Immune Response in Severe Infection: Could Life‐Saving Drugs Be Potentially Harmful?

Šurbatović, Maja; Jevdjić, Jasna; Veljović, Milić; Popović, Nikola; Djordjević, Dragan; Radaković, Sonja

doi:10.1155/2013/961852

Cited by 13 publications

(15 citation statements)

References 66 publications

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“…An MPO assay was performed in the peritoneal fluid as described elsewhere (2,5,11,12). Briefly, 200 μl of peritoneal fluid was incubated with 800 μl hexadecyltrimethylammoniumbromide (HTAB) buffer and the mixture was transferred into microcentrifuge tube and centrifuged at 20,000 × g for 4 min.…”

Section: Methodsmentioning

confidence: 99%

“…Bacteria in the peritoneum during polymicrobial sepsis interact with pattern recognition receptors (1) resulting in CXCL1 production by hematopoietic and resident cells (2). CXCL1 controls neutrophil recruitment (one arm) and neutrophil function (other arm).…”

Section: Figurementioning

confidence: 99%

“…The pathogenesis of sepsis is characterized by an early, overwhelming systemic pro-inflammatory response that leads to multiple organ damage; the later phases are characterized by anti-inflammatory responses and negative regulation of immune signaling pathways (2). However, the molecular and cellular mechanisms that regulate immune responses to polymicrobial sepsis are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

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CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions

Jin

Batra

Douda

et al. 2014

The Journal of Immunology

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Severe bacterial sepsis leads to a pro-inflammatory condition that can manifest as septic shock, multiple organ failure, and death. Neutrophils are critical for the rapid elimination of bacteria, however, the role of neutrophil chemoattractant CXCL1 in bacterial clearance during sepsis remains elusive. To test the hypothesis that CXCL1 is critical to host defense during sepsis. We used CXCL1-deficient mice and bone marrow chimeras to demonstrate the importance of this molecule in sepsis. We demonstrate that CXCL1 plays a pivotal role in mediating host defense to polymicrobial sepsis following cecal ligation and puncture (CLP) in gene-deficient mice. CXCL1 appears to be essential for restricting bacterial outgrowth and death in mice. CXCL1 derived from both hematopoietic and resident cells contributed to bacterial clearance. Moreover, CXCL1 is essential for neutrophil migration, expression of pro-inflammatory mediators, activation of Nuclear-Factor-κ-B (NF-κB) and Mitogen-Activated Protein (MAP) kinases and upregulation of adhesion molecule Intercellular Adhesion Molecule-1 (ICAM-1). Recombinant interleukin 17 (IL-17) rescued impaired host defenses in cxcl1−/− mice. CXCL1 is important for IL-17A production via Th17 differentiation. CXCL1 is essential for Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase-mediated reactive oxygen species production and neutrophil extracellular trap (NET) formation. This study reveals a novel role for CXCL1 in neutrophil recruitment via modulating T cell function and neutrophil-related bactericidal functions. These studies suggest that modulation of CXCL1 levels in tissues and blood could reduce bacterial burden in sepsis.

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Section: Methodsmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions

Jin

Batra

Douda

et al. 2014

The Journal of Immunology

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“…The upregulated genes in the VAP group identified in the present study were mainly enriched in the GO terms of immune system processes and immune responses, which have been verified to have a pivotal role in the development of VAP ( 24 ). The immune system has a central role in controlling the duration and amplitude of the inflammatory response ( 25 ). A previous study on sepsis revealed that the innate and adaptive immune response is considerably different between patients with VAP and those without this type of nosocomial infection ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Gene expression profile analysis of ventilator-associated pneumonia

Yuan

Liang

et al. 2015

Molecular Medicine Reports

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Based on the gene expression profile of patients with ventilator-associated pneumonia (VAP) and patients not affected by the disease, the present study aimed to enhance the current understanding of VAP development using bioinformatics methods. The expression profile GSE30385 was downloaded from the Gene Expression Omnibus database. The Linear Models for Microarray Data package in R language was used to screen and identify differentially expressed genes (DEGs), which were grouped as up- and down-regulated genes. The up- and downregulated genes were functionally enriched using the Database for Annotation, Visualization and Integrated Discovery system and then annotated according to TRANSFAC, Tumor Suppressor Gene and Tumor Associated Gene databases. Subsequently, the protein-protein interaction (PPI) network was constructed, followed by module analysis using CFinder software. A total of 69 DEGs, including 33 up- and 36 downregulated genes were screened out in patients with VAP. Upregulated genes were mainly enriched in functions and pathways associated with the immune response (including the genes ELANE and LTF) and the mitogen-activated protein kinase (MAPK) signaling pathway (including MAPK14). The PPI network comprised 64 PPI pairs and 44 nodes. The top two modules were enriched in different pathways, including the MAPK signaling pathway. Genes including ELANE, LTF and MAPK14 may have important roles in the development of VAP via altering the immune response and the MAPK signaling pathway.

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“…Sepsis, as a systematic inflammatory response to infection, compromises a number of very complex pathophysiological processes: diffuse endothelial and epithelial injury, increased capillary permeability, impaired hemodynamics, microvascular thrombosis, tissue ischemia, apoptosis and can result in multiple organ dysfunction [1][2][3][4] . It is one of the most frequent reasons for intensive care hospitalization.…”

Section: Introductionmentioning

confidence: 99%

Beta-lactam antibiotics use in intensive care units - the pathophysiological, pharmacokinetic, pharmacodynamic and pharmacoeconomic approach

et al. 2015

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Immune Response in Severe Infection: Could Life‐Saving Drugs Be Potentially Harmful?

Cited by 13 publications

References 66 publications

CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions

CXCL1 Contributes to Host Defense in Polymicrobial Sepsis via Modulating T Cell and Neutrophil Functions

Gene expression profile analysis of ventilator-associated pneumonia

Beta-lactam antibiotics use in intensive care units - the pathophysiological, pharmacokinetic, pharmacodynamic and pharmacoeconomic approach

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