innate immune effectors likely contribute to the inflammatory state in CRS. This section will cover antimicrobial proteins, PRR, and bitter taste receptors in innate immunity. The contribu tion of innate immune cells and epithelial-derived innate cytokines are further described in Table IX-15. Key Antimicrobial Proteins and Peptides. Seven stud ies revealed that the activities of select innate antimicro bial proteins and peptides are increased in patients with CRSsNP. Only 1 study showed that the activity of an innate immunity antimicrobial protein was decreased in patients with CRSsNP. Lee et al. 801 showed that surfactant protein A (SP- A) mRNA and protein levels were significantly increased in the sinonasal tissue of CRSsNP compared to that of normal controls. Woods et al. 802 found that immunostain ing of lysozyme was significantly increased in mucosal biopsy specimens of CRSsNP compared to control, but not at the mRNA level. Schlosser et al. and others 803,804 demonstrated that factor B, complement components C3 and C5 mRNAs level were significantly higher in sinus mucosa biopsy specimens of CRSsNP compared to that of