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Peer-reviewedCC BYOpen life sciences

Honey in wound healing: molecular and cellular mechanisms of inflammation control, immune modulation, and antimicrobial defense

  1. 1Faculty of Sciences, Arab American University, P.O. Box 240, Jenin, Palestine
  2. 2Faculty of Medicine, Arab American University, P.O. Box 240, Jenin, Palestine
  3. 3Qasemi Research Center and Faculty of Medicine, Arab American University, P.O. Box 240, Jenin, Palestine

Abstract

Wound healing is a complex process involving inflammation control, protection against infection, oxidative balance, and tissue regeneration. Honey has attracted considerable attention due to its multifunctional biological activities. In addition to its anti-inflammatory and antioxidant actions, honey exhibits broad antimicrobial activity that helps prevent microbial colonization and biofilm formation, thereby facilitating a favorable environment for healing. It also limits oxidative stress through reactive oxygen species (ROS) scavenging and erythroid 2–related factor 2 (Nrf2) activation, resulting in better control of inflammation and improved tissue repair. However, despite promising experimental and clinical evidence, the clinical translation of honey remains limited by variability in composition, lack of standardization, and methodological weaknesses in existing trials, and robust, well-controlled studies and standardized formulations are therefore essential to confirm efficacy and support its integration into evidence-based wound care. This review summarizes current knowledge on how honey supports wound healing, focusing on its antimicrobial, anti-inflammatory, antioxidant, and immunomodulatory effects. The analysis is based on a literature search of MEDLINE, Google Scholar, Scopus, and Web of Science. Overall, honey reduces pro-inflammatory mediators (e.g., tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, nuclear factor kappa B (NF-κB)) and enhances anti-inflammatory responses such as IL-10 and M2 macrophage activity.

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BibTeX
@article{kmail2026honey,
  title = {{Honey in wound healing: molecular and cellular mechanisms of inflammation control, immune modulation, and antimicrobial defense}},
  author = {Abdalsalam Kmail and Bashar Saad},
  journal = {Open life sciences},
  year = {2026},
  month = oct,
  doi = {10.1515/biol-2025-1397},
  url = {https://europepmc.org/article/PMC/PMC13718990},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Honey in wound healing: molecular and cellular mechanisms of inflammation control, immune modulation, and antimicrobial defense
AU  - Abdalsalam Kmail
AU  - Bashar Saad
PY  - 2026
DA  - 2026/10/30
JO  - Open life sciences
DO  - 10.1515/biol-2025-1397
UR  - https://europepmc.org/article/PMC/PMC13718990
AB  - Wound healing is a complex process involving inflammation control, protection against infection, oxidative balance, and tissue regeneration. Honey has attracted considerable attention due to its multifunctional biological activities. In addition to its anti-inflammatory and antioxidant actions, honey exhibits broad antimicrobial activity that helps prevent microbial colonization and biofilm formation, thereby facilitating a favorable environment for healing. It also limits oxidative stress through reactive oxygen species (ROS) scavenging and erythroid 2–related factor 2 (Nrf2) activation, resulting in better control of inflammation and improved tissue repair. However, despite promising experimental and clinical evidence, the clinical translation of honey remains limited by variability in composition, lack of standardization, and methodological weaknesses in existing trials, and robust, well-controlled studies and standardized formulations are therefore essential to confirm efficacy and support its integration into evidence-based wound care. This review summarizes current knowledge on how honey supports wound healing, focusing on its antimicrobial, anti-inflammatory, antioxidant, and immunomodulatory effects. The analysis is based on a literature search of MEDLINE, Google Scholar, Scopus, and Web of Science. Overall, honey reduces pro-inflammatory mediators (e.g., tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, nuclear factor kappa B (NF-κB)) and enhances anti-inflammatory responses such as IL-10 and M2 macrophage activity.
SN  - 2391-5412
ER  -