Modulation of early cellular events in wound healing in mice.

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.