Editing Sinusitis (section)

==Pathophysiology==
Chronic rhinosinusitis is multifactorial process hypothesized to be caused by inflammatory processes driven by dysfunction between local host and environmental interactions.<ref name=":12">{{Cite journal |last1=Fokkens |first1=W.J. |last2=Lund |first2=V.J. |last3=Hopkins |first3=C. |last4=Hellings |first4=P.W. |last5=Kern |first5=R. |last6=Reitsma |first6=S. |last7=Toppila-Salmi |first7=S. |last8=Bernal-Sprekelsen |first8=M. |last9=Mullol |first9=J. |last10=Alobid |first10=I. |last11=Terezinha Anselmo-Lima |first11=W. |last12=Bachert |first12=C. |last13=Baroody |first13=F. |last14=von Buchwald |first14=C. |last15=Cervin |first15=A. |date=2020-02-01 |title=European Position Paper on Rhinosinusitis and Nasal Polyps 2020 |url=https://www.rhinologyjournal.com/Documents/Supplements/supplement_29.pdf |journal=Rhinology  |volume=58 |issue=Suppl S29 |pages=1–464 |doi=10.4193/Rhin20.600|pmid=32077450 }}</ref>  It is divided into two [[phenotype]]s that depend on the presence or absence of [[nasal polyp]]s.<ref name=":22">{{Cite journal |last1=Kato |first1=Atsushi |last2=Schleimer |first2=Robert P. |last3=Bleier |first3=Benjamin S. |date=May 2022 |title=Mechanisms and pathogenesis of chronic rhinosinusitis |journal=Journal of Allergy and Clinical Immunology |volume=149 |issue=5 |pages=1491–1503 |doi=10.1016/j.jaci.2022.02.016 |issn=0091-6749 |pmc=9081253 |pmid=35245537}}</ref> Chronic rhinosinusitis with nasal polyps and chronic rhinosinusitis without nasal polyps are thought to have two different inflammatory pathways, with the latter form driven by a [[Th1 response]] and the former driven by a [[T helper cell|Th2 response]].<ref>{{Cite book |last1=Scholes |first1=Melissa A. |title=ENT secrets |last2=Ramakrishnan |first2=Vijay R. |date=May 9, 2022 |publisher=Elsevier Health Sciences |isbn=9780323733588 |edition=5th |pages=155–160}}</ref>  Both pathways result in an increase in inflammatory molecules ([[Cytokine|cytokines]]). The Th1 response is characterized by secretion of [[interferon gamma]].<ref name=":22" /> The Th2 response is characterized by secretion of [[interleukin-4 receptor]], [[interleukin 5]], and [[interleukin 13]].<ref name=":22" /> Both forms of chronic rhinosinusitis are considered to be highly heterogenous, each with the ability to demonstrate three inflammatory [[endotype]]s, the third being a [[T helper cell|Th17 response]].<ref name=":22" />