The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum

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In guinea pigs, the role of the monocyte/macrophage in wound repair (skin excisions) was investigated in wounds depleted of this cell and/or its phagocytic activity. Hydrocortisone acetate, administered s.c., was used to induce a prolonged monocytopenia in guinea pigs, and antimacrophage serum (AMS) was used for local elimination of tissue macrophages. In vitro, in the presence of complement, macrophages are rapidly lysed and killed by AMS. In the absence of complement, AMS is not cytotoxic; the AMS titers were obtained by observation of adherence and phagocytosis of opsonized erythrocytes in serial dilutions of AMS. Six groups of animals were studied: untreated animals, animals receiving daily s.c. injections of normal rabbit serum (NRS) around each wound, animals receiving daily subcutaneous AMS around each wound, animals receiving systemic hydrocortisone, animals receiving systemic hydrocortisone and daily AMS around each wound. Wounds consisted of a series of 6 linear incisions in the dorsal skin. Subcutaneous AMS alone had no effect on the number of circulating monocytes, nor was there any observalbe effect on the number or the phagocytic ability of wound macrophages. Fibrosis in these wounds was unaffected. Systemic hydrocortisone induced a prolonged monocytopenia. The macrophage level in the wounds of these monocytopenic animals was reduced to approximately 1/3 that of controls; the phagocytic activity of the monocytes/macrophages that did appear in these wounds was, however, similar to that of controls. Some inhibition of wound debridement was observed in these wounds, but fibrosis was virtually unaffected. Collagen synthesis, as judged morphometrically, was similar to that of control wounds at all stages of repair. Conjoint systemic hydrocortisone and subcutaneous AMS around each wound resulted in the almost complete disappearance of macrophages from the wounds. Wound fibrin levels were elevated, and clearance of fibrin, neutrophils, erythrocytes and other miscellaneous debris from these wounds was delayed. Fibroblasts, which in control wounds first appear by 3 days postwounding and reach maximal levels by day 5, did not appear in these wounds until day 5, and their subsequent rate of proliferation was slower than that of controls. Seven and 10 day wounds appeared immature both in terms of the degree of debridement, and extent of fibrosis. These studies indicate that, in the repair process, the principle cell type responsible for wound debridement is the macrophage. In addition, the macrophage may be required to stimulate fibroblast proliferation in some as yet unidentified manner.

Original languageEnglish (US)
Pages (from-to)71-99
Number of pages29
JournalAmerican Journal of Pathology
Issue number1
StatePublished - 1975
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

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