Sepsis and septic shock: New definitions, new diagnostic and therapeutic approaches

Esposito, Silvano; Simone, Giuseppe De; Boccia, Giovanni; De, Francesco; Pagliano, Pasquale

doi:10.1016/j.jgar.2017.06.013

Cited by 142 publications

(127 citation statements)

References 69 publications

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“…Recent improvements in the therapeutic approaches to sepsis have significantly decreased the associated rate of mortality at least in high-income countries. However, sepsis remains a leading cause of death worldwide [ 1 , 2 ].…”

Section: Introductionmentioning

confidence: 99%

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Kim

Yeo

et al. 2017

IJMS

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Tussilagone, extracted from Tussilago farfara is an oriental medicine used for asthma and bronchitis. We investigated its mechanism of action, its inhibitory effects on lipopolysaccharide-induced inflammation in macrophages, and its impact on viability in a cecal ligation and puncture (CLP)-induced mouse model of sepsis. Tussilagone suppressed the expression of the inflammatory mediators, nitric oxide and prostaglandin E2, and the inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and high-mobility group box 1 (HMGB1), in lipopolysaccharide-stimulated RAW 264.7 cells and peritoneal macrophages. Tussilagone also reduced the activation of the mitogen-activated protein kinases and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) involved in the activation of various inflammatory mediators in activated macrophages. Moreover, tussilagone administration (1 mg/kg and 10 mg/kg) produced decreased mortality and lung injury in CLP-activated septic mice. Augmented expression of cyclooxygenase (COX)-2 and TNF-α in pulmonary alveolar macrophages of septic mice were attenuated by tussilagone administration. Tussilagone also suppressed the induction of nitric oxide, prostaglandin E2, TNF-α and HMGB1 in the serum of the septic mice. Overall, tussilagone exhibited protective effects against inflammation and polymicrobial sepsis by suppressing inflammatory mediators possibly via the inhibition of NF-κB activation and the MAP kinase pathway. These results suggest the possible use of tussilagone for developing novel therapeutic modalities for sepsis and other inflammatory diseases.

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Section: Introductionmentioning

confidence: 99%

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Kim

Yeo

et al. 2017

IJMS

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“…Septik şoklu hastaların tanımlanması için klinik parametreler şunlardır; ortalama arter basıncının 65 mmHg veya daha fazla olması için vazopressör kullanım gerekliliğinin olması ve hipovolemi olmadan serum laktat seviyesinin 2 mmol/L'den (>18 mg/dL) daha yüksek olmasıdır. 1,3 Sepsis her yıl dünya çapında yaklaşık 18 milyon insanı etkilemekte ve yüksek mortalite ve morbidite oranı taşımaktadır. Dünya çapında ölümlerin dörtte birinden sepsis ve septik şokun sorumlu olduğu bilinmektedir.…”

Section: Acil Serviste Gizli Tehlikeunclassified

“…Bu organ işlev bozukluğu Sepsis ile ilişkili Organ Yetmezliği Değerlendirmesi [Sepsis-Related Organ Failure Assessment (SOFA)] skorunda *2 puan veya daha üstü ile karakterizedir. 1,3,9 Sepsisi tanımlamak için iki veya daha fazla sistemik inflamatuar yanıt sendromu kriteri ve "şiddetli sepsis" tanımının kullanımı bu kılavuzda oy birliğiyle yararsız olarak değerlendirilmiştir. 3 Yeni tanıma ek olarak; kılavuz, yoğun bakım ünitesi dışındaki yerlerde (örneğin; ambulans, acil servisler, dâhiliye ve cerrahi klinikleri) kullanılmak üzere yeni geliştirilen hızlı-SOFA (Quick-Sepsis Related Organ Failure Assesment -qSOFA) aracının kullanımını önermektedir.…”

Section: Acil Serviste Gizli Tehlikeunclassified

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The Hidden Danger in Emergency Department: Sepsis and New Definition

Taş¹,

Özbudak²,

Türeyen³

2019

Turkiye Klinikleri J Nurs Sci

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“…Sepsis is a serious and increasingly common condition that contributes to the morbidity and mortality of many hospitalized patients and, thus, is costly to the healthcare system . Sepsis was most recently defined by the third International Consensus Panel (Sepsis‐3) as a dysregulated host response to infection that leads to life‐threatening organ dysfunction . The increased focus on organ dysfunction is based on the recognition that morbidity and mortality in sepsis are principally due to organ dysfunction, especially MOD .…”

Section: Introductionmentioning

confidence: 99%

Quantification of adherens junction disruption and contiguous paracellular protein leak in human lung endothelial cells under septic conditions

et al. 2019

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Objective Sepsis is associated with dysfunction of MVEC resulting in organ edema and inflammation. VE‐cadherin, a component of MVEC adherens junctions, may be disrupted in sepsis. However, the direct connection between individual MVEC VE‐cadherin disruption and increased paracellular permeability is uncertain. Methods Human pulmonary MVEC were cultured on a biotin matrix and treated with cytomix, as a model of sepsis, vs PBS. MVEC permeability was assessed by trans‐MVEC monolayer leak of Oregon green 488‐conjugated avidin, which bound subcellular biotin to localize sites of paracellular leak. Leak was correlated with individual cell‐specific MVEC surface VE‐cadherin continuity by fluorescence microscopy. Results Cytomix treatment reduced total MVEC VE‐cadherin density, disrupted surface VE‐cadherin continuity, was associated with intercellular gap formation, and enhanced paracellular avidin leak. Cytomix‐induced MVEC paracellular avidin leak was strongly correlated temporally and was highly contiguous with focal MVEC surface VE‐cadherin disruption. Total cellular VE‐cadherin density was less strongly correlated with MVEC paracellular avidin leak and individual cell‐specific focal surface VE‐cadherin discontinuity. Conclusions These data support a mechanistic link between septic human lung MVEC VE‐cadherin disruption and contiguous paracellular protein leak, and will permit more detailed assessment of individual cell‐specific mechanisms of septic MVEC barrier dysfunction.

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Sepsis and septic shock: New definitions, new diagnostic and therapeutic approaches

Cited by 142 publications

References 69 publications

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

Tussilagone Inhibits the Inflammatory Response and Improves Survival in CLP-Induced Septic Mice

The Hidden Danger in Emergency Department: Sepsis and New Definition

Quantification of adherens junction disruption and contiguous paracellular protein leak in human lung endothelial cells under septic conditions

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