Recent advances in biosensors for diagnosis and detection of sepsis: A comprehensive review

Kumar, Sukriti; Tripathy, Suryasnata; Jyoti, Anupam; Singh, Shiv Govind

doi:10.1016/j.bios.2018.10.034

Cited by 123 publications

(99 citation statements)

References 115 publications

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“…Sepsis, a systemic inflammatory response syndrome (SIRS), is caused by infection, can induce multiple organs dysfunction and even death (Bellomo et al, 2017). According to the 2018 World Health Organization report, more than 30 million people worldwide are diagnosed with sepsis each year (Kumar et al, 2019). The mortality rate of patients with sepsis is more than 10%, but increases to 40% in severe cases, such as septic shock (Assinger et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Enhancing Autophagy Through Inhibition of the PI3K/AKT/mTOR Pathway

et al. 2020

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Background: Acute kidney injury (AKI) is often secondary to sepsis. Previous studies suggest that damaged mitochondria and the inhibition of autophagy results in AKI during sepsis, but dexmedetomidine (DEX) alleviates lipopolysaccharide (LPS)-induced AKI. However, it is uncertain whether the renoprotection of DEX is related to autophagy or the clearance of damaged mitochondria in sepsis-induced AKI. Methods: In this study, AKI was induced in rats by injecting 10 mg/kg of LPS intraperitoneally (i.p.). The rats were also pretreated with DEX (30 mg/kg, i.p.) 30 min before the injection of LPS. The structure and function of kidneys harvested from the rats were evaluated, and the protein levels of autophagy-related proteins, oxidative stress levels, and apoptosis levels were measured. Further, atipamezole (Atip) and 3-Methyladenine (3-MA), which are inhibitors of DEX and autophagy, respectively, were administered before the injection of DEX to examine the protective mechanism of DEX. Results: Pretreatment with DEX ameliorated kidney structure and function. DEX decreased the levels of blood urea nitrogen (BUN) and creatinine (Cre), urine kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), reactive oxygen species (ROS), and apoptosis proteins (such as cleaved caspase-9 and cleaved caspase-3). However, DEX upregulated the levels of autophagy and mitophagy proteins, such as Beclin-1, LC3 II and PINK1. These results suggest that DEX ameliorated LPS-induced AKI by reducing oxidative stress and apoptosis and enhancing autophagy. To promote autophagy, DEX inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Furthermore, the administration of Atip and 3-MA inhibitors blocked the renoprotection effects of DEX. Conclusions: Here, we demonstrate a novel mechanism in which DEX protects against LPS-induced AKI. DEX enhances autophagy, which results in the removal of damaged

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Section: Introductionmentioning

confidence: 99%

Dexmedetomidine Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Enhancing Autophagy Through Inhibition of the PI3K/AKT/mTOR Pathway

et al. 2020

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“…1,2 In 2018, the World Health Organization reported more than 30 million sepsis diagnoses. 3 Sepsis can induce disorders in many organs and can lead to death. 4 Lipopolysaccharide (LPS), the main component of the gramnegative bacteria cell wall, is thought to induce the release of variety of inflammatory cytokines that are considered fundamental components in the basis of sepsis.…”

Section: Introductionmentioning

confidence: 99%

Oleuropein protects against lipopolysaccharide‐induced sepsis and alleviates inflammatory responses in mice

et al. 2020

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Sepsis results from a major systemic inflammatory response and can induce disorders in multiple organs. The present study evaluated the potential protective effects of oleuropein (OLE) against hyperinflammatory responses during lipopolysaccharide (LPS)‐induced sepsis in mice. Sixty male Balb/c mice were randomly categorized into five groups of 12 animals each: control, intraperitoneally injected with OLE (50 mg/kg), injected with LPS (10 mg/kg, intraperitoneal), and two groups administered OLE (25 and 50 mg/kg) for 3 days prior to LPS injection. Twenty‐four hours after lipopolysaccharide injection, the animals were sacrificed. Serum, liver, and kidney tissue samples were collected for biochemical analyses, histopathological examinations, and investigation of inflammation‐related gene expression. OLE pretreatment significantly reduced liver damage parameters (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase) and kidney damage parameters (blood urea nitrogen, creatinine, and kidney injury molecule‐1) in the septic mice. OLE pretreatment ameliorated LPS‐induced liver and kidney histological changes. OLE significantly mitigated the increased levels of malondialdehyde in the liver and kidneys and reduced levels of reduced glutathione induced by LPS. LPS injection also resulted in increased expression of the proinflammatory cytokines (TNF‐α, IL‐1β, and IL‐6) and inflammation‐related genes (Nos2, Hmgb1, Mpo, Cd46, Map2k4, and Map2k7) in the hepatic and renal tissues. OLE reduced these expressions to ameliorate the inflammatory response. Moreover, OLE pretreatment enhanced the survival rate of septic mice. In conclusion, OLE alleviated the inflammatory response to protect against LPS‐induced sepsis in mice.

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“…Thus, biosensors are portable analytical devices equipped with biological elements, potentially capable of controlling biochemical parameters of physiological and pathological processes, which are inaccessible to modern analytical tools [7,29,30]. These are a kind of detectors with their action based on the specific interaction of biomolecules and bioreceptors, used for detecting and measuring minimum concentrations of various analytes [6,29,31,32].…”

Section: Main Types Of Biosensors and Their Functionsmentioning

confidence: 99%

Label-Free Biosensors for Laboratory-Based Diagnostics of Infections: Current Achievements and New Trends

et al. 2020

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Infections pose a serious global public health problem and are a major cause of premature mortality worldwide. One of the most challenging objectives faced by modern medicine is timely and accurate laboratory-based diagnostics of infectious diseases. Being a key factor of timely initiation and success of treatment, it may potentially provide reduction in incidence of a disease, as well as prevent outbreak and spread of dangerous epidemics. The traditional methods of laboratory-based diagnostics of infectious diseases are quite time- and labor-consuming, require expensive equipment and qualified personnel, which restricts their use in case of limited resources. Over the past six decades, diagnostic technologies based on lateral flow immunoassay (LFIA) have been and remain true alternatives to modern laboratory analyzers and have been successfully used to quickly detect molecular ligands in biosubstrates to diagnose many infectious diseases and septic conditions. These devices are considered as simplified formats of modern biosensors. Recent advances in the development of label-free biosensor technologies have made them promising diagnostic tools that combine rapid pathogen indication, simplicity, user-friendliness, operational efficiency, accuracy, and cost effectiveness, with a trend towards creation of portable platforms. These qualities exceed the generally accepted standards of microbiological and immunological diagnostics and open up a broad range of applications of these analytical systems in clinical practice immediately at the site of medical care (point-of-care concept, POC). A great variety of modern nanoarchitectonics of biosensors are based on the use of a broad range of analytical and constructive strategies and identification of various regulatory and functional molecular markers associated with infectious bacterial pathogens. Resolution of the existing biosensing issues will provide rapid development of diagnostic biotechnologies.

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Recent advances in biosensors for diagnosis and detection of sepsis: A comprehensive review

Cited by 123 publications

References 115 publications

Dexmedetomidine Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Enhancing Autophagy Through Inhibition of the PI3K/AKT/mTOR Pathway

Dexmedetomidine Protects Against Lipopolysaccharide-Induced Acute Kidney Injury by Enhancing Autophagy Through Inhibition of the PI3K/AKT/mTOR Pathway

Oleuropein protects against lipopolysaccharide‐induced sepsis and alleviates inflammatory responses in mice

Label-Free Biosensors for Laboratory-Based Diagnostics of Infections: Current Achievements and New Trends

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