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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: Curr Dermatol Rep. 2022 Mar 25;11(2):60–72. doi: 10.1007/s13671-022-00354-9

Fig. 1.

Fig. 1

Molecular pathology of chronic wound biofilms. Chronic wounds exhibit a hyperproliferative and non-migratory epidermis, unresolved inflammation, and fibrosis. Biofilm presence, which can incorporate a diverse community of bacteria and fungi, promotes impaired keratinocyte migration, dysregulated inflammatory response, and inflammatory cell dysfunction. Additionally, biofilm damages host tissue through increased neutrophilic reactive oxygen species production, imbalance of metalloproteases and inhibitors, and breakdown of keratinocyte tight junctions. These processes further perpetuate chronic wound pathogenesis. (DAMP, damage-associated molecular patterns; MMP, matrix metalloprotease; ROS, reactive oxygen species; TIMP, tissue inhibitor of matrix metalloprotease; TEWL, transepidermal water loss)