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Role of haem oxygenase-1 in microbial host defence
Chung, Su Wol,Hall, Sean R.,Perrella, Mark A. Blackwell Publishing Ltd 2009 Cellular microbiology Vol.11 No.2
<P>Summary</P><P>Haem oxygenase (HO)-1 is a cytoprotective enzyme that plays a critical role in defending the body against oxidant-induced injury during inflammatory processes. HO catalydes the degradation of haem to carbon monoxide (CO), biliverdin and ferrous iron. Biliverdin is converted to bilirubin, a potent endogenous antioxidant. CO has a number of biological functions, including anti-inflammatory properties. In various models of disease, HO-1 is known to play a critical role by ameliorating the pathological consequences of injury. In many of these models, the beneficial effects of HO-1 and its products of haem catabolism are by suppressing an inflammatory response. However, when investigating diseases due to microbial infections, inhibition of the inflammatory response could disrupt the ability of the immune system to eradicate an invading pathogen. Thus, questions remain regarding the role of HO-1 in microbial host defence. This microreview will address our present understanding of HO-1 and its functional significance in a variety of microbial infections.</P>
Elk-3 is a KLF4-regulated gene that modulates the phagocytosis of bacteria by macrophages
Tsoyi, Konstantin,Geldart, Adriana M.,Christou, Helen,Liu, Xiaoli,Chung, Su Wol,Perrella, Mark A. Federation of American Societies for Experimental 2015 Journal of Leukocyte Biology Vol.97 No.1
<P>Down-regulation of Elk-3 by bacterial LPS, in part through the transcriptional repressor KLF4, allows for up-regulation of HO-1 and a compensatory phagocytic response in macrophages.</P><P>ETS family proteins play a role in immune responses. A unique member of this family, Elk-3, is a transcriptional repressor that regulates the expression of HO-1. Elk-3 is very sensitive to the effects of inflammatory mediators and is down-regulated by bacterial endotoxin (LPS). In the present study, exposure of mouse macrophages to <I>Escherichia coli</I> LPS resulted in decreased, full-length, and splice-variant isoforms of Elk-3. We isolated the Elk-3 promoter and demonstrated that LPS also decreased promoter activity. The Elk-3 promoter contains GC-rich regions that are putative binding sites for zinc-finger transcription factors, such as Sp1 and KLFs. Mutation of the GC-rich region from bp –613 to –603 blunted LPS-induced down-regulation of the Elk-3 promoter. Similar to the LPS response, coexpression of KLF4 led to repression of Elk-3 promoter activity, whereas coexpression of Sp1 increased activity. ChIP assays revealed that KLF4 binding to the Elk-3 promoter was increased by LPS exposure, and Sp1 binding was decreased. Thus, down-regulation of Elk-3 by bacterial LPS is regulated, in part, by the transcriptional repressor KLF4. Overexpression of Elk-3, in the presence of <I>E. coli</I> bacteria, resulted in decreased macrophage phagocytosis. To determine whether limited expression of HO-1 may contribute to this response, we exposed HO-1-deficient bone marrow-derived macrophages to <I>E. coli</I> and found a comparable reduction in bacterial phagocytosis. These data suggest that down-regulation of Elk-3 and the subsequent induction of HO-1 are important for macrophage function during the inflammatory response to infection.</P>
Eicker, Ursula,Strzalka, Aneta,Erhart, Tobias,Balestieri, Jose Antonio Perrella Sustainable Building Research Center 2011 International journal of sustainable building tech Vol.2 No.1
The paper presents monitoring results from the implementation of energy efficient buildings, renewable energy supply systems and energy management in a sustainable neighborhood in Germany. The whole quarter has low energy standard buildings, which have been monitored for heating and electricity consumption. About 80% of the heating energy demand and 50% of the electricity consumption of the whole area is supplied by a wood fired co-generation plant with 1 MW electrical output and 5.3 MW thermal power output. In summer the heat from the network is used for decentralized absorption cooling in one of the office buildings. The main performance results of this monitored area are presented and the potential for replication are discussed.
Lee, Seonmin,Lee, Seon-Jin,Coronata, Anna A.,Fredenburgh, Laura E.,Chung, Su Wol,Perrella, Mark A.,Nakahira, Kiichi,Ryter, Stefan W.,Choi, Augustine M.K. Mary Ann Liebert 2014 Antioxidants & redox signaling Vol.20 No.3
<P>Sepsis, a systemic inflammatory response to infection, represents the leading cause of death in critically ill patients. However, the pathogenesis of sepsis remains incompletely understood. Carbon monoxide (CO), when administered at low physiologic doses, can modulate cell proliferation, apoptosis, and inflammation in pre-clinical tissue injury models, though its mechanism of action in sepsis remains unclear.</P>