Gender differences in kidney function.

Sex hormones influence the development of female (F) and male (M) specific traits and primarily affect the structure and function of gender-specific organs. Recent studies also indicated their important roles in regulating structure and/or function of nearly every tissue and organ in the mammalian body, including the kidneys, causing gender differences in a variety of characteristics. Clinical observations in humans and studies in experimental animals in vivo and in models in vitro have shown that renal structure and functions under various physiological, pharmacological, and toxicological conditions are different in M and F, and that these differences may be related to the sex-hormone-regulated expression and action of transporters in the apical and basolateral membrane of nephron epithelial cells. In this review we have collected published data on gender differences in renal functions, transporters and other related parameters, and present our own microarray data on messenger RNA expression for various transporters in the kidney cortex of M and F rats. With these data we would like to emphasize the importance of sex hormones in regulation of a variety of renal transport functions and to initiate further studies of gender-related differences in kidney structure and functions, which would enable us to better understand occurrence and development of various renal diseases, pharmacotherapy, and drug-induced nephrotoxicity in humans and animals.

Muramyl dipeptide-induced enhancement of phagocytosis of antibiotic pretreated Escherichia coli by macrophages.

Treatment of mice with muramyl dipeptide, a known immunoadjuvant, resulted in marked augmentation of the phagocytic activity of peritoneal macrophages incubated in vitro with Escherichia coli. Even greater phagocytosis occurred when the E. coli were pretreated for 2 hr with subinhibitory concentrations of the semisynthetic penicillins cyclacillin or ampicillin, but not penicillin G to which they were resistant. The antibiotic-pretreated E. coli were more rapidly ingested by the macrophages derived from MDP-treated mice as compared to similar cells from normal mice. Optimum augmentation of phagocytosis of untreated or antibiotic-pretreated E. coli occurred 2 to 3 days after administration of MDP to the mice. Similar augmentation of phagocytosis occurred by treating cultures of peritoneal macrophages from normal mice in vitro with MDP prior to incubation with the antibiotic-pretreated bacteria. These results indicate that macrophages from MDP stimulated mice interact with antibiotic-pretreated bacteria to a greater extent than with untreated E. coli, resulting in increased phagocytosis and killing of the bacteria.