Infection induced inflammation impairs wound healing through IL-1b signaling
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA994500 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25258800_1.fastq.gz | Fastqsanger.gz | |||
| SRR25258800_2.fastq.gz | Fastqsanger.gz | |||
| SRR25258801_1.fastq.gz | Fastqsanger.gz | |||
| SRR25258801_2.fastq.gz | Fastqsanger.gz | |||
| SRR25258802_1.fastq.gz | Fastqsanger.gz |
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Project description:Wound healing is impaired by infection; however, how microbe-induced inflammation modulates tissue repair remains unclear. We took advantage of the optical transparency of zebrafish and a genetically tractable microbe, Listeria monocytogenes, to probe the role of infection and inflammation in wound healing. We found a critical window of microbial clearance necessary to limit persistent inflammation and enable efficient wound repair. Infection with bacteria engineered to activate the inflammasome, Lm-Pyro, induced persistent inflammation and impaired healing despite low bacterial burden. In contrast, infection with an anti-inflammatory, apoptosis inducing strain, Lm-Apo, had similar infectious burden but was associated with rapid wound repair. Inflammatory infections induced il-1b expression and blocking IL-1R signaling partially rescued wound healing in the presence of persistent infection. Taken together, our findings suggest that the dynamics of microbe-induced tissue inflammation impacts repair in complex tissue damage independent of bacterial load, with a critical early window for efficient tissue repair.
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Project description:To facilitate the recovery process of chronic and hard-to-heal wounds novel pro-resolving treatment options are urgently needed. We investigated the pro regenerative properties of soluble CD83 (sCD83) on cutaneous wound healing, where sCD83 accelerated wound healing not only after systemic but also after topical application, which is of high therapeutic interest. Cytokine profile analyses revealed an initial upregulation of inflammatory mediators such as TNFa and IL-1b, followed by a switch towards pro-resolving factors, including YM-1 and IL-10, both expressed by tissue repair macrophages. These cells are known to mediate resolution of inflammation and stimulate wound healing processes by secretion of growth factors such as epidermal growth factor (EGF) and vascular endothelial growth factor (VEGF), which promote vascularization as well as fibroblast and keratinocyte differentiation. In conclusion, we have found strong wound healing capacities of sCD83 beyond the previously described role in transplantation and autoimmunity. This makes sCD83 a promising candidate for the treatment of chronic- and hard-to-heal wounds
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