Wound healing and microbiome, an unexpected relationship

Abstract

Skin wounds are common and represent a major public health and economical problem, with risks of complications and a significant negative impact on the quality of life of patients. Cutaneous wound healing is a tightly regulated process resulting in the restoration of tissue integrity. Wound healing involves the interaction of several skin, immune and vascular cells, growth factors and cytokines. However, external actors can play an important role in wound healing, such as the skin microbiome, which is the microbial commensal collection of bacteria, fungi and viruses inhabiting the skin. Indeed, recent advances have featured the interactions, within the wound environment, between different microbial species and between microbial species and the host immune system. This article reviews the relationship between the skin microbiome and the wound healing process. Although cutaneous wounds are a potential entry site for infection, the wound microbiome can have either a detrimental or a beneficial role on wound healing. Thus, targeting the skin microbiome could represent an essential part of wound healing management.

Janus Paper‐Based Wound Dressings for Effective Exudate Absorption and Antibiotic Delivery

“…The blue ink was not focused but spread over the wound bed, potentially decreasing the therapeutic effect, and generating a side effect by killing the beneficial skin microbiome. [ 6 ] Uncontrollable drug delivery may cause antibiotic resistance as well.…”

“…[4,5] In particular, the inflammatory phase is essential to successful wound healing by secreting a small amount of exudate to activate the innate immune system, which will remove potential pathogens from the wound bed. [6,7] However, excessive wound exudate during inflammation can create an ideal microenvironment for bacterial breeding and potential infections because the exudate is nutrient-rich containing many vitamins, growth factors, and leukocytes. [8,9] Traditional hydrophilic wound dressings (e.g., gauzes, bandages, and hydrogels) integrated with antibiotic substances partially improved wound healing by absorbing excessive exudate and inhibiting bacterial growth.…”

“…[8,9] Traditional hydrophilic wound dressings (e.g., gauzes, bandages, and hydrogels) integrated with antibiotic substances partially improved wound healing by absorbing excessive exudate and inhibiting bacterial growth. [1,6,7,9,10] Even the emerging Janus membranes with a hydrophobic-hydrophilic interface (e.g., fiber-, sponge-, hydrogel-, and polymerbased dressings with asymmetric wettability) accelerated drainage of excessive biofluid around wounds through unidirectional water-transfer capability from the skin-facing hydrophobic side to the exposed hydrophilic side while preventing favorable conditions for bacterial growth. [11][12][13][14][15][16] Moreover, the integration of antimicrobial materials into the Janus membranes [16][17][18][19][20] or advanced Janus multilayer membranes for effective antibiotic delivery substantially prevented the growth and reproduction of pathogens.…”

A bismuth-based double-network hydrogel-mediated synergistic photothermal-chemodynamic therapy for accelerated wound healing

“…The healing of infected wounds is a complex biological process involving infection, inflammation, proliferation, and remodeling. 45,46 We further examined the various hallmarks involved in wound healing to elucidate the important role of double-network Bi@P-Cu hydrogel-mediated synergistic PTT and CDT. Hematoxylin-eosin (H&E) staining, as shown in Fig.…”

Signaling Pathways Triggering Therapeutic Hydrogels in Promoting Chronic Wound Healing

“…[50] Chronic wounds also frequently stem from an excessive bacterial colonization, prominently involving Staphylococcus aureus, which can secrete toxins, trigger a proinflammatory response, and facilitate the spread of bacteria through tissue damage and heightened vascular permeability. [51] Additionally, bacteria can establish biofilms characterized by antiphagocytosis properties, thereby disrupting the immune response. This disruption occurs by activating neutrophils and proinflammatory macrophages, while concurrently limiting the penetration of drugs and antibodies, and hindering the movement of immune cells.…”