An anti-eCIRP strategy for necrotizing enterocolitis.


Journal

Molecular medicine (Cambridge, Mass.)
ISSN: 1528-3658
Titre abrégé: Mol Med
Pays: England
ID NLM: 9501023

Informations de publication

Date de publication:
20 Sep 2024
Historique:
received: 20 05 2024
accepted: 11 09 2024
medline: 21 9 2024
pubmed: 21 9 2024
entrez: 20 9 2024
Statut: epublish

Résumé

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease characterized by intestinal inflammation and injury, with high mortality risk. Extracellular cold-inducible RNA-binding protein (eCIRP) is a recently discovered damage-associated molecular pattern that propagates inflammation and tissue injury; however, the role of eCIRP in NEC remains unknown. We hypothesize that eCIRP exacerbates NEC pathogenesis and the novel eCIRP-scavenging peptide, milk fat globule-epidermal growth factor-factor VIII (MFG-E8)-derived oligopeptide 3 (MOP3), attenuates NEC severity, serving as a new therapeutic strategy to treat NEC. Stool samples from premature neonates were collected prospectively and eCIRP levels were measured. Wild-type (WT) and CIRP Stool samples from NEC neonates had elevated eCIRP levels compared to healthy age-matched controls (p < 0.05). CIRP eCIRP exacerbates NEC evidenced by protection with CIRP-deficiency and administration of MOP3, a CIRP-directed therapeutic, in a murine model. Thus, eCIRP is a novel target with human relevance, and MOP3 is a promising treatment for lethal NEC.

Sections du résumé

BACKGROUND BACKGROUND
Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease characterized by intestinal inflammation and injury, with high mortality risk. Extracellular cold-inducible RNA-binding protein (eCIRP) is a recently discovered damage-associated molecular pattern that propagates inflammation and tissue injury; however, the role of eCIRP in NEC remains unknown. We hypothesize that eCIRP exacerbates NEC pathogenesis and the novel eCIRP-scavenging peptide, milk fat globule-epidermal growth factor-factor VIII (MFG-E8)-derived oligopeptide 3 (MOP3), attenuates NEC severity, serving as a new therapeutic strategy to treat NEC.
METHODS METHODS
Stool samples from premature neonates were collected prospectively and eCIRP levels were measured. Wild-type (WT) and CIRP
RESULTS RESULTS
Stool samples from NEC neonates had elevated eCIRP levels compared to healthy age-matched controls (p < 0.05). CIRP
CONCLUSIONS CONCLUSIONS
eCIRP exacerbates NEC evidenced by protection with CIRP-deficiency and administration of MOP3, a CIRP-directed therapeutic, in a murine model. Thus, eCIRP is a novel target with human relevance, and MOP3 is a promising treatment for lethal NEC.

Identifiants

pubmed: 39304832
doi: 10.1186/s10020-024-00935-3
pii: 10.1186/s10020-024-00935-3
doi:

Substances chimiques

RNA-Binding Proteins 0
Cirbp protein, mouse 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

156

Subventions

Organisme : Foundation for the National Institutes of Health
ID : R01GM129633
Organisme : Foundation for the National Institutes of Health
ID : U01AI170018
Organisme : Foundation for the National Institutes of Health
ID : R35GM118337
Organisme : Foundation for the National Institutes of Health
ID : R01HL076179
Organisme : Foundation for the National Institutes of Health
ID : R01AA028947
Organisme : Foundation for the National Institutes of Health
ID : U01AI170018

Informations de copyright

© 2024. The Author(s).

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Auteurs

Colleen P Nofi (CP)

Center for Immunology and Inflammation, the Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY, 11030, USA.
Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, 11030, USA.
Department of Surgery, Zucker School of Medicine, Manhasset, NY, 11030, USA.

Jose M Prince (JM)

Center for Immunology and Inflammation, the Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY, 11030, USA.
Department of Surgery, Zucker School of Medicine, Manhasset, NY, 11030, USA.

Mariana R Brewer (MR)

Department of Pediatrics, Zucker School of Medicine, Manhasset, NY, 11030, USA.

Monowar Aziz (M)

Center for Immunology and Inflammation, the Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY, 11030, USA. maziz1@northwell.edu.
Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, 11030, USA. maziz1@northwell.edu.
Department of Surgery, Zucker School of Medicine, Manhasset, NY, 11030, USA. maziz1@northwell.edu.
Department of Molecular Medicine, Zucker School of Medicine, Manhasset, NY, 11030, USA. maziz1@northwell.edu.

Ping Wang (P)

Center for Immunology and Inflammation, the Feinstein Institutes for Medical Research, 350 Community Dr., Manhasset, NY, 11030, USA. pwang@northwell.edu.
Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, 11030, USA. pwang@northwell.edu.
Department of Surgery, Zucker School of Medicine, Manhasset, NY, 11030, USA. pwang@northwell.edu.
Department of Molecular Medicine, Zucker School of Medicine, Manhasset, NY, 11030, USA. pwang@northwell.edu.

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