Morphological examination of primary foci several hours after intramuscular infection of rats with Pseudomonas aeruginosa, Staphylococcus aureus, or Staphylococcus epidermidis showed that bacteriopyknosis is associated with deficiency of compounds necessary for the microorganisms or excess of secreted microbial metabolites. Motility is a factor of virulence, since it inhibits bacteriopyknosis. The biological significance of divalent antibodies and agglutination provided by them probably lies in considerable stimulation of bacteriopyknosis in agglutinates. Formation of IgM also enhances bacteriopyknosis.

Electron-autoradiographic study of normal and tumor-transformed adipose tissue (common lipoma and destructive lipoma, i.e. infiltrating and degrading lipoma) showed the capacity of adipose tissue cells in lipomas, especially in destructive lipomas, to proliferation and differentiation. In vivo synthesis of DNA in mature adipocytes not observed previously is described. The role of microvascular wall cells as mesenchymal multipotent precursors in the formation of the adipose tissue is discussed. The involvement of the bone marrow mesenchymal stem cell in this process cannot be ruled out.

The process of concentration of microorganisms, which leads to inhibition of their growth and death, is a mechanism of nonspecific resistance and immunity in bacterial infection. It was suggested that inhibition and death of microorganisms are caused by deficiency of essential substances in the concentration site, which determines the significance of agglutination in the immunity. Agglutination of microbial bodies increases their concentration in tissues. By contrast, dispersion of bacteria in the tissues weakens the effect of the concentration factor and, consequently, increases the virulence of the bacteria.

Rats were immunized with Pseudomonas aeruginosa. A suspension of bacteria of the same strain was mixed with a sufficient amount of serum from the immunized rats to produce agglutination. This bacteria-serum mixture was injected intramuscularly to intact rats. Rapid dissolution of bacteria (during 1-3 h) was noted in the intercellular space, where microbial cells were reduced to pyknomorphic detritus. The formation of detritus from destroyed bacteria was demonstrated by detecting the radioactivity of the detritus in cases where animals were infected with bacteria labeled with tritium. The phenomenon described is a mechanism of bacterial dissolution in the organism differing from phagocytosis and complement-dependent lysis. Key Words: antibodies; wound infection; immunology of bacterial infectionsKnowledge of how microbial cells die in the organism of homoiothermic animal is essential for combating bacterial infections. Two bactericidal factors are now associated with antYoody action, namely extracellular lysis by complement [8] and intraceUular killing and digestion by phagocytes [4,6,7]. Both mechanisms can be initiated and boosted by antibodies unable themselves to kill bacteria [5,9]. In the present article we describe one more mechanism of the killing and breakdown of bacteria, one that depends on antibodies, occurs in the intercellular space, is morphologically manifested by bacteriopyknosis, and, at least in some cases, acts faster and is more effective than complement or phagocytes. MATERIALS AND METHODSOutbred rats weighing 220-280 g were infected with a 24-h Pseudomonas aeruginosa ( In some experiments microbial cells were labeled with 3H prior to administration. For this purpose 100 ~tCi/ml 3H-uridine were added to agar. Control animals were injected with 0.3 ml of bacterial suspension in Hanks' solution in a concentration of 8• cells/ml to the right m. gastrocnemius. The same dose of bacteria agglutinated by homologous immune serum in a volume of 5-10% of the bacterial suspension was administered to experimental animals. For preparation of the immune serum rats were injected i.m. with a P. aeruginosa (strain 453) culture containing 2• cells/m] in Hanks' solution 3 times at 7-day intervals. Blood for serum preparation was taken 7-60 days after the third injection of bacteria.Animals were killed under ketamine anesthesia 1, 2, 3, 8, and 20 hours and 1, 2, 3, and 15 days after infection. The primary foci were studied by electron microscopy and electron autoradiography. The latter was performed in two ways: 1) contamination with bacteria preliminarily labeled in vitro; 2)