{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T04:34:32Z","timestamp":1789619672748,"version":"build-2803163510"},"reference-count":58,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T00:00:00Z","timestamp":1759881600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T00:00:00Z","timestamp":1759881600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2025,10,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Conidia are the primary infection structures in\n                      <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                      , the etiologic agent of aspergillosis. Here, we characterized CrpA (a\n                      <jats:underline>c<\/jats:underline>\n                      ysteine-\n                      <jats:underline>r<\/jats:underline>\n                      ich\n                      <jats:underline>p<\/jats:underline>\n                      rotein), a conidial surface-associated protein important for fungal evasion and host immunity modulation. \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      conidia elicited decreased production of proinflammatory cytokines and increased production of anti-inflammatory cytokine IL-10 from murine macrophages and in the lungs of infected mice. Murine macrophages exposed to \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      conidia produce significantly higher levels of prostaglandins PGE2 and PGD2, suggesting that deletion of CrpA modulates cytokine production through effects on eicosanoid signaling. While \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      spores have lower virulence in larval zebrafish, this difference is abrogated in larvae that cannot produce prostaglandins. The CrpA protein can directly modulate PGE2 and cytokine production by macrophages, and solid-state NMR shows that \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      swollen conidia present lower \u03b2\u22121,3-glucan and chitin than the wild-type strain, suggesting that the effects of the \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      mutant on macrophages are due to the combinatorial effects of direct CrpA action and altered cell wall PAMP recognition. \u0394\n                      <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                      mutants are avirulent in an immunocompetent murine model of aspergillosis, and high CrpA-specific IgG responses were found in antisera from individual patients with invasive pulmonary aspergillosis, suggesting a role for CrpA in\n                      <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                      pathogenesis.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Conidia serve as the primary infectious units of\n                        <jats:italic toggle=\"yes\">Aspergillus fumigatus<\/jats:italic>\n                        , the causative agent of aspergillosis. This study identifies CrpA, a cysteine-rich protein found on the conidial surface, as a crucial regulator of immune modulation and fungal virulence. Loss of CrpA (\u0394\n                        <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                        ) alters host immune responses, resulting in reduced production of proinflammatory cytokines and increased IL-10 levels in both murine macrophages and infected lungs. \u0394crpA conidia also stimulate elevated levels of prostaglandins PGE2 and PGD2. This immunomodulatory effect is dependent on eicosanoid signaling as the virulence of \u0394\n                        <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                        is restored in prostaglandin-deficient zebrafish larvae. CrpA directly modulates macrophage production of PGE2 and cytokines. Solid-state NMR analysis shows that \u0394\n                        <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                        conidia expose lower levels of \u03b2\u22121,3-glucan and chitin, suggesting that CrpA influences both cell wall composition and host pattern recognition receptor engagement. \u0394\n                        <jats:italic toggle=\"yes\">crpA<\/jats:italic>\n                        strains are avirulent in immunocompetent mice, and patients with invasive pulmonary aspergillosis exhibit elevated CrpA-specific IgG. These results highlight CrpA as a key virulence factor in\n                        <jats:italic toggle=\"yes\">A. fumigatus<\/jats:italic>\n                        and a promising target for antifungal therapy.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02481-25","type":"journal-article","created":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T13:27:14Z","timestamp":1757683634000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["<i>Aspergillus fumigatus<\/i>\n                    effector crpA orchestrates host prostaglandin signaling to promote fungal virulence"],"prefix":"10.1128","volume":"16","author":[{"given":"Camila Figueiredo","family":"Pinzan","sequence":"first","affiliation":[{"name":"Faculdade de Ci\u00eancias Farmac\u00eauticas de Ribeir\u00e3o Preto, Universidade de S\u00e3o Paulo","place":["Ribeir\u00e3o Preto, 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