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Mast cells control lung type 2 inflammation via prostaglandin E2-driven soluble ST2.
Alhallak, Kinan; Nagai, Jun; Zaleski, Kendall; Marshall, Sofia; Salloum, Tamara; Derakhshan, Tahereh; Hayashi, Hiroaki; Feng, Chunli; Kratchmarov, Radomir; Lai, Juying; Kuchibhotla, Virinchi; Nishida, Airi; Balestrieri, Barbara; Laidlaw, Tanya; Dwyer, Daniel F; Boyce, Joshua A.
Afiliación
  • Alhallak K; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Nagai J; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Zaleski K; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Marshall S; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Salloum T; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Derakhshan T; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Hayashi H; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Feng C; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Kratchmarov R; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Lai J; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Kuchibhotla V; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Nishida A; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Balestrieri B; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Laidlaw T; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Dwyer DF; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA.
  • Boyce JA; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, MA, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, MA, USA. Electronic address: jboyce@rics.bwh.harvard.edu.
Immunity ; 57(6): 1274-1288.e6, 2024 Jun 11.
Article en En | MEDLINE | ID: mdl-38821053
ABSTRACT
Severe asthma and sinus disease are consequences of type 2 inflammation (T2I), mediated by interleukin (IL)-33 signaling through its membrane-bound receptor, ST2. Soluble (s)ST2 reduces available IL-33 and limits T2I, but little is known about its regulation. We demonstrate that prostaglandin E2 (PGE2) drives production of sST2 to limit features of lung T2I. PGE2-deficient mice display diminished sST2. In humans with severe respiratory T2I, urinary PGE2 metabolites correlate with serum sST2. In mice, PGE2 enhanced sST2 secretion by mast cells (MCs). Mice lacking MCs, ST2 expression by MCs, or E prostanoid (EP)2 receptors by MCs showed reduced sST2 lung concentrations and strong T2I. Recombinant sST2 reduced T2I in mice lacking PGE2 or ST2 expression by MCs back to control levels. PGE2 deficiency also reversed the hyperinflammatory phenotype in mice lacking ST2 expression by MCs. PGE2 thus suppresses T2I through MC-derived sST2, explaining the severe T2I observed in low PGE2 states.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Dinoprostona / Ratones Noqueados / Interleucina-33 / Proteína 1 Similar al Receptor de Interleucina-1 / Pulmón / Mastocitos Límite: Animals / Female / Humans / Male Idioma: En Revista: Immunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Dinoprostona / Ratones Noqueados / Interleucina-33 / Proteína 1 Similar al Receptor de Interleucina-1 / Pulmón / Mastocitos Límite: Animals / Female / Humans / Male Idioma: En Revista: Immunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos