Author
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Holt, Peter |
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Submitted to: American College of Poultry Veterinarians
Publication Type: Proceedings Publication Acceptance Date: 2/28/2011 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: A variety of bacterial agents reside in and around the environment that can cause illness and death in a poultry flock. Many cause disseminated disease while others exert more local effects such as the respiratory or gastrointestinal tract. The host, for our current purposes the laying hen, has developed multiple mechanisms to combat microbial invasion. While substantial research has been undertaken to understand the host/pathogen interactions involved between the hen and the multiple bacterial disease agents, the amount of indepth information on immune mechanisms of protection are lacking. However, because of the bird health and food safety issues caused by paratyphoid salmonellae, much more is known about immunity in the avian host as it relates to clearing or preventing infection by these organisms. The two bacteria of interest are Salmonella enterica serovar Enteritidis (S. enteritidis) and Salmonella enterica serovar Typhimurium (S. typhimurium). These organisms generally enter the avian host via ingestion and they migrate down the alimentary tract until they reach the ileum, colon and cecum where they replicate, invade the intestinal epithelium and then disseminate to multiple organs (Barrow et al. 1987). In the case of S. enteritidis, this dissemination can result in the infection of the reproductive tract and the ultimate entry into eggs either during egg formation or via penetration through the shell (Gantois et al. 2009), resulting in a potentially significant food safety issue. In most cases, the hen immune system helps clear the infection over time. This short review will focus on the different immune parameters as they relate to infection in chickens There are two primary types of immunity that protect the host from infection: innate and adaptive. Innate immunity represents all of the nonspecific protective mechanisms such as barriers (skin, mucus, respiratory cilia), soluble (complement, cytokines, acute phase proteins) and leukocytes (heterophils, macrophages/monocytes, NK cells). These provide protection for the host during the early phase of the infection. Adaptive immunity represents the humoral and cell-mediated immune (CMI) systems, which are activated specifically against foreign agents that enter the body. Development of this response requires the activation of cells and production of antibodies specific for the pathogen and is therefore delayed for a period of a week or longer. The innate and adaptive immune systems are not mutually exclusive and interact with each other to enhance protection. When the Salmonella bacteria reach the intestinal tract, they must breach several of the gut innate defenses to cause infection. They must migrate through the mucus layer covering the gut epithelium and then penetrate and invade the epithelial cells, moving down through the cell layer into deeper tissue. At this point, the bacteria meet the first line of active defense, the phagocytic cells heterophils and macrophages. These cells engulf and phagocytize the bacteria. In many cases, the bacteria are able to survive and hitch a ride within the phagocytic cells to disseminate to other parts of the body. If the cells are sufficiently activated, however, they will be able to subsequently kill the bacteria. Many factors come into play to activate heterophils and macrophages. CXCli2, the avian ortholog of mammalian interleukin 8 (Bedard et al. 1987), is a chemokine produced during invasion of many cell types, including the epithelial cells of the gut, and serves as a chemotactic signal to activate and attract phagocytic cells to the area of microbial invasion (Willems et al 1989; Agace et al. 1993). Phagocytic cell activation can also occur via the binding of various cellular pattern recognition receptors (PRR) such as Toll-like receptors (TLR), to their specific ligands. This activation increases |
