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Article: Nuclear control of the inflammatory response in mammals by peroxisome proliferator-activated receptors.

Mandard, Stéphane / Patsouris, David

2013 Volume 2013, Page(s) 613864

Abstract: Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that play pivotal roles in the regulation of a very large number of biological processes including inflammation. Using specific examples, this paper focuses on ...

Abstract	Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that play pivotal roles in the regulation of a very large number of biological processes including inflammation. Using specific examples, this paper focuses on the interplay between PPARs and innate immunity/inflammation and, when possible, compares it among species. We focus on recent discoveries establishing how inflammation and PPARs interact in the context of obesity-induced inflammation and type 2 diabetes, mostly in mouse and humans. We illustrate that PPAR γ ability to alleviate obesity-associated inflammation raises an interesting pharmacologic potential. In the light of recent findings, the protective role of PPAR α and PPAR β / δ against the hepatic inflammatory response is also addressed. While PPARs agonists are well-established agents that can treat numerous inflammatory issues in rodents and humans, surprisingly very little has been described in other species. We therefore also review the implication of PPARs in inflammatory bowel disease; acute-phase response; and central, cardiac, and endothelial inflammation and compare it along different species (mainly mouse, rat, human, and pig). In the light of the data available in the literature, there is no doubt that more studies concerning the impact of PPAR ligands in livestock should be undertaken because it may finally raise unconsidered health and sanitary benefits.
Language	English
Publishing date	2013-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2237981-2
ISSN	1687-4765 ; 1687-4757
ISSN (online)	1687-4765
ISSN	1687-4757
DOI	10.1155/2013/613864
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Article ; Online: Catecholamines Induce Endoplasmic Reticulum Stress Via Both Alpha and Beta Receptors.

Abdullahi, Abdikarim / Wang, Vivian / Auger, Christopher / Patsouris, David / Amini-Nik, Saeid / Jeschke, Marc G

Shock (Augusta, Ga.)

2019 Volume 53, Issue 4, Page(s) 476–484

Abstract: Severely burned patients suffer from a hypermetabolic syndrome that can last for years after the injury has resolved. The underlying cause of these metabolic alterations most likely involves the persistent elevated catecholamine levels that follow the ... ...

Abstract	Severely burned patients suffer from a hypermetabolic syndrome that can last for years after the injury has resolved. The underlying cause of these metabolic alterations most likely involves the persistent elevated catecholamine levels that follow the surge induced by thermal injury. At the cellular level, endoplasmic reticulum (ER) stress in metabolic tissues is a hallmark observed in patients following burn injury and is associated with several detrimental effects. Therefore, ER stress could be the underlying cellular mechanism of persistent hypermetabolism in burned patients. Here, we show that catecholamines induce ER stress and that adreno-receptor blockers reduce stress responses in the HepG2 hepatocyte cell line. Our results also indicate that norepinephrine (NE) significantly induces ER stress in HepG2 cells and 3T3L1 mouse adipocytes. Furthermore, we demonstrate that the alpha-1 blocker, prazosin, and beta blocker, propranolol, block ER stress induced by NE. We also show that the effects of catecholamines in inducing ER stress are cell type-specific, as NE treatment failed to evoke ER stress in human fibroblasts. Thus, these findings reveal the mechanisms used by catecholamines to alter metabolism and suggest inhibition of the receptors utilized by these agents should be further explored as a potential target for the treatment of ER stress-mediated disease.
MeSH term(s)	Adrenergic alpha-1 Receptor Antagonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Catecholamines/physiology ; Cell Culture Techniques ; Endoplasmic Reticulum Stress/physiology ; Fibroblasts/drug effects ; Fibroblasts/physiology ; Hep G2 Cells/drug effects ; Hep G2 Cells/physiology ; Humans ; Prazosin/pharmacology ; Propranolol/pharmacology ; Receptors, Adrenergic, alpha/physiology ; Receptors, Adrenergic, beta/physiology
Chemical Substances	Adrenergic alpha-1 Receptor Antagonists ; Adrenergic beta-Antagonists ; Catecholamines ; Receptors, Adrenergic, alpha ; Receptors, Adrenergic, beta ; Propranolol (9Y8NXQ24VQ) ; Prazosin (XM03YJ541D)
Language	English
Publishing date	2019-07-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000001394
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Zs.A 3985: Show issues

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Book ; Thesis: Transcriptional regulation of nutrient metabolism by PPARalpha, gamma and LXRalpha

Patsouris, David

2006

Author's details	David Patsouris
Language	English
Size	160 p. :, ill. ;, 24 cm.
Publisher	s.n
Publishing place	Wageningen
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Thesis (doctoral)--Wageningen Universiteit, 2006
Note	Summary in French. ; Vita.
ISBN	9085044634 ; 9789085044635
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Modeling Acute ER Stress in Vivo and in Vitro.

Abdullahi, Abdikarim / Stanojcic, Mile / Parousis, Alexandra / Patsouris, David / Jeschke, Marc G

Shock (Augusta, Ga.)

2017 Volume 47, Issue 4, Page(s) 506–513

Abstract: The endoplasmic reticulum (ER) is a critical organelle that synthesizes secretory proteins and serves as the main calcium storage site of the cell. The accumulation of unfolded proteins at the ER results in ER stress. Although the association between ER ... ...

Abstract	The endoplasmic reticulum (ER) is a critical organelle that synthesizes secretory proteins and serves as the main calcium storage site of the cell. The accumulation of unfolded proteins at the ER results in ER stress. Although the association between ER stress and the pathogenesis of many metabolic conditions have been well characterized using both in vivo and in vitro models, no standardized model concerning ER stress exists. Here, we report a standardized model of ER stress using two well-characterized ER stress-inducing agents, thapsigargin and tunicamycin. Our aim in this current study was 2-fold: to characterize and establish which agent is optimal for in vitro use to model acute ER stress and to evaluate which agent is optimal for in vivo use. To study the first aim we used two well-established metabolic cell lines; human hepatocellular carcinoma (HepG2s) and differentiated mouse adipocytes (3T3-L1). In the second aim we utilized C57BL/6J mice that were randomized into three treatment groups of sham, thapsigargin, and tunicamycin. Our in vitro results showed that tunicamycin worked as a rapid and efficacious inducer of ER stress in adipocytes consistently, whereas thapsigargin and tunicamycin were equally effective in inducing ER stress in hepatocytes. In regards to our in vivo results, we saw that tunicamycin was superior in not only inducing ER stress but also recapturing the metabolic alterations associated with ER stress. Thus, our findings will help guide and inform researchers as to which ER stress agent is appropriate with regards to their model.
Language	English
Publishing date	2017-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000000759
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Article ; Online: Lipidomic analysis enables prediction of clinical outcomes in burn patients.

Qi, Peter / Abdullahi, Abdikarim / Stanojcic, Mile / Patsouris, David / Jeschke, Marc G

Scientific reports

2016 Volume 6, Page(s) 38707

Abstract: Recent discoveries have highlighted the novel metabolic functions of adipose tissue in enhancing hypermetabolism after trauma. As the exact function and expression profiles of serum lipids and free fatty acids (FFA) are essentially unknown, we determined ...

Abstract	Recent discoveries have highlighted the novel metabolic functions of adipose tissue in enhancing hypermetabolism after trauma. As the exact function and expression profiles of serum lipids and free fatty acids (FFA) are essentially unknown, we determined the lipidomic expression profile after burn in correlation to clinical outcomes to identify important lipid mediators affecting post-burn outcomes. We conducted a prospective cohort study with 46 adult burn patients and 5 healthy controls at the Ross Tilley Burn Center in Toronto, Canada. Patients were stratified based on major demographic and clinical variables, including age, burn severity, mortality, and sepsis. Serum FFAs and inflammatory markers were measured during acute hospital stay. We found that FFAs were acutely elevated post-burn and returned to baseline over time. Greater burn severity and age were associated with an impaired acute response in unsaturated FFAs and pro-inflammatory cytokines. Elevations in saturated and mono-unsaturated FFAs correlated significantly to increased mortality. In summary, persistent elevation of unsaturated lipids was associated with a functionally altered inflammatory-immunological milieu and worse clinical outcomes. The present lipidomic analysis indicates profound alterations in the lipid profile after burn by characterizing key lipids as potential diagnostic and outcome indicators in critically injured patients.
Language	English
Publishing date	2016-12-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep38707
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Article ; Online: Alternative Mechanism for White Adipose Tissue Lipolysis after Thermal Injury.

Diao, Li / Patsouris, David / Sadri, Ali-Reza / Dai, Xiaojing / Amini-Nik, Saeid / Jeschke, Marc G

Molecular medicine (Cambridge, Mass.)

2015 Volume 21, Issue 1, Page(s) 959–968

Abstract: Extensively burned patients often suffer from sepsis, a complication that enhances postburn hypermetabolism and contributes to increased incidence of multiple organ failure, morbidity and mortality. Despite the clinical importance of burn sepsis, the ... ...

Abstract	Extensively burned patients often suffer from sepsis, a complication that enhances postburn hypermetabolism and contributes to increased incidence of multiple organ failure, morbidity and mortality. Despite the clinical importance of burn sepsis, the molecular and cellular mechanisms of such infection-related metabolic derangements and organ dysfunction are still largely unknown. We recently found that upon endoplasmic reticulum (ER) stress, the white adipose tissue (WAT) interacts with the liver via inflammatory and metabolic signals leading to profound hepatic alterations, including hepatocyte apoptosis and hepatic fatty infiltration. We therefore hypothesized that burn plus infection causes an increase in lipolysis of WAT after major burn, partially through induction of ER stress, contributing to hyperlipidemia and profound hepatic lipid infiltration. We used a two-hit rat model of 60% total body surface area scald burn, followed by intraperitoneal (IP) injection of
Language	English
Publishing date	2015-12-29
Publishing country	England
Document type	Journal Article
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.2119/molmed.2015.00123
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Zs.A 4456: Show issues

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Article ; Online: Alternatively Activated Macrophages Drive Browning of White Adipose Tissue in Burns.

Abdullahi, Abdikarim / Auger, Christopher / Stanojcic, Mile / Patsouris, David / Parousis, Alexandra / Epelman, Slava / Jeschke, Marc G

Annals of surgery

2017 Volume 269, Issue 3, Page(s) 554–563

Abstract: Objective: The aim of this study was to uncover the mediators and mechanistic events that facilitate the browning of white adipose tissue (WAT) in response to burns.: Background: In hypermetabolic patients (eg, burns, cancer), the browning of WAT has ...

Abstract	Objective: The aim of this study was to uncover the mediators and mechanistic events that facilitate the browning of white adipose tissue (WAT) in response to burns. Background: In hypermetabolic patients (eg, burns, cancer), the browning of WAT has presented substantial clinical challenges related to cachexia, atherosclerosis, and poor clinical outcomes. Browning of the adipose tissue has recently been found to induce and sustain hypermetabolism. Although browning appears central in trauma-, burn-, or cancer-induced hypermetabolic catabolism, the mediators are essentially unknown. Methods: WAT and blood samples were collected from patients admitted to the Ross Tilley Burn Centre at Sunnybrook Hospital. Wild type, CCR2 KO, and interleukin (IL)-6 KO male mice were purchased from Jax laboratories and subjected to a 30% total body surface area burn injury. WAT and serum collected were analyzed for browning markers, macrophages, and metabolic state via histology, gene expression, and mitochondrial respiration. Results: In the present study, we show that burn-induced browning is associated with an increased macrophage infiltration, with a greater type 2 macrophage profile in the fat of burn patients. Similar to our clinical findings in burn patients, both an increase in macrophage recruitment and a type 2 macrophage profile were also observed in post burn mice. Genetic loss of the chemokine CCR2 responsible for macrophage migration to the adipose impairs burn-induced browning. Mechanistically, we show that macrophages recruited to burn-stressed subcutaneous WAT (sWAT) undergo alternative activation to induce tyrosine hydroxylase expression and catecholamine production mediated by IL-6, factors required for browning of sWAT. Conclusion: Together, our findings uncover macrophages as the key instigators and missing link in trauma-induced browning.
MeSH term(s)	Adipose Tissue, Brown/physiopathology ; Adipose Tissue, White/physiopathology ; Adult ; Animals ; Biomarkers/blood ; Burns/blood ; Burns/immunology ; Burns/physiopathology ; Case-Control Studies ; Female ; Flow Cytometry ; Humans ; Immunohistochemistry ; Interleukin-6/metabolism ; Macrophage Activation/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Polymerase Chain Reaction
Chemical Substances	Biomarkers ; Interleukin-6
Language	English
Publishing date	2017-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	340-2
ISSN	1528-1140 ; 0003-4932
ISSN (online)	1528-1140
ISSN	0003-4932
DOI	10.1097/SLA.0000000000002465
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Article ; Online: Burn Induces Browning of the Subcutaneous White Adipose Tissue in Mice and Humans.

Patsouris, David / Qi, Peter / Abdullahi, Abdikarim / Stanojcic, Mile / Chen, Peter / Parousis, Alexandra / Amini-Nik, Saeid / Jeschke, Marc G

Cell reports

2015 Volume 13, Issue 8, Page(s) 1538–1544

Abstract: Burn is accompanied by long-lasting immuno-metabolic alterations referred to as hypermetabolism that are characterized by a considerable increase in resting energy expenditure and substantial whole-body catabolism. In burned patients, the length and ... ...

Abstract	Burn is accompanied by long-lasting immuno-metabolic alterations referred to as hypermetabolism that are characterized by a considerable increase in resting energy expenditure and substantial whole-body catabolism. In burned patients, the length and magnitude of the hypermetabolic state is the highest of all patients and associated with profoundly increased morbidity and mortality. Unfortunately, the mechanisms involved in hypermetabolism are essentially unknown. We hypothesized that the adipose tissue plays a central role for the induction and persistence of hypermetabolism post-burn injury. Here, we show that burn induces a switch in the phenotype of the subcutaneous fat from white to beige, with associated characteristics such as increased mitochondrial mass and UCP1 expression. Our results further demonstrate the significant role of catecholamines and interleukin-6 in this process. We conclude that subcutaneous fat remodeling and browning represent an underlying mechanism that explains the elevated energy expenditure in burn-induced hypermetabolism.
MeSH term(s)	Adipose Tissue, White/metabolism ; Animals ; Burns/metabolism ; Catecholamines/metabolism ; Energy Metabolism/physiology ; Female ; Humans ; Interleukin-6/metabolism ; Ion Channels/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Uncoupling Protein 1
Chemical Substances	Catecholamines ; Interleukin-6 ; Ion Channels ; Mitochondrial Proteins ; UCP1 protein, human ; Ucp1 protein, mouse ; Uncoupling Protein 1
Language	English
Publishing date	2015-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2015.10.028
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Article ; Online: Pathophysiologic Response to Burns in the Elderly.

Jeschke, Marc G / Patsouris, David / Stanojcic, Mile / Abdullahi, Abdikarim / Rehou, Sarah / Pinto, Ruxandra / Chen, Peter / Burnett, Marjorie / Amini-Nik, Saeid

EBioMedicine

2015 Volume 2, Issue 10, Page(s) 1536–1548

Abstract: Over the last decades advancements have improved survival and outcomes of severely burned patients except one population, elderly. The Lethal Dose 50 (LD50) burn size in elderly has remained the same over the past three decades, and so has morbidity and ... ...

Abstract	Over the last decades advancements have improved survival and outcomes of severely burned patients except one population, elderly. The Lethal Dose 50 (LD50) burn size in elderly has remained the same over the past three decades, and so has morbidity and mortality, despite the increased demand for elderly burn care. The objective of this study is to gain insights on why elderly burn patients have had such a poor outcome when compared to adult burn patients. The significance of this project is that to this date, burn care providers recognize the extreme poor outcome of elderly, but the reason remains unclear. In this prospective translational trial, we have determined clinical, metabolic, inflammatory, immune, and skin healing aspects. We found that elderly have a profound increased mortality, more premorbid conditions, and stay at the hospital for longer, p < 0.05. Interestingly, we could not find a higher incidence of infection or sepsis in elderly, p > 0.05, but a significant increased incidence of multi organ failure, p < 0.05. These clinical outcomes were associated with a delayed hypermetabolic response, increased hyperglycemic and hyperlipidemic responses, inversed inflammatory response, immune-compromisation and substantial delay in wound healing predominantly due to alteration in characteristics of progenitor cells, p < 0.05. In summary, elderly have substantially different responses to burns when compared to adults associated with increased morbidity and mortality. This study indicates that these responses are complex and not linear, requiring a multi-modal approach to improve the outcome of severely burned elderly.
MeSH term(s)	Aged ; Aged, 80 and over ; Biomarkers ; Blood Glucose ; Burns/diagnosis ; Burns/epidemiology ; Burns/etiology ; Burns/metabolism ; Cohort Studies ; Comorbidity ; Cytokines/metabolism ; Dermis/metabolism ; Dermis/pathology ; Energy Metabolism ; Epidermis/metabolism ; Epidermis/pathology ; Female ; Humans ; Inflammasomes/metabolism ; Inflammation Mediators/metabolism ; Lipid Metabolism ; Male ; Middle Aged ; Mortality ; Severity of Illness Index ; Wound Healing
Chemical Substances	Biomarkers ; Blood Glucose ; Cytokines ; Inflammasomes ; Inflammation Mediators
Language	English
Publishing date	2015-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2015.07.040
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Article ; Online: Endoplasmic reticulum stress in adipose tissue augments lipolysis.

Bogdanovic, Elena / Kraus, Nicole / Patsouris, David / Diao, Li / Wang, Vivian / Abdullahi, Abdikarim / Jeschke, Marc G

Journal of cellular and molecular medicine

2015 Volume 19, Issue 1, Page(s) 82–91

Abstract: The endoplasmic reticulum (ER) is an organelle important for protein synthesis and folding, lipid synthesis and Ca(2+) homoeostasis. Consequently, ER stress or dysfunction affects numerous cellular processes and has been implicated as a contributing ... ...

Abstract	The endoplasmic reticulum (ER) is an organelle important for protein synthesis and folding, lipid synthesis and Ca(2+) homoeostasis. Consequently, ER stress or dysfunction affects numerous cellular processes and has been implicated as a contributing factor in several pathophysiological conditions. Tunicamycin induces ER stress in various cell types in vitro as well as in vivo. In mice, a hallmark of tunicamycin administration is the development of fatty livers within 24-48 hrs accompanied by hepatic ER stress. We hypothesized that tunicamycin would induce ER stress in adipose tissue that would lead to increased lipolysis and subsequently to fatty infiltration of the liver and hepatomegaly. Our results show that intraperitoneal administration of tunicamycin rapidly induced an ER stress response in adipose tissue that correlated with increased circulating free fatty acids (FFAs) and glycerol along with decreased adipose tissue mass and lipid droplet size. Furthermore, we found that in addition to fatty infiltration of the liver as well as hepatomegaly, lipid accumulation was also present in the heart, skeletal muscle and kidney. To corroborate our findings to a clinical setting, we examined adipose tissue from burned patients where increases in lipolysis and the development of fatty livers have been well documented. We found that burned patients displayed significant ER stress within adipose tissue and that ER stress augments lipolysis in cultured human adipocytes. Our results indicate a possible role for ER stress induced lipolysis in adipose tissue as an underlying mechanism contributing to increases in circulating FFAs and fatty infiltration into other organs.
MeSH term(s)	Adipose Tissue/drug effects ; Adipose Tissue/pathology ; Animals ; Burns/pathology ; Burns/surgery ; Cell Separation ; Cells, Cultured ; Endoplasmic Reticulum Stress/drug effects ; Fatty Acids/metabolism ; Hepatocytes/drug effects ; Hepatocytes/pathology ; Humans ; Lipolysis/drug effects ; Male ; Mice, Inbred BALB C ; Organ Specificity/drug effects ; Tunicamycin/pharmacology
Chemical Substances	Fatty Acids ; Tunicamycin (11089-65-9)
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.12384
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