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Updated: Aug 19, 2026
Murine Model of Wound Healing
Published on: May 28, 2013
Modulation of early cellular events in wound healing in mice
Abstract:
Wound healing experiments were conducted in random-bred Swiss mice to determine the effect on antimicrobial surfactants and macrophage stimulators on wound measurements, histologic repair, and wound breaking strengths. In selection of mice, Sendai virus antibody-positive mice healed more slowly than did mice with no detectable titer to Sendai virus. Studies were conducted with Sendai virus-free mice that had C31G (an antimicrobial surfactant), alkyl amine oxide, zymosan, glucan, or phosphate-buffered isotonic saline solution instilled into full-thickness incised wounds. The early events in the repair process indicated a greater degree of inflammatory response comprised mainly of polymorphonuclear leukocytes with subsequent large numbers of monocytes in C31G and alkyl amine oxide-treated wounds. Although zymosan did not induce as large a number of monocytes, the degree of fibroplasia was as great as in wounds in which numbers were higher. The effect of zymosan could be blocked by the addition of N-alpha-p-tosyl-L-lysine chloromethyl ketone to wounds. Wound breaking strength 3 days after surgery was greatest for glucan-treated mice (134 +/- 37 g) whereas that in C31G-treated mice (77 +/- 31 g) was less than that of the controls (92 +/- 37 g). By day 7, there was no significant difference in breaking strength between control and glucan-treated wounds; however, C31G-treated wounds remained substantially weaker than control wounds.
Insights
Antimicrobial surfactants like C31G impaired wound healing and reduced breaking strength in mice. However, glucan enhanced wound strength initially, with no significant difference by day 7 compared to controls.
Area of Science:
- Wound Healing Research
- Biomaterials Science
- Immunology
Background:
- Sendai virus infection can negatively impact wound healing rates.
- Investigating compounds that modulate the inflammatory and repair processes is crucial for improving wound outcomes.
Purpose of the Study:
- To evaluate the efficacy of antimicrobial surfactants and macrophage stimulators on wound healing in mice.
- To assess the impact of C31G, alkyl amine oxide, zymosan, and glucan on wound measurements, histology, and breaking strength.
Main Methods:
- Full-thickness incised wounds were created in Sendai virus-free mice.
- Wounds were treated with C31G, alkyl amine oxide, zymosan, glucan, or saline solution.
- Wound healing, inflammatory response, fibroplasia, and breaking strength were analyzed.
Main Results:
- C31G and alkyl amine oxide induced early inflammatory responses with increased polymorphonuclear leukocytes and monocytes.
- Zymosan promoted fibroplasia, an effect blocked by N-alpha-p-tosyl-L-lysine chloromethyl ketone.
- Glucan-treated wounds showed the highest breaking strength at day 3, while C31G-treated wounds were weaker than controls at both 3 and 7 days.
Conclusions:
- Antimicrobial surfactants like C31G may impede wound healing and reduce tissue strength.
- Glucan shows potential for enhancing early wound breaking strength, though its long-term effects require further study.
- Modulating inflammatory responses and macrophage activity influences the wound healing cascade.
