Biofilm-Innate Immune Interface: Contribution to Chronic Wound Formation

Abstract

Delayed wound healing can cause significant issues for immobile and ageing individuals as well as those living with co-morbid conditions such as diabetes, cardiovascular disease, and cancer. These delays increase a patient’s risk for infection and, in severe cases, can result in the formation of chronic, non-healing ulcers (e.g., diabetic foot ulcers, surgical site infections, pressure ulcers and venous leg ulcers). Chronic wounds are very difficult and expensive to treat and there is an urgent need to develop more effective therapeutics that restore healing processes. Sustained innate immune activation and inflammation are common features observed across most chronic wound types. However, the factors driving this activation remain incompletely understood. Emerging evidence suggests that the composition and structure of the wound microbiome may play a central role in driving this dysregulated activation but the cellular and molecular mechanisms underlying these processes require further investigation. In this review, we will discuss the current literature on: 1) how bacterial populations and biofilms contribute to chronic wound formation, 2) the role of bacteria and biofilms in driving dysfunctional innate immune responses in chronic wounds, and 3) therapeutics currently available (or underdevelopment) that target bacteria-innate immune interactions to improve healing. We will also discuss potential issues in studying the complexity of immune-biofilm interactions in chronic wounds and explore future areas of investigation for the field.

The Comparison of Breast Reconstruction Using Two Types of Acellular Dermal Matrix after Breast-Conserving Surgery

“…This process promotes tissue damage and delays wound healing. In addition, excessive inflammatory cell recruitment and biofilm formation due to bacterial infection cause a chronic wound [ 13 ]. These processes increase wound inflammation and delay wound healing, which may be associated with an increase in inflammatory cases.…”

Skin Wound Healing: Normal Macrophage Function and Macrophage Dysfunction in Diabetic Wounds

“…and Peptostreptococcus spp. have been found in DFUs [ 62 , 63 ]. DFUs are thought to have higher microbial loads than venous leg ulcers [ 63 ].…”

“…have been found in DFUs [ 62 , 63 ]. DFUs are thought to have higher microbial loads than venous leg ulcers [ 63 ]. The diversity of these loads also impacts wound healing.…”

Immunomodulatory Properties of Host Defence Peptides in Skin Wound Healing

“…Although the reciprocity of either deficiency or overproduction of HDPs in the presence of inflammation and thus balance between pro-or anti-inflammatory effects is not so easy to define directly, this can lead to a pathological inflammatory response [99,100]. Endogenous host defence peptides, stored intracellularly at high concentrations as inactive precursors in granules, are released locally at infection and inflammation sites, whereas the expression of others is induced in response to pathogen-associated molecules [101].…”