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. 2015 Jan-Feb;81(1 Suppl 1):S1-S49.
doi: 10.1016/j.bjorl.2015.01.003.

Rhinosinusitis: evidence and experience: October 18 and 19, 2013 - São Paulo

Affiliations

Rhinosinusitis: evidence and experience: October 18 and 19, 2013 - São Paulo

Wilma T Anselmo-Lima et al. Braz J Otorhinolaryngol. 2015 Jan-Feb.

Erratum in

  • Braz J Otorhinolaryngol. 2015 Jul-Aug;81(4):454. multiple author names added
No abstract available

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Figures

Figure 1
Figure 1
Visual Analogue Scale (VAS).
Figure 2
Figure 2
Rhinosinusitis symptoms of acute infection caused by rhinovirus in relation to the start time and duration. (Adapted from Gwaltney et al. [1967]).
Figure 3
Figure 3
Figure illustrating the participation of innate immunity in the pathogenesis of chronic rhinosinusitis (CRS): once the toll-like (TLR) or nod-like (NLR) receptors bind to pathogen-associated molecular pattern (PAMP), the production of Th1 and Th2 cytokines is stimulated, in addition to the decrease in Treg cytokines through two pathways: myeloid differentiation primary response-88 (MyD88) and TIR domain containing adapter inducing interferon-β TRIF). Furthermore, lactoferrins and lysozymes are produced.
Figure 4
Figure 4
Specific response to chronic rhinosinusitis without nasal polyps (CRSsNP). After stimulation of innate immunity in the presence of high concentrations of IL-6, there is a polarized adaptive response to Th1, with associated increase in Treg. That results in neutrophil response and a modulated inflammatory process.
Figura 5
Figura 5
Specific response to chronic rhinosinusitis with nasal polyps (CRSwNP). After stimulation of innate immunity, polarized adaptive response to Th2 occurs and Treg response decreases. As a result, the response is primarily eosinophilic and exacerbated, resulting in edema.

References

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