Is there an association between fetal viral infection and fetal malformation? I. Detection of specific IgM antibodies in the serum of malformed fetuses.

Determinations of IgG and IgM antibodies specific for cytomegalovirus (CMV), herpes simplex virus (HSV1), herpes simplex virus (HSV2), varicella-zoster virus (VZV), rubella, echo, Coxsackie and morbilli viruses were performed in 20 sera from malformed fetuses. Demonstration of a fetal infection by increased fetal serum IgM permits linkage to a detected fetal malformation. In parallel, 14 maternal sera and 17 amniotic fluid samples were examined. Laser nephelometry (a quantitative method) was used for the determination of IgM and IgG class immunoglobulins. None of the fetal sera were found to contain IgM class antibodies specific for the viral antigens studies. While IgM CMV-specific antibodies were present in one maternal serum, the specific IgM was absent in the fetus. The absence of specific IgM antibodies appears to warrant the conclusion that the malformed fetuses were uninfected by any of the above viruses. IgM antibodies were detected in two fetal sera by quantitative methods. The IgM antibodies present in two fetuses probably were generated in response to some other introduced antigen.

A peptidoglycan monomer as an antitumor agent in mice: stimulation of phagocytosis by resident peritoneal macrophages with peptidoglycan monomer.

Peptidoglycan monomer (dissacharide-pentapeptide, PGM) from Brevibacterium divaricatum is an immunomodulator and an antitumor agent. As part of our investigation of the antitumor properties of PGM in mice, its potential to stimulate phagocytosis by resident peritoneal macrophages was assessed. Inbred CBA/H/Zg tau mice (kept under conventional conditions) were used, and a simple and brief method was developed to evaluate phagocytosis. It consisted of a short (10 min) coincubation of yeast cells (YCs) with peritoneal cells (PCs) and microscopic (phase-contrast) scoring of YC ingestion. Three samples of PGM were injected intravenously into mice (60 mg/kg), and PCs were collected from groups of recipients 8, 16, 24, 48, or 72 h later. All samples temporarily increased phagocytosis, but the extent and duration of the effect varied. Stimulation of phagocytosis also occurred after in vitro exposure (3 h) of PCs to PGM, or to the pentapeptide (PP) part of its molecule. We concluded that PGM could enhance phagocytosis by resident peritoneal macrophages in vivo and in vitro, the PP being the active component in vitro.