HIGH YIELD IMMUNOLOGY 2ND EDITION PDF

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High-Yield Immunology book. Read reviews from world's largest community for readers. This book extracts the most important information on immunology and. High-yield immunology by Arthur G. Johnson; 2 editions; First published in ; Subjects: Hypersensitivity, Immunity, Immunologic Factors. High-Yield Immunology / Edition 2. Add to Wishlist. ISBN ; ISBN- ; Pub. Date: 08/28/; Publisher: LWW.

Adequate immune functions are essential for host defence against IMIs. MG immunity depends on the complex combination and coordination of nonspecific and specific protective elements, including the anatomical features of the gland as well as cellular and humoral defence components [ 5 ].

Nevertheless, MG immune defence varies over different stages of lactation in dairy animals and is typically depressed with exposure to stress and around drying-off and parturition, thus increasing susceptibility to mastitis [ 6 , 7 ].

However, a considerable body of evidence has accumulated suggesting that mastitis is a multifactorial complex, and several management and environmental factors must interact to increase host exposure to mastitis pathogens, reduce the natural resistance of animals to disease, or aid pathogens in gaining entrance to the MG environment to cause infection [ 2 , 4 ].

Teat Skin and Teat Canal Defence System Structural Defence The primary defence mechanism of the MG is represented structurally in the teat canal [ 3 , 8 , 9 ], which acts as both a physical barrier and a source of antimicrobial substances.

The physical barrier is provided by the smooth muscle sphincter surrounding the teat canal, which prevents escape of milk and constitutes a barricade against the entry of different pathogens by maintaining tight closure [ 2 , 3 , 9 ]. The antimicrobial defence, on the other hand, comprises several components.

Normally, the healthy teat skin is coated with a protective mantle of fatty acids FAs that slow the growth of bacterial pathogens [ 2 ]. Additionally, the stratified squamous epithelium of the teat duct produces keratin, a waxy material lining the teat canal, which traps invading bacteria and hinders the migration of microorganisms into the gland cistern.

Keratin also contains antimicrobial agents that assist in combating infection [ 9 ]. This keratin is composed of I bacteriostatic FAs of both esterified and nonesterified types, such as lauric, myristic, palmitoleic, and linolenic acids and II fibrous proteins, which bind electrostatically to microorganisms, altering the cell wall and rendering it more susceptible to osmotic pressure changes and, thus, to lysis and death [ 9 ].

Additionally, these cationic proteins were found to have an inhibitory effect against some pathogens as Staph. The lipid content and composition of teat duct keratin have been shown to vary throughout the milking process [ 12 ], between lactating and dry dairy animals [ 13 ], and according to the severity of IMI.

SCM was found to not affect the lipid content of teat duct keratin, while CM was shown to be associated either with significantly higher levels of total lipids [ 14 ] or with similar lipid composition of uninfected quarters [ 15 ]. Additionally, the free FAs in milk from clinical quarters contained fewer short-chain FAs, whereas polyunsaturated FAs were significantly higher [ 14 ].

Recently, sentinel functions for the teat towards invading pathogens have been documented, as the teat canal tissue responded rapidly and intensely, with both expression of several Toll-like receptors TLRs and production of cytokines and antimicrobial peptides [ 16 , 17 ].

Damage of keratin, perhaps as a result of incorrect intramammary therapy infusion [ 18 ] or by faulty machine milking [ 19 ], has been reported to increase susceptibility of the teat canal to bacterial invasion and colonisation [ 20 ]. However, the antimicrobial effectiveness of keratin is limited [ 9 , 21 ] and, despite the potent physical and chemical protection in the teat canal, there are several ways by which bacteria can penetrate the teat canal and cause IMI, so much so that a number of pathogens are able to colonize the teat canal for prolonged periods, such as Corynebacterium bovis, or CNS.

The survival for several days of Staph. Also, during milking, it is common for keratin to be flushed out with distention of the teat canal [ 25 ].

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Because the sphincter takes approximately 2 h to regain its contracted position, there is a chance for outside pathogens to enter the teat canal, causing trauma and damage to the keratin or mucous membranes lining the teat sinus [ 2 , 21 ]. Additionally, during mechanical milking, microorganisms present at the teat end may be propelled into or through the teat duct into the cistern. This mechanism is considered the chief mechanism behind the spreading of contagious mastitis pathogens [ 26 ].

Innate and Adaptive Acquired Immunity The MG is normally protected by both innate and adaptive immune responses IRs , which coordinate and operate together to provide an optimal defence against infections. The IRs also facilitate the constitutive or acute transient presence of a wide range of immune-related components in milk [ 5 ].

The adaptive immune system AIS responds more robustly to threats to which it has previously been exposed [ 27 ]; however, it is slow to respond to novel threats [ 33 ]. In contrast, the innate immune system IIS is the first line of defence against pathogens once they have penetrated the physical barrier of the teat canal and before the AIS comes into play, and it evolves into a highly effective host defence [ 33 , 34 ].

This process is mediated via several intracellular signal transduction cascades that trigger an acute upregulation of several innate immune components including different leukocytes, adhesion molecules, and cytokines [ 35 — 37 ].

The two most critical components of host innate immunity are pathogen recognition PR and the ability to mount a proinflammatory response, a complex interaction of cellular and molecular processes aimed at detecting and subsequently eliminating harmful pathogens [ 25 , 34 ].

A wide variety of components linked to the innate IR IIR have been identified in milk, including cellular defence components [e. Many of these components originate from specialised cells that traffic to the MG [ 33 , 34 ].

The ability of the IIS to recognise and respond to a broad spectrum of pathogens that may or may not have been previously encountered, combined with the speed in mounting a proinflammatory response following initial PR, greatly contributes to the host's ability to control invading pathogens [ 37 ].

Below, there is a detailed overview of the roles and mechanisms of action of some innate immune factors. The viable leukocytes inside the MG offer some degree of cellular protection against microbial invasion through their ability to recognise microorganisms and induce a rapid inflammatory response in an attempt to resolve the IMI immediately.

Thus, MG-resident leukocytes likely provide a surveillance function in the uninfected gland. Also, these cells may aid in the restructuring of the MG that occurs during involution i. In addition to microbicidal functions of phagocytosis, MG leukocytes secrete a variety of immune-related components into milk including cytokines, chemokines, ROS, and antimicrobial proteins and peptides LF, defensins, and cathelicidins [ 40 ].

Leukocytes also assist in the repair of damaged tissue caused by shedding and renewal processes [ 41 ]. Despite the presence of considerable numbers of immune cells in the MG environment, it has been suggested that the MG is immune-compromised when compared to the rest of the body [ 42 ]. Moreover, the activities of all types of leukocytes in milk have been shown to be reduced compared to those in blood [ 28 , 43 , 44 ]. The migration of immune cells during IMI plus desquamation of MG epithelia results in an increase of somatic cell count SCC accompanied with decreased milk production according to the severity of the process [ 1 , 45 ].

Even under healthy conditions, PMNs are permanently present inside the MG environment, and nursing or milking stimuli accompanied with milk removal were found to induce directed migration of fresh PMN into mammary tissue [ 46 ]. Bovine neutrophils cross the MG epithelium by diapedesis without causing epithelial cell damage [ 47 ] unless the migration is extensive, in which case both mechanical and chemical damage are possible [ 48 ].

The neutrophil's multilobulated nucleus allows for easy and rapid migration between endothelial cells, thus arriving as the first recruited immune cell to sites of infection [ 49 ]. Because only small numbers of mature PMNs are stored in the bone marrow, the number of immature neutrophils in circulation increases as a result of mobilisation into circulation during inflammatory conditions.

Thus, the number of circulating mature neutrophils negatively correlates with severity of mastitis [ 6 ]. Several important functions are not fully developed in immature neutrophils, including those pertaining to phagocytosis, intracellular killing, and chemotaxis [ 50 ].

Neutrophils are delineated by a plasma membrane that has a number of functionally important receptors. Membrane receptors for the Fc portion of the IgG2 and IgM classes of Igs and for complement components C3b and iC3b are necessary for the phagocytosis of invading bacteria [ 52 , 53 ].

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In addition to microbicidal functions of phagocytosis, MG leukocytes secrete a variety of immune-related components into milk including cytokines, chemokines, ROS, and antimicrobial proteins and peptides LF, defensins, and cathelicidins [ 40 ]. Lymphocytes recognise a variety of antigenic structures via membrane receptors, which define their specificity, diversity, and memory characteristics.

Visit Seller's Storefront. This trusted resource features sweeping content updates, rewritten chapters, a highly clinical perspective, and an easy-to-use organization designed to enhance your diagnosis and management skills in daily practice. Frew; Cornelia M. Pillai; Ronald C. Grace Caparas marked it as to-read May 15,