Fibronectin Binding Protein A
Fibronectin binding protein A, denoted as FnBPs are implicated when disease causing organisms adhere to and the take over of bovine mammary glands. This leads to mastitis infection. In vitro research shows that in most cases, FnBPs aids the pathogen to adhere to the epithelial cells of the mammary glands. While this is the case, in vivo analysis, do not show this relationship between FnBPs and the pathogen. In this paper, we shall discuss Fibronectin binding protein A and its support for pathogens in the development of mastitis.
It is important that bovine mastitis is one of the most expensive diseases in the dairy industry. When it strikes, the loss associated to it is enormous and unimaginable. In most cases, mastitis presents itself with the inflammation of the mammary glands, which is as a result of microbial infection. Moreover, Streptococcus agalactiae and Staphylococcus aureus account for more than 75% of inflammatory diseases, including mastitis. Notably, S. aureus causes about 19% of the infections and is responsible for mastitis cases, which are not easy to cure. It is adaptive and has adhhesins, which can bind on different proteins of the host, especially in the extracellular matrix of the host. Some of these sites include collagen, fibrinogen, and Fibronectin. Research shows that fibronectin-binding proteins A and B are the primary adhesins, which bind purified Fibronectin. One of these genes of FnBP is always found in most S. aureus strains. Furthermore, researchers note that the first step of mammary gland infection is when pathogens adhere to the teat canal of the udder. Based on this finding, FnBP has been put forth as virulence requirement in bovine mastitis. No evidence has been found to link FnBPs with the colonization of the mammary glands.
It is worth noting that science is replete with studies, conducted to determine the role of FnBP in bacterial adherence to cells like eukaryotic carried out in vitro. There are also various reviews, which show that in vivo experiments do not illustrate FnBPs as virulence factors. By using a predetermined strain of bacteria and cell, research has revealed that an isogenic mutant, which does not have FnBPs is likely to have a 40% drop in its ability to adhere to bovine mammary glands. This was in comparison with S. aureus 8325-4, which is a wild-type laboratory strain.
In understanding this phenomenon, it important to note that other factors influences the adherence of these pathogens. A good example is the stress that comes from milking or suckling of mammals. This affects the presence of milk and serum, which may have direct impact on the expression of genes and bacterial adaptation to the mammary gland. There is also enough research evidence showing that when you vary in vivo conditions, you are likely to experience different effects for the adherence of pathogens in the mammary glands of animals. It is essential to underscore the fact that when mammary glands inflame, they lead to high level of serum percentage in the milk of a cow. Nonetheless, there is need to conduct more research and investigations concerning adherence levels in different animals, which suffer from the bovine mastitis.
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