however, this is dependent on the type virus.

19.1.4 Phagocyte-Pathogen Interactions Phagocytosis

Various receptors on phagocytes including complement, Fc, fibronectin, and mannose receptors mediate attachment to, and phagocytosis of pathogens. These receptors either induce or suppress certain metabolic events of phagocytes. Binding of IgG-coated particles with Fc receptors induces endocytosis and triggers multiple biological activities, including the production of ROI.28 In contrast, the complement receptor pathway may provide intracellular parasites with safe passage into mono-nuclear phagocytes, since ligation of CR1 and CR3 receptors by particles coated with C3b or C3bi causes endocytosis but does not consistently stimulate the release of oxygen metabolites, such as hydrogen peroxide, or superoxide or the release of mediators of inflammation such as metabolites

29-32 33

of arachidonic acid. Consistent with this hypothesis, Legionella pneumophila, Mycobacterium leprae,34 and Toxoplasma gondii35 have been found to elicit little or no metabolic burst upon entering mononuclear phagocytes. Because intracellular predators often enter their prey without inducing reactive oxygen metabolites, their growth in activated macrophages must ultimately be controlled by nonoxidative mechanisms.36-39 Pathogen Survival in Phagocytes

To survive within professional phagocytes, intracellular pathogens have a variety of evasion mechanisms. In principle, these include (1) interference with, or resistance to, oxidative killing, (2) inhibition of phagosome-lysosome fusion,40-42 (3) interference with or resistance to lysosomal enzymes43 or microbicidal peptides, and (4) escape into the cytoplasm.

Precise identification of the molecules responsible for intracellular survival is just beginning. Lipoarabinomannan in mycobacteria has been shown to scavenge cytotoxic oxygen free radicals.44,45 Phenolic glycolipid-1 of M. leprae and lipophosphoglycan of Leishmania donovani scavenge reactive oxygen metabolites in a cell free system.44,46 Mycobacterium avium survives intracellularly by inhibiting superoxide anion production by macrophages,47,48 as well as phagolysosomal fusion following phagocytosis.49,50 Activation of Phagocyte Function

Phagocytic function can be regulated by cytokines. Tumor necrosis factor (TNF) can stimulate bacteriostatic and bactericidal activities in macrophages,51 which may be important in the immune response against M. avium,52,53 M. tuberculosis,1,54 Chlamydia trachomatis,55 Listeria monocytoge-nes,56'51 Candida albicans,5 Legionella pneumophila.59 It has been proposed that interferon-/ (IFN-/) produced by T cells activates macrophages to secrete TNF which, in turn, sensitizes the same or other macrophages to secrete ROI that rapidly destroy parasites through a process of lipid peroxidation.60

IFN-/ also directly enhances macrophage antimicrobial6162 and oxidative63 64 activities in such a way that they kill or inhibit the multiplication of L. pneumophila,65'66 Toxoplasma gondii,67-69 Chlamydia psittaci,70 Leishmania donovani,11'12 L. major,13 and Trypanosoma cruzi.14

Macrophages and monocytes exposed to rIFN-/ develop the ability to secrete ROI, as well as to kill nonspecifically obligate or facultative intracellular microorganisms.68,15,16 Growth inhibition of M. bovis by IFN-/-activated macrophages is an oxygen-independent process and may involve phagosome-lysosome fusion.16,11 For some facultative intracellular pathogens, such as Listeria monocytogenes, M. avium, and Salmonella typhimurium, IFN-/ is not capable of sufficiently activating the antibacterial effector function.18,19 Illustration of Bacterial-Phagocyte Interaction with Haemophilus somnus

Haemophilus somnus is a Gram-negative, small, fastidious bacterium that has been recognized as a facultative intracellular pathogen of cattle. It causes a wide variety of clinical syndromes in cattle including myocarditis, pneumonia, encephalitis, and arthritis, which are collectively known as bovine hemophilosis.80-85 Haemophilus somnus is able to interact with a number of cells types in the host, including phagocytes. In vitro studies have established that bovine PMN are unable to kill H. somnus, and that H. somnus can replicate within bovine monocytes.83 Moreover, H. somnus is able to suppress the chemiluminescence activity of both bovine PMN and monocytes.85,86 These findings suggest that the ability of the bacterium to persist and proliferate within these cells could contribute to the pathogenesis of hemophilosis. The objective of this study was to use chemilumi-nescence and phagocytosis assays to investigate the phagocytic function and ROI-mediated killing mechanisms of bovine mononuclear phagocytes following interaction with H. somnus.

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