| First Author | Chen Z | Year | 2024 |
| Journal | Mol Oral Microbiol | Volume | 39 |
| Issue | 3 | Pages | 113-124 |
| PubMed ID | 37902166 | Mgi Jnum | J:355512 |
| Mgi Id | MGI:7715058 | Doi | 10.1111/omi.12442 |
| Citation | Chen Z, et al. (2024) Primed inflammatory response by fibroblast subset is necessary for proper oral and cutaneous wound healing. Mol Oral Microbiol 39(3):113-124 |
| abstractText | Fibroblasts are ubiquitous mesenchymal cells that exhibit considerable molecular and functional heterogeneity. Besides maintaining stromal integrity, oral fibroblast subsets are thought to play an important role in host-microbe interaction during injury repair, which is not well explored in vivo. Here, we characterize a subset of fibroblast lineage labeled by paired-related homeobox-1 promoter activity (Prx1Cre(+)) in oral mucosa and skin and demonstrate these fibroblasts readily respond to microbial products to facilitate the normal wound healing process. Using a reporter mouse model, we determined that Prx1Cre(+) fibroblasts had significantly higher expression of toll-like receptors 2 and 4 compared to other fibroblast populations. In addition, Prx1 immunopositive cells exhibited heightened activation of inflammatory transcription factor NF-kappaB during the early wound healing process. At the cytokine level, CXCL1 and CCL2 were significantly upregulated by Prx1Cre(+) fibroblasts at baseline and upon LPS stimulation. Importantly, lineage-specific knockout to prevent NF-kappaB activation in Prx1Cre(+) fibroblasts drastically impaired both oral and skin wound healing processes, which was linked to reduced macrophage infiltration, failure to resolve inflammation, and clearance of bacteria. Together, our data implicate a pro-healing role of Prx1-lineage fibroblasts by facilitating early macrophage recruitment and bacterial clearance. |
