Biomedical subjects

C Romano-Carratelli

Publications and source records attributed to C Romano-Carratelli.

6 recordsLinked to original sources

PubMed1997

Polyclonal T cell elimination by prolonged immunostimulation in an experimental model.

An experimental model of immunological deficiency obtained by treating mice for 6 months with serum of human blood drawn from different healthy individuals has been studied. The results show that an alteration of a circulating lymphocyte population with alterations of the ratio CD4+/CD8+ appeared in mice stimulated for a long period with immunogens. Mice treated for 2-4 months showed an increase in B lymphocytes and a decrease in the total number of T lymphocytes, with a decrease in CD4+ lymphocytes and an increase in CD8+ lymphocytes. After 4 months, the CD8+ lymphocyte population started to decrease, with a ratio of CD4+/CD8+ reaching almost 1. In animals treated for 2-3 months, the mean survival time (MST) following experimental infection with Salmonella typhimurium presented a decrease to 5 days, and after 5-6 months of treatment presented a decrease to 3-2.5 days. The bacteraemia was modified in comparison with controls. Prolonged exposure to antigens also induced lymphocyte apoptosis: cells of animals treated for 4-6 months presented increased levels of apoptosis with a percentage that reached 30-35%. A semiquantitative evaluation of the level of heat shock protein (hsp) in splenic lymphocytes showed an increase in the presence of hsp60 and hsp70 in the first 3 months of treatment, which then remained constant for up to 6 months.

Animals↗

PubMed1995

In vivo inhibition of cell-mediated and humoral immune responses to cellular antigens by SV-IV, a major protein secreted from the rat seminal vesicle epithelium.

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.

Animals↗

PubMed1993

HLA class II antigens and interleukin-1 in patients affected by type-II diabetes mellitus and hyperlipemia.

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.

Adult↗

PubMed1992

Iak antigen and interleukin-1 secretion by lymphocytes and monocytes of mice fed a lipid-rich diet.

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.

Animals↗

PubMed1988

Toxicity in uremia. 1. Correlation between PTH levels and depressed cell proliferation.

Cell proliferation is significantly depressed in uremia; to assess the influence of PTH on it, normal lymphocytes were cultured in presence of uremic patients' serum with low or high plasma PTH levels (Group A; PTH less than 2.5 ng/ml; Group B: PTH greater than 12 ng/ml), and serum of normal subjects (Group C). Cell proliferation was lowered by serum from both groups (p A vs C less than 0.004; p B vs C less than 0.001). However, the depressing effect was more evident when group B serum was employed (p A vs B less than 0.002).

Cell Division↗

PubMed1988

Toxicity in uremia. 2. Correlation between PTH levels and impaired aspecific immunity.

The role of PTH in depressing polynuclear leucocyte (PMN) phagocytosis in uremia was investigated. The hydrophobicity and phagocytic activity of normal PMN was tested in presence of uremic patients' serum with low (Group A) or high (Group B) levels of plasma PTH. The PMN phagocytic index was lowered by serum of both groups, but more in presence of Group B serum (p A vs B less than 0.002). Similarly, the contact angle of cells was affected more in presence of serum of patients with high PTH levels (p B vs A less than 0.003; p B vs C less than 0.002).

Cytotoxins↗