{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T19:29:31Z","timestamp":1791919771809,"version":"4.3.4"},"reference-count":67,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T00:00:00Z","timestamp":1721779200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Allergic fungal rhinosinusitis (AFRS) is a severe phenotype of chronic rhinosinusitis with nasal polyposis (CRSwNP), characterised by localised and exaggerated type 2 inflammation. While fungal antigenic stimulation of unregulated Th2\u2010mediated inflammation is the core pathophysiological mechanism, the direct and synergistic role of bacteria in disease modification is a pervasive hypothesis. We set out to define the microenvironment of AFRS to elucidate virulent organisms that may be implicated in the pathophysiology of AFRS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methodology<\/jats:title>\n                    <jats:p>We undertook a cross\u2010sectional study of AFRS patients and non\u2010fungal CRSwNP patients. Demographics, disease severity, culture and microbiome sequences were analysed. Multimodality microbiome sequencing included short\u2010read next\u2010generation sequencing (NGS) on the Illumina Miseq (16S rRNA and ITS) and full\u2010length 16S rRNA sequencing on the Oxford Nanopore Technologies GridION (ONT).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Thirty\u2010two AFRS and 29 non\u2010fungal CRSwNP patients (NF) were included in this study.\n                      <jats:italic>Staphylococcus aureus<\/jats:italic>\n                      was the dominant organism cultured and sequenced in both AFRS and NF groups (AFRS 27.54%; NF 18.04%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.07).\n                      <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n                      (AFRS 12.31%; NF 0.98%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.03) and\n                      <jats:italic>Haemophilus influenzae<\/jats:italic>\n                      (AFRS 15.03%; NF 0.24%;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.005) were significantly more abundant in AFRS. Bacterial diversity (Shannon's index) was considerably lower in AFRS relative to NF (AFRS 0.6; NF 1.0,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u2009.008).\n                      <jats:italic>Aspergillus<\/jats:italic>\n                      was the most cultured fungus in AFRS (10\/32, 31.3%). The AFRS sequenced mycobiome was predominantly represented by\n                      <jats:italic>Malassezia<\/jats:italic>\n                      (43.6%), Curvularia (18.5%) and\n                      <jats:italic>Aspergillus<\/jats:italic>\n                      (16.8%), while the NF mycobiome was nearly exclusively\n                      <jats:italic>Malassezia<\/jats:italic>\n                      (84.2%) with an absence of\n                      <jats:italic>Aspergillus<\/jats:italic>\n                      or dematiaceous fungi.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      A low diversity, dysbiotic microenvironment dominated by\n                      <jats:italic>Staphylococcus aureus, Streptococcus pneumoniae<\/jats:italic>\n                      and\n                      <jats:italic>Haemophilus influenzae<\/jats:italic>\n                      characterised the bacterial microbiome of AFRS, with a mycobiome abundant in\n                      <jats:italic>Malassezia<\/jats:italic>\n                      ,\n                      <jats:italic>Aspergillus<\/jats:italic>\n                      and\n                      <jats:italic>Curvularia<\/jats:italic>\n                      . While\n                      <jats:italic>Staphylococcus aureus<\/jats:italic>\n                      has been previously implicated in AFRS through enterotoxin superantigen potential,\n                      <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n                      and\n                      <jats:italic>Haemophilus influenzae<\/jats:italic>\n                      are novel findings that may represent alternate cross\u2010kingdom pathophysiological mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.16240","type":"journal-article","created":{"date-parts":[[2024,7,24]],"date-time":"2024-07-24T05:26:42Z","timestamp":1721798802000},"page":"3082-3094","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Characterising the allergic fungal rhinosinusitis microenvironment using full\u2010length\n                    <scp>16S rRNA<\/scp>\n                    gene amplicon sequencing and fungal\n                    <scp>ITS<\/scp>\n                    sequencing"],"prefix":"10.1111","volume":"79","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3081-5433","authenticated-orcid":false,"given":"J. 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