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The capacity of liposomes constituted by dycetyl-phosphate (0.009 mM), cholesterol (0.017 mM), lecithin (0.003 mM), and myristic (0.1 mM), stearic (0.1 mM), or oleic acid (0.1 mM) to modify the lymphocyte response to Brucella melitensis antigens in mice was studied. Mice treated with antigens mixed with liposomes containing myristic, stearic or oleic acid had higher antibody titres than mice given antigen suspended in a saline solution. Liposomes alone, without Brucella antigens, resulted in increased 3H-thymidine incorporation by lymphocytes both in vivo and in vitro. The addition of polyclonal activators (LPS and ConA) caused a further increase of 3H-thymidine uptake. Moreover, spleen lymphocytes from mice inoculated with Brucella antigens mixed with the liposomes had a significantly lower population of B lymphocytes (10%), and a notable increase in the Tc lymphocytes (20%). Autoradiography of sections of popliteal ganglia of treated mice showed that the radioactivity was concentrated mainly in the membrane structures of the cell.

Microgram amounts of protein SV-IV, a major secretory protein produced by adult rat seminal vesicle epithelium, markedly decrease the mouse humoral immune response to cellular xenogeneic or allogeneic antigens (sheep red blood cells (SRBC) or mouse epididymal spermatozoa). The significant reduction in the total number of splenocytes and their main cell subsets in SRBC-immunized mice, the dramatic decrease in the number of Ia+ splenic T cells and the marked inhibition of splenocyte ability to respond in vitro to polyclonal mitogen stimuli suggest that the macrophage accessory cells are the primary target of the SV-IV immunosuppressive activity in vivo. Moreover, the infection of SV-IV-treated mice with Salmonella typhimurium produced an increased mortality of the experimental animals associated with a marked decrease of the phagocytic and intracellular killing activities of their peritoneal macrophages.

Liposomes consisting of dicetyl-phosphate, cholesterol, lecithin and stearic or myristic or oleic acid, exert a protective effect for mice against experimental infection by Salmonella typhimurium, and delay both the onset and mortality B16 melanoma in these animals. Liposomes labelled with 3H-myristic acid were used as probes in the spleen and liver. We found that the treatment schedule rather than route of administration of liposomes, is important. The results show that in order to induce protection, preventive treatment must start at least three days before. Longer treatments do not increase the degree of protection, and treatments started at the same time as, or following experimental infection or tumor transplantation, have no effect.

The immunoregulatory role of prolactin (PRL) has been well established. In order to clarify if the hormone is also able to stimulate a protective activity against pathogens-induced infections we have studied the modifications of the infective capacity of Salmonella typhimurium induced in mice by repeated treatments with ovine PRL. A significant dose-dependent reduction in the mortality rate was observed in comparison to controls. This activity is probably related to the observed increases in phagocytosis and intracellular killing of the peritoneal macrophages and chemotaxis of the peritoneal granulocytes induced by the hormonal treatment. On the contrary, the number of leukocytes in blood was not modified by PRL treatment excluding a mobilization of cells from other districts. Our findings confirm the existence of a linkage between the neuroendocrine and immune systems suggesting a possible role for PRL in the regulation of non-specific immune response.

In order to evaluate the influence of hyperlipemia on the specific cell defence reaction in type-II diabetes mellitus in humans, 20 diabetics were recruited in this study. They were divided into two groups on the basis of the absence or coexistence of abnormal serum lipid pattern. The lymphocyte and monocyte cells drawn from the type-II diabetic patients with abnormally elevated serum levels of cholesterol and triglycerides showed a decreased expression of major histocompatibility complex (MHC) class-II antigens and an impaired secretion of interleukin (IL-1). Values of MHC class-II antigen expression in diabetics without lipid metabolic alterations were not significantly different from those found in healthy subjects. In conclusion, abnormalities of lipid metabolism often found in type-II diabetes mellitus may play a key role in the impaired specific cell reaction toward infectious diseases of these patients.

Rabbits immunized for 6 months with different amounts of sterile human serum showed weight loss and a decrease in leukocytes. The lymphocyte population reacting to ConA contained autoreactive cells capable of causing 51Cr release from labeled cells from a culture consisting of splenic and peripheral lymphocytic cells from the same animal.

Female mice were maintained on a lipid-rich diet. After 33 days, the mice showed a decrease in the cell population bearing MHC class II molecules, and in the production of interleukin-1 (IL-1). After 60 days, we reported a further decrease of the cell population with MHC class II molecules and the secretion IL-1.

In a prospective study 76 children were divided into three groups on the basis of severity of head injury as defined by the Glasgow Coma Scale and duration of increased intracranial pressure. The children were administered a neuropsychological test battery and behavioural ratings were made by parents and teachers at three intervals: time of hospital discharge and 3 and 9 months post-initial testing. There were cognitive deficits related to severity of injury with the greatest difference in abilities observed between the severe and the other two groups. The greatest differences in skills were on the Performance IQ and timed tests of visual-motor speed and co-ordination. The greatest improvement in skills occurred in the first 3 months post-injury. Several children in coma for up to 4 weeks were able to obtain normal IQ scores. In the mild and moderate injury groups very few had behavioural change while in the severe group approximately 90% had one learning or adjustment difficulty and 40% had three or more problems.

Our study considered the possibility of modifying the functional response of human neutrophils, of mouse lymphocytes and macrophages treated with phospholipids having different polar groups, different isomerisms with saturated and unsaturated fatty acids from C12 to C20 carbon atoms. The results are as follows. a) Most of the phospholipids containing fatty acids from C12 to C20 cause inhibition of the blastogenic capacity of the polyclonal activators tested. b) The phospholipids tested cause a decrease in adherence of polymorphonuclear leukocytes with the exception of the phosphatidyl-choline containing saturated and unsaturated fatty acids. c) A decrease in polymorphonuclear leukocytes migrational capacity almost always occurs. d) The cells treated with L-phosphatidyl-ethanolamine having fatty acids from C14 to C17 show an increase in chemiluminescence; those treated with phosphatidyl-choline and L-phosphatidyl-glycerol show a decrease of the chemiluminescence; L-phosphatidic acid and L-phosphatidyl-ethanolamine having Microbial fatty acids (FAs) at C16 cause a decrease in the formation of phagolisosomes in the macrophages tested.

A study was conducted on the granulocytic phagocytosis of bacterial aggregates obtained under ideal environmental conditions. For the strains studied, aggregation was favored by low salt concentrations, low pH and temperatures between 30 degrees C and 40 degrees C. Our results show that the phagocytic capacity of granulocytes depends on the type and size of these aggregates. Those formed by a smaller number of cells are more easily phagocytized than the larger ones.

This study examines the action of the cell wall components of enterobacteria on the vitality of human spermatozoa. Lipopolysaccharides extracted from Escherichia coli K12 killed about 80% of the spermatozoa at a concentration of 50 micrograms/ml. Porins extracted from E. coli, Proteus mirabilis and Salmonella typhimurium killed between 80% and 100% of the spermatozoa at a concentration of 50 micrograms/ml. Muramic acid and N-acetylmuramic acid caused about 60% mortality at a concentration of 50 micrograms/ml. The possibility that the products of cellular lysis in the course of gram-negative infections cause temporary sterility is discussed.

Studies have been carried out on protein and fatty acid patterns present in the outer layers of E. coli strains which are considered pathogenic in relation to their serogroup. The patterns were related to surface properties of hydrophobicity of the same cells and to their resistance to phagocytosis. The results obtained demonstrate the presence in the pathogenic serogroups of a proteic band of high molecular weight as well as differences in the percentages of fatty acids with respect to the non-pathogenic serogroups. Furthermore, these serogroups are more resistant to phagocytosis; this resistance seems to be correlated to a greater surface hydrophilia of the pathogenic serogroups, leading to different relations of the lipidic and protein fraction of the outer layers.

In our present study we have examined the phagocytosis by polynucleates towards bacteria exposed to macrophages or lymphocytes. Our results show that for almost all the bacterial strains, the contact with lymphocytes determines changes in hydrophobicity correlated to variations in the possibility of being phagocytized and of more significant intracellular killing with respect to bacteria treated with macrophages.

Female mice were maintained on lipid diet for 20 days. The nonspecific and immunological defense capability was determined by in vitro and in vivo methods. It was found that mice held mostly on a lipid diet demonstrate an all-round lowered response. Following 20 days of lipid diet the splenocytes exhibit: (1) an inversed lipid-protein ratio; (2) an inability to respond to sheep erythrocytes; (3) a reduction in [3H] thymidine incorporation in splenocytes stimulated with lipopolysaccharide (LPS) or with concanavalin A; (4) a reduction in the number of cells bearing surface immunoglobulins in splenocytes stimulated with LPS; (5) an inhibition of phagocytosis and intracellular killing in macrophages; (6) a lowering in granulocyte chemotaxis and adherence capacity; (7) a higher mortality to LPS after loading with galactosamine; and (8) a lowered complement activity even following LPS activation.