@article {1749,
	title = {Cationic polyelectrolytes from leukocytes might kill bacteria by\&nbsp;activating their autolytic systems: Enigmatically, the relevance\&nbsp;of this phenomenon to post-infectious sequelae is disregarded},
	journal = {Intensive Care Medicine},
	volume = {28},
	number = {8},
	year = {2002},
	pages = {1188},
	abstract = {Linear polymers of lysine and arginine, phagocyte-derived lysozyme, PLA, elas- tase, cathepsin G, myeloperoxidases, nu- clear histone and bacterial/permeability-en- hancing peptide (BPI) and defensins all possess bactericidal activities [1, 2, 3, 4, 5, 6]. The highly cationic BPI and defensins might kill Gram-negatives primarily by de- polarizing their outer membrane to en- hance its permeability [3]. However, it had also been proposed that many of these polycations might also function as {\textquotedblleft}Trojan Horses{\textquotedblright} to disrupt the intracellular regula- tion of the autolytic wall enzyme systems (muramidases).This can lead to cleavage of the peptidoglycan, to bacteriolysis, and to cell death [4, 5, 6].The highly cationic, ly- sozyme, PLA2, and elastase probably do not function solely as enzymes, but rather as highly cationic agents. The bactericidal and bacteriolytic effects of polycations might therefore mimic the bacteriolytic ef- fects caused by beta-lactam antibiotics. Sulfated compounds (heparin, dextran sul- fate, polyaenthole sulfonate) very efficient-
CORRESPONDENCE
ly inhibited the activation of bacterial au- tolysis induced either by cationic agents or by beta-lactam antibiotics [4, 5, 6, 7]. Therefore, it is highly likely that polycat- ions of plasma and leukocyte origins might be actively involved in the pathophysiolo- gy of post-infectious sequelae by their ca- pacity to induce a massive release of high- ly phlogistic lipoteichoic acid [7] endotox- in, lipoprotein, and peptidoglycan [8].
Combinations among these agents might act on mononuclear cells to generate reactive oxygen species, NO, NOO-, hy- drolases, and also to activate the coagula- tion, complement, and cytokine cascades, all involved in septic shock. Based on the above arguments, it is tempting to specu- late that the failure to depress early bacteri- olysis in the bloodstream might be the main cause for the inability to cope with the multiple synergistic interactions lead- ing to post-infectious sequelae [9]. The clinical use of polyanions when combined with mutli drug strategies might therefore be recommended as potent anti-bacteriolyt- ic and anti-inflammatory agents [10]. It is enigmatic why publications that have pro- posed the role of polycations in bacterioly- sis and the possibility to inhibit its unto- ward effects by polyanions, findings so rel- evant to the patholysiology of post-infec- tious sequelae, are consistently disregarded [11] either in basic science publications on the bactericidal effects of polycations or in the clinical literature dealing with post-in- fectious sequelae.},
	author = {Isaac Ginsburg}
}
