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Aim: Inflammatory reactions are essential for wound healing and a physiological response to injuries. Excessive inflammation delays the transition to the proliferation phase, thus representing one key aspect in the development of wound healing disorders. Here, we monitored inflammatory responses in physiological and delayed wound healing. Method: Gene expression and dermal interstitial fluid (dISF) abundance of inflammatory and regeneration factors were monitored in superficial wounds of different healing stages in pigs. Inflammation was induced in some wounds by using resiquimod, a TLR7/8 agonist, to prolong the inflammatory phase for up to 6 days after wounding. Results / Discussion: During physiological wound healing, pro-inflammatory cytokines (IL6, CXCL8) and prostaglandin E2 showed a peak of abundance in the dISF on day 2 after wounding and declined back to baseline on day 6. Wounds induced with resiquimod for 6 days showed only 20% healing rate as compared to 75% in control wounds. Further, resiquimod induction significantly increased gene expression, production as well as secretion of pro-inflammatory factors (IL6, CXCL8, PGE2). Gene expression levels of regeneration markers such as TGFB1 and HIF1A were also upregulated in inflamed wounds. Histological analysis demonstrated decreased re-epithelization in resiquimod induced wounds, but increased infiltration of immune cells. Resiquimod induction led to a sustained inflammatory response until at least day 6 post wounding. Conclusion: This study gave insight into the time and location dependent expression, production and secretion of relevant cytokines, growth factors and markers of tissue regeneration in the context of physiological as well as delayed wound healing. [ABSTRACT FROM AUTHOR]