title: Injury-induced immune responses in Hydra.
abstract: The impact of injury-induced immune responses on animal regenerative processes is highly variable, positive or negative depending on the context. This likely reflects the complexity of the innate immune system that behaves as a sentinel in the transition from injury to regeneration. Early-branching invertebrates with high regenerative potential as Hydra provide a unique framework to dissect how injury-induced immune responses impact regeneration. A series of early cellular events likely require an efficient immune response after amputation, as antimicrobial defence, epithelial cell stretching for wound closure, migration of interstitial progenitors toward the wound, cell death, phagocytosis of cell debris, or reconstruction of the extracellular matrix. The analysis of the injury-induced transcriptomic modulations of 2636 genes annotated as immune genes in Hydra identified 43 genes showing an immediate/early pulse regulation in all regenerative contexts examined. These regulations point to an enhanced cytoprotection via ROS signaling (Nrf, C/EBP, p62/SQSMT1-l2), TNFR and TLR signaling (TNFR16-like, TRAF2l, TRAF5l, jun, fos-related, SIK2, ATF1/CREB, LRRC28, LRRC40, LRRK2), proteasomal activity (p62/SQSMT1-l1, Ced6/Gulf, NEDD8-conjugating enzyme Ubc12), stress proteins (CRYAB1, CRYAB2, HSP16.2, DnaJB9, HSP90a1), all potentially regulating NF-κB activity. Other genes encoding immune-annotated proteins such as NPYR4, GTPases, Swap70, the antiproliferative BTG1, enzymes involved in lipid metabolism (5-lipoxygenase, ACSF4), secreted clotting factors, secreted peptidases are also pulse regulated upon bisection. By contrast, metalloproteinases and antimicrobial peptide genes largely follow a context-dependent regulation, whereas the protease inhibitor α2macroglobulin gene exhibits a sustained up-regulation. Hence a complex immune response to injury is linked to wound healing and regeneration in Hydra.
authors.affiliation: Department of Genetics and Evolution, Faculty of Sciences, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva 04, Switzerland.
authors.forename: Yvan
authors.initials: Y
authors.lastname: Wenger
authors.affiliation: Department of Genetics and Evolution, Faculty of Sciences, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva 04, Switzerland.
authors.forename: Wanda
authors.initials: W
authors.lastname: Buzgariu
authors.affiliation: Department of Genetics and Evolution, Faculty of Sciences, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva 04, Switzerland.
authors.forename: Silke
authors.initials: S
authors.lastname: Reiter
authors.affiliation: Department of Genetics and Evolution, Faculty of Sciences, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva 04, Switzerland. Electronic address: brigitte.galliot@unige.ch.
authors.forename: Brigitte
authors.initials: B
authors.lastname: Galliot
mesh_terms: D000818:Animals; D006829:Hydra / Q000276:immunology* / Q000502:physiology*; D007113:Immunity, Innate; D010944:Plants / Q000276:immunology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012038:Regeneration; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species
keywords: Evolution of innate immune system; Injury-induced immune response; ROS signaling in Hydra; Tissue repair and regeneration; Transcriptomic signature; Wound healing