@proceedings {2194,
	title = {HOW ARE CELL-WALL COMPONENTS OF PATHOGENIC MICROORGANISMS DEGRADEDIN INFECTIOUS AND INFLAMMATORY SITES? FACTS AND MYTHS},
	journal = {Biological Properties of Peptidoglycan},
	year = {1986},
	pages = {167-185},
	abstract = {Introduction.
Although a voluminous literature exists today which describes, in
great detail, the role played by "professional" phagocytes and by
serum components in the killing of pathogenic bacteria in vitro
and in vivo (l-7) very surprisingly, however, little is actually
known about the fate and mode of disposal of microorganisms once
they had been rendered non-viable by the defence systems of the
host. It is expected that the rich arsenal of lysosomal hydro-
lases, including the key muralytic enzyme lysozyme (LYZ), present
in leukocytes and in body fluids might be adequate to biodegrade
the complex structures of the microbial cells. Paradoxically,
however, the majority of bacteria are highly refractory to LYZ
action. There is also some confusion in the literature concerning
the distinction between bactericidal and bacteriolytic processes.
It is conceivable that while a major degradation of microbial cell
walls may be followed by a bactericidal reaction, the mere killing
of bacteria either by oxygen radicals (2) or by complement-dependent cytlytic antibodies (7) may not necessarily be accompanied by a
significant cell wall degradation. Many experimental models, with
laboratory animals, have distinctly shown the persistence, for very long periods, of non-viable bacteria and of undergraded microbial cell wall components, within macrophages, in chronic inflammatory sites (8-l8). Thus, one should categorically differentiate
between bactericidal and bacteriolytic phenomena. It is apparent,
therefore, that mammalian tissues fail, for still not/fully known
reasons, to biodegrade and eliminate microbial cell wall components. Peptidoglycan (PPG)-polysaccharide (PS) complexes derived
from microbial cell walls possess distinct pathobiological and and pathophysiological properties (19-21). These include the capacity to activate the complement cascade and to generate chemotactic agents, to induce fever, to activate the respiratory burst in
leukocytes and to modulate the immune responses (19-24), to mention only a few of the plethora of functions ascribed to PPG.
These properties may also explain the very complex interrelationships which exist between the parasite and the host during microbial infections and the possible reasons for the development of
certain post-infectious sequelae, which involve the prolonged persistence of bacterial cell wall components in tissues (10-15).
},
	author = {Isaac Ginsburg}
}
