Host defence

Gale M Jr, Eoy EM (2005) Evasion of intracellular host defence by hepatitis C virus. Nature 436 939-945... 

Mmphy J.W. (1996) Slick ways Cryptococcus neoformans foih host defences, Soc Microbiol News,... 

Immunological tests were performed for studying the reactive of peritoneal-exudative cells, especially peritonial macrophages, which are the main effector cells involved in natural resistance (host defence system) against bacterial infection. 

It is misleading to consider that ROS are always deleterious, and that to prevent release or action of ail ROS will be of therapeutic value. One could reason that some ROS are released without control or purpose, as by-products of the normal metabolism of eicosanoids, or during oxidative phosphorylation in the mitochondria. However, during normal function, inflammatory ceUs appropriately release ROS both intracellularly into vacuoles and extracellularly in order to kill foreign organisms in host defence. Also, nitric oxide is a radical species whose principal role in the lung appears to be the control of pulmonary vascular tone and platelet function. Nevertheless, there are clear examples where fhistrated phagocytosis could explain an excessive release of ROS in... 

In summary, the in vivo protective effects of Tyv-specific antibodies, exclusion and immobility, can now be effectively studied using an in vitro model of the intestinal epithelium. Larvae are prevented from entering epithelial cells by caps of immune complexes or by binding of antibody to Tyv in the absence of immune complex formation. These effects would correlate with exclusion of larvae from epitheha observed in passively immunized rats. Larvae are encumbered as they migrate within epithelial monolayers, an effect that may correlate with immobility of larvae observed in vivo. It is reasonable to conclude that in the animal host the different effects work in combination, most iikeiy in cooperation with innate host defences, to cause nematode expuision from the intestine. 

Parasitism by T. spiralis has been a subject of scientific interest for over 150 years. Recently, considerable attention has been paid to the parasite by immunologists interested in immunity to nematodes in general, and mucosal immunity in particular. It has been shown that glycan-specific antibodies are highly effective mediators of host defence against intestinal 7. spiralis infection. Protective monoclonal antibodies have been used to elucidate mechanisms of worm expulsion, as well as to identify molecules that the parasite uses to create its niche. In the future, detailed characterization of these molecules and their functions should afford additional insights into parasitism by Trichinella spiralis, and possibly also by other types of pathogen. 

Kazura, J.W. and Aikawa, M. (1980) Host defence mechanisms against Trichinella spiralis infection in the mouse eosinophil mediated destruction of newborn larvae in vitro. Journal of Immunology 124, 355-361. 

Dykhuizen R., Frazer R., Benjamin N., Duncan C., Smith C.C., Golden M. and Leifert C. (1996). Antimicrobial effect of acidified nitrite on gut pathogens the importance of dietary nitrate in host defence . J Antimicrob Agents Chemothe, 40, 1422-1425. 

Apponyi, M.A. et al., Host-defence peptides of Australian anurans structure, mechanisms of action and evolutionary significance. Peptides, 25, 1035, 2004. 

Low levels of mercuric chloride in polymorphonuclear cells may profoundly alter the cell respiratory burst, measured as chemiluminiscence, oxygen consumption and H2Oz production [171-173], depress phagocytic capacity [172, 173] and enhance release of lysosomal enzymes [ 172] with minimal loss of cell viability. A stimulation of oxygen metabolism in vivo might promote tissue injury, via the local production of free oxygen metabolites, in addition to depression of host defence [173],... 

Neutrophils and host defence The fight against infection... 

Myeloperoxidase is an extremely potent, antimicrobial protein that is present in neutrophils at up to 5% of the total cell protein. Its role in the killing of a wide range of bacteria, fungi, viruses, protozoa and mammalian cells (e.g. tumour cells) is well established from in vitro studies. It also plays an important role in the inactivation of toxins and the activation of latent proteases, as well as in other functions described in section 5.4.1. In view of this apparent central role in neutrophil function during host defence, one would think that any deficiencies in this enzyme would have disastrous consequences on the ability of the host to combat infections. Until the early 1980s, this key role for myeloperoxidase in host protection seemed substantiated by the extremely low incidence of reports of patients with deficiencies of this enzyme. Indeed, up to this time, only 15 cases from 12 families had been reported worldwide. Sometimes these patients were asymptomatic but often suffered Candida infections, particularly if their myeloperoxidase deficiency was also associated with diabetes mellitus. 

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