Mitochondrial Membrane Potential and Apoptosis Peripheral Blood Monocytes in Severe Human Sepsis

Adrie, Christophe; Bachelet, Maria; Vayssier‐Taussat, Muriel; Russo‐Marie, Françoise; Bouchaert, Isabelle; Adib‐Conquy, Minou; Cavaillon, Jean‐Marc; Pinsky, Michael R.; Dhainaut, Jean-François; Polla, Barbara S.

doi:10.1164/ajrccm.164.3.2009088

Cited by 194 publications

(131 citation statements)

References 49 publications

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“…Pioneering autopsy studies by Hotchkiss and colleagues (80,139,140) disclosed a profound, progressive, apoptosis-induced loss of cells of the adaptive immune system in the spleen, blood, and (146). Furthermore, among septic patients, this percentage was significantly higher in nonsurvivors than survivors.…”

Section: Monitoring Of Apoptosismentioning

confidence: 99%

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

Monneret

Venet

Pachot

et al. 2008

Mol Med

306

323

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Section: Monitoring Of Apoptosismentioning

confidence: 99%

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

Monneret

Venet

Pachot

et al. 2008

Mol Med

306

323

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“…34) DY m was determined by the ratio-metric analysis of orange fluorescence emitted by JC1 aggregates (FL2) and that emitted by the free probe (FL1).…”

Section: Animals Modelmentioning

confidence: 99%

Effects of Chitooligosaccharide Lactate Salt on Sleep Deprivation-Induced Fatigue in Mice

Cho

Lee

Song

et al. 2010

Biological & Pharmaceutical Bulletin

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Fatigue is defined as difficulty in initiating or sustaining voluntary activity.1) Despite the prevalence of fatigue in developed countries, the pathophysiology and etiology of fatigue are unknown. Several underlying mechanisms of chronic fatigue syndrome (CFS) have been suggested: for example, allergic and psychological factors, 2) heavy exercise, viral infection, 3) muscle damage, 4,5) CNS disorders and immunological factors.6) Recent studies have demonstrated that energy metabolism is involved in the pathophysiology of fatigue. 7) At the biochemical level, fatigue is represented as the depletion of metabolic energy available to the cells that perform a myriad of functions vital to the survival of an organism.7) Metabolic energy is generated in the form of ATP through oxidative metabolism in the mitochondria. During energy generation, however, reactive oxygen species (ROS) are produced which have the potential to cause mitochondrial damage. The accumulation of mitochondrial dysfunction induced by ROS is proposed as "the mitochondrial theory of aging." 8) In addition, in CFS, impairment of mitochondrial function is frequently observed as represented by reduced oxidative metabolism, 9) increased anaerobic metabolism and subsequently increased lactate production.10,11) Mitochondrial abnormalities and degeneration are also frequently found in patients with CFS,12) reflecting the crucial role of mitochondria in the development of fatigue syndrome. In line with this, a wide variety of natural health products are used or are being developed to replenish the production of cellular energy in the mitochondria. 13)Chitooligosaccharides (COS) is an oligosaccharide made from chitin or chitosan by chemical or enzymatic decomposition.14,15) COS has attracted huge attention as a new biomedical material owing to its water-soluble character and versa- COS is also used as a health food for the treatment of fatigue. It has been suggested that the anti-fatigue effect of COS is related to its improvement of peripheral circulation, anti-oxidation, immunomodulation and nutritional effects. However, the exact mechanism underlying the anti-fatigue effect of COS remains to be elucidated. Sleep disturbance causes excessive energy consumption which leads to daytime fatigue and mental enervation. 26,27) Sleep deprivation increases the levels of the stress hormone cortisol, 28) and elevated cortisol levels induce the development of depression. 29) Researchers from the Karolinska Institute recently reported that decreased production of ATP in mitochondria may aggravate depressive disorders through the induction of high levels of somatization (physical symptoms). 30)In this study, we investigated the effect of COS in a sleep deprivation-induced fatigue model 31) in an effort to explore the utility of COS as a novel functional food with anti-fatigue effects, and examined its efficacy in terms of mitochondrial function and antioxidant activities. We discovered that COS lactate markedly decreased the severity of fatigue, as demonstrated by the d...

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“…It has been proposed that apoptosis is a significant event mediating the phagocytic and inflammatory behaviors of monocytes during sepsis (27). Thus, the lifespan of monocytes dictates the duration during which microorganisms are ingested and proinflammatory factors are released.…”

Section: Effect Of Activated Protein C On Camptothecin-induced Thp-1 mentioning

confidence: 99%

“…This observation is intriguing since it is unclear if prolonged monocyte survival is beneficial or detrimental to the host during sepsis. One perspective is that although monocytes mediate the immediate host response to invading microorganisms, prolonged release of proinflammatory mediators by monocytes may lead to persistence of tissue injury (27). In other words, the monocyte response may be a dual-edged sword: monocytes phagocytose invading pathogens but also produce various inflammatory cytokines, chemokines, and growth factors that can amplify the inflammatory response.…”

mentioning

confidence: 99%

Modulation of Monocyte Function by Activated Protein C, a Natural Anticoagulant

Stephenson¹,

Toltl²,

Beaudin

et al. 2006

The Journal of Immunology

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Activated protein C is the first effective biological therapy for the treatment of severe sepsis. Although activated protein C is well established as a physiological anticoagulant, emerging data suggest that it also exerts anti-inflammatory and antiapoptotic effects. In this study, we investigated the ability of activated protein C to modulate monocyte apoptosis, inflammation, phagocytosis, and adhesion. Using the immortalized human monocytic cell line THP-1, we demonstrated that activated protein C inhibited camptothecin-induced apoptosis in a dose-dependent manner. The antiapoptotic effect of activated protein C requires its serine protease domain and is dependent on the endothelial cell protein C receptor and protease-activated receptor-1. In primary blood monocytes from healthy individuals, activated protein C inhibited spontaneous apoptosis. With respect to inflammation, activated protein C inhibited the production of TNF, IL-1β, IL-6, and IL-8 by LPS-stimulated THP-1 cells. Activated protein C did not influence the phagocytic internalization of Gram-negative and Gram-positive bioparticles by THP-1 cells or by primary blood monocytes. Activated protein C also did not affect the expression of adhesion molecules by LPS-stimulated blood monocytes nor the ability of monocytes to adhere to LPS-stimulated endothelial cells. We hypothesize that the protective effect of activated protein C in sepsis reflects, in part, its ability to prolong monocyte survival in a manner that selectively inhibits inflammatory cytokine production while maintaining phagocytosis and adherence capabilities, thereby promoting antimicrobial properties while limiting tissue damage.

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Mitochondrial Membrane Potential and Apoptosis Peripheral Blood Monocytes in Severe Human Sepsis

Abstract: mitochondria; apoptosis; sepsis; heat-shock protein 70; proto-oncogene protein c-Bcl-2

Cited by 194 publications

References 49 publications

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

Effects of Chitooligosaccharide Lactate Salt on Sleep Deprivation-Induced Fatigue in Mice

Modulation of Monocyte Function by Activated Protein C, a Natural Anticoagulant

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