@article {17406,
	title = {Thiazolidinedione-8 Alters Symbiotic Relationship in C. albicans-S. mutans Dual Species Biofilm},
	journal = {Frontiers  in Microbiology},
	volume = {10},
	year = {2016},
	month = {2016},
	abstract = {The small molecule, thiazolidinedione-8 (S-8) was shown to impair biofilm formation of various microbial pathogens, including the fungus\&nbsp;Candida albicans\&nbsp;and\&nbsp;Streptococcus mutans. Previously, we have evaluated the specific molecular mode of S-8 action against\&nbsp;C. albicans\&nbsp;biofilm-associated pathogenicity. In this study we investigated the influence of S-8 on dual species,\&nbsp;C. albicans-S. mutans\&nbsp;biofilm. We show that in the presence of S-8 a reduction of the co-species biofilm formation occurred with a major effect on\&nbsp;C. albicans. Biofilm biomass and exopolysaccharide (EPS) production were significantly reduced by S-8. Moreover, the agent caused oxidative stress associated with a strong induction of reactive oxygen species and hydrogen peroxide uptake inhibition by a mixed biofilm. In addition, S-8 altered symbiotic relationship between these species by a complex mechanism. Streptococcal genes associated with quorum sensing (QS) (comDE\&nbsp;and\&nbsp;luxS), EPS production (gtfBCD\&nbsp;and\&nbsp;gbpB), as well as genes related to protection against oxidative stress (nox\&nbsp;and\&nbsp;sodA) were markedly upregulated by S-8. In contrast, fungal genes related to hyphae formation (hwp1), adhesion (als3), hydrophobicity (csh1), and oxidative stress response (sod1,\&nbsp;sod2, and\&nbsp;cat1) were downregulated in the presence of S-8. In addition,\&nbsp;ywp1\&nbsp;gene associated with yeast form of\&nbsp;C. albicans\&nbsp;was induced by S-8, which is correlated with appearance of mostly yeast cells in S-8 treated dual species biofilms. We concluded that S-8 disturbs symbiotic balance between\&nbsp;C. albicans\&nbsp;and\&nbsp;S. mutans\&nbsp;in dual species biofilm.},
	url = {http://journal.frontiersin.org/article/10.3389/fmicb.2016.00140/full},
	author = {Mark Feldman and Isaac Ginsburg and Abed Al-Quntar1 and Steinberg, Doron}
}
@article {17405,
	title = {Nuclear histones: major virulence factors or just additional early sepsis markers? A comment},
	journal = {Inflammopharmacology},
	volume = {24},
	number = {5},
	year = {2016},
	month = {2016},
	pages = {287-289},
	abstract = {In 2009, Xu et al. and Chaput et al. in Nature Medicine had argued that the main cause of death in sepsis is the release from neutrophil nets of nuclear histone, highly toxic to endothelial cells and that these polycations are major and unique virulence factors. Since 2009, numerous researchers have also suggested the involvement of histones in the pathophysiology of many clinical disorders. If histones are indeed major unique virulence toxic agents, then heparin, activated protein C and antibodies to histone should prove excellent antisepsis agents. However, this is provided that these agents are administered to patients early enough before the activation of the cytokine storms, immune responses and the coagulation cascades are irreversibly unleashed. This may not be practical, since a diagnosis of sepsis is usually made much later. Future identifications of novel early markers are therefore needed and a compilation of cocktails of antagonists may replace the faulty single antagonists tried for many years, but in vain, to prevent death in sepsis.},
	url = {https://www.ncbi.nlm.nih.gov/pubmed/27613722},
	author = {Ginsburg, I. and Koren, E. and Varani, J. and Kohen, R.}
}
