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Delayed wound healing in mice associated with viral alteration of macrophages
Abstract:
Mice acutely and chronically infected with Sendai virus had impaired healing of incisional wounds. This impairment could be overcome by instilling the macrophage-stimulators zymosan and glucan into full-thickness incised wounds, whereas levamisole, an immunomodulator, had no effect on tensile strength of these wounds (breaking strengths). Another commonly occurring murine virus, murine hepatitis virus, also reduced wound tensile strength in infected mice. However, the murine strain of herpes simplex virus, type 1, which caused greater morbidity, did not reduce tensile strength. Although measurements of wound length and wound breaking strength clearly showed the adverse effect of viral infection, histologic evaluation of wounds did not consistently reveal a similar change in composition of wound "cell aggregation centers" for mice infected with the Sendai and murine hepatitis viruses.
Insights
Viral infections like Sendai virus impair wound healing in mice. Macrophage stimulators, zymosan and glucan, restored wound tensile strength, suggesting a role for macrophage activation in viral-impaired wound repair.
Area of Science:
- Immunology
- Virology
- Wound Healing Research
Background:
- Viral infections can impact physiological processes beyond the primary infection site.
- Impaired wound healing is a potential complication of viral infections, affecting tissue repair mechanisms.
- The role of specific viruses and immune modulators in wound healing requires further investigation.
Purpose of the Study:
- To investigate the effect of viral infections on incisional wound healing in mice.
- To determine if macrophage stimulators can overcome virus-induced impairment of wound healing.
- To assess the impact of different viruses on wound tensile strength.
Main Methods:
- Mice were infected with Sendai virus, murine hepatitis virus, or herpes simplex virus type 1.
- Incisional wounds were created, and their healing was assessed by measuring tensile strength (breaking strength) and length.
- Macrophage stimulators (zymosan, glucan) and an immunomodulator (levamisole) were instilled into wounds.
- Histologic evaluation of wound "cell aggregation centers" was performed.
Main Results:
- Sendai virus infection impaired incisional wound healing, evidenced by reduced tensile strength.
- Zymosan and glucan treatments restored wound tensile strength in Sendai virus-infected mice.
- Murine hepatitis virus also reduced wound tensile strength, but herpes simplex virus type 1 did not.
- Histologic examination did not consistently correlate with the observed changes in wound breaking strength.
Conclusions:
- Viral infections, particularly Sendai virus and murine hepatitis virus, adversely affect incisional wound healing in mice.
- Macrophage activation through zymosan and glucan can restore impaired wound healing caused by viral infections.
- The study highlights the complex interplay between viral infections, immune responses, and tissue repair processes.
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