Innate and adaptive immunity at mucosal surfaces of the female reproductive tract: stratification and integration of immune protection against the transmission of sexually transmitted infections.

This review examines the multiple levels of pre-existing immunity in the upper and lower female reproductive tract. In addition, we highlight the need for further research of innate and adaptive immune protection of mucosal surfaces in the female reproductive tract. Innate mechanisms include the mucus lining, a tight epithelial barrier and the secretion of antimicrobial peptides and cytokines by epithelial and innate immune cells. Stimulation of the innate immune system also serves to bridge the adaptive arm resulting in the generation of pathogen-specific humoral and cell-mediated immunity. Less understood are the multiple components that act in a coordinated way to provide a network of ongoing protection. Innate and adaptive immunity in the human female reproductive tract are influenced by the stage of menstrual cycle and are directly regulated by the sex steroid hormones, progesterone and estradiol. Furthermore, the effect of hormones on immunity is mediated both directly on immune and epithelial cells and indirectly by stimulating growth factor secretion from stromal cells. The goal of this review is to focus on the diverse aspects of the innate and adaptive immune systems that contribute to a unique network of protection throughout the female reproductive tract.

Lipolysis in cheddar cheese made from raw, thermized, and pasteurized milks.

The evolution of free fatty acids (FFA) was monitored over 168 d of ripening in Cheddar cheeses manufactured from good quality raw milk (RM), thermized milk (TM; 65 degrees C x 15 s), and pasteurized milk (PM; 72 degrees C x 15 s). Heat treatment of the milk reduced the level and diversity of raw milk microflora and extensively or wholly inactivated lipoprotein lipase (LPL) activity. Indigenous milk enzymes or proteases from RM microflora influenced secondary proteolysis in TM and RM cheeses. Differences in FFA in the RM, TM, and PM influenced the levels of FFA in the subsequent cheeses at 1 d, despite significant losses of FFA to the whey during manufacture. Starter esterases appear to be the main contributors of lipolysis in all cheeses, with LPL contributing during production and ripening in RM and, to a lesser extent, in TM cheeses. Indigenous milk microflora and nonstarter lactic acid bacteria appear to have a minor contribution to lipolysis particularly in PM cheeses. Lipolytic activity of starter esterases, LPL, and indigenous raw milk microflora appeared to be limited by substrate accessibility or environmental conditions over ripening.