Amnion responses to intrauterine inflammation and effects of inhibition of TNF signaling in preterm Rhesus macaque.
- Resource Type
- Academic Journal
- Authors
- Presicce P; Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Cappelletti M; Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Morselli M; Department of Molecular, Cell and Developmental Biology Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Institute for Quantitative and Computational Biosciences - Collaboratory at the University of California Los Angeles, Los Angeles, CA, USA.; Ma F; Department of Molecular, Cell and Developmental Biology Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Institute for Quantitative and Computational Biosciences - Collaboratory at the University of California Los Angeles, Los Angeles, CA, USA.; Senthamaraikannan P; Division of Neonatology/Pulmonary Biology, Cincinnati Children's Hospital Research Foundation, The University of Cincinnati College of Medicine, Cincinnati, OH, USA.; Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, The University of Cincinnati College of Medicine, Cincinnati, OH, USA.; Protti G; Institute for Quantitative and Computational Biosciences - Collaboratory at the University of California Los Angeles, Los Angeles, CA, USA.; Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.; Nadel BB; Department of Molecular Cellular and Developmental Biology, and Institute for Genomics and Proteomics, University of California Los Angeles, Los Angeles, CA, USA.; California National Primate Research Center, University of California Davis, Davis, CA, USA.; Aryan L; Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Eghbali M; Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Salwinski L; UCLA-DOE Institute of Genomics and Proteomics, University of California Los Angeles, Los Angeles, CA, USA.; Pithia N; Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; De Franco E; Department of Obstetrics/Gynecology, Maternal-Fetal Medicine, University of Cincinnati, Cincinnati, OH, USA.; Miller LA; Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California Davis, CA, USA.; Pellegrini M; Department of Molecular, Cell and Developmental Biology Medicine at the University of California Los Angeles, Los Angeles, CA, USA.; Institute for Quantitative and Computational Biosciences - Collaboratory at the University of California Los Angeles, Los Angeles, CA, USA.; Jobe AH; Division of Neonatology/Pulmonary Biology, Cincinnati Children's Hospital Research Foundation, The University of Cincinnati College of Medicine, Cincinnati, OH, USA.; Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, The University of Cincinnati College of Medicine, Cincinnati, OH, USA.; Chougnet CA; Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, OH, USA.; Kallapur SG; Divisions of Neonatology and Developmental Biology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
- Source
- Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
- Subject
- Language
- English
Intrauterine infection/inflammation (IUI) is a frequent complication of pregnancy leading to preterm labor and fetal inflammation. How inflammation is modulated at the maternal-fetal interface is unresolved. We compared transcriptomics of amnion (a fetal tissue in contact with amniotic fluid) in a preterm Rhesus macaque model of IUI induced by lipopolysaccharide with human cohorts of chorioamnionitis. Bulk RNA sequencing (RNA-seq) amnion transcriptomic profiles were remarkably similar in both Rhesus and human subjects and revealed that induction of key labor-mediating genes such as IL1 and IL6 was dependent on nuclear factor κB (NF-κB) signaling and reversed by the anti-tumor necrosis factor (TNF) antibody Adalimumab. Inhibition of collagen biosynthesis by IUI was partially restored by Adalimumab. Interestingly, single-cell transcriptomics, flow cytometry, and immunohistology demonstrated that a subset of amnion mesenchymal cells (AMCs) increase CD14 and other myeloid cell markers during IUI both in the human and Rhesus macaque. Our data suggest that CD14 + AMCs represent activated AMCs at the maternal-fetal interface.
Competing Interests: The authors declare no competing interests.
(© 2023 The Author(s).)