Bacterial lipopolysaccharide-induced systemic inflammation alters perfusion of white matter-rich regions without altering flow in brain-irrigating arteries: Relationship to blood-brain barrier breakdown?

Dhaya, Ibtihel; Griton, Marion; Raffard, Gérard; Amri, Mohamed; Hiba, Bassem; Konsman, Jan Pieter

doi:10.1016/j.jneuroim.2017.11.009

Cited by 12 publications

(6 citation statements)

References 64 publications

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“…In normal circumstances, only a small number of inflammatory factors such as TNF-α, IL-1, and IL-6, from the systemic circulation may pass through the BBB to enter the brain ( Tauber et al, 2017 ). However, the disruption of BBB will make a wide range of inflammatory cytokines, neurotoxins, complement as well as pathogens to enter the brain tissue when systemic inflammation occurs ( Dhaya et al, 2018 ; Nwafor et al, 2019 ; Ren et al, 2020 ). Not only that, the NVU that makes up the BBB also mediates partial inflammatory responses, oxidative stress, and other reactions, for example, activating microglia to release NO, cytokines, and ROS, to aggravate BBB dysfunction in turn, so BBB disruption can be not only a cause but also a consequence of SAE ( da Fonseca et al, 2014 ; Danielski et al, 2018 ).…”

Section: Bbb and Saementioning

confidence: 99%

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Peng

Luo

et al. 2021

Front. Cell. Infect. Microbiol.

131

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As a complex multicellular structure of the vascular system at the central nervous system (CNS), the blood-brain barrier (BBB) separates the CNS from the system circulation and regulates the influx and efflux of substances to maintain the steady-state environment of the CNS. Lipopolysaccharide (LPS), the cell wall component of Gram-negative bacteria, can damage the barrier function of BBB and further promote the occurrence and development of sepsis-associated encephalopathy (SAE). Here, we conduct a literature review of the direct and indirect damage mechanisms of LPS to BBB and the relationship between these processes and SAE. We believe that after LPS destroys BBB, a large number of inflammatory factors and neurotoxins will enter and damage the brain tissue, which will activate brain immune cells to mediate inflammatory response and in turn further destroys BBB. This vicious circle will ultimately lead to the progression of SAE. Finally, we present a succinct overview of the treatment of SAE by restoring the BBB barrier function and summarize novel opportunities in controlling the progression of SAE by targeting the BBB.

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Section: Bbb and Saementioning

confidence: 99%

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Peng

Luo

et al. 2021

Front. Cell. Infect. Microbiol.

131

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“…This could be besides the fact that systemic inflammation and ischemic events tends to disrupt the blood–brain barrier. 38 – 41…”

Section: Discussionmentioning

confidence: 99%

Biomarker Profiling of Neurovascular Diseases in Patients with Stage 5 Chronic Kidney Disease

Lee

Bontekoe

Trac

et al. 2018

Clin Appl Thromb Hemost

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Patients with stage 5 chronic kidney disease (CKD5D) have a higher risk of developing neurocognitive deficits. Stroke, cervical carotid artery disease (CCAD), and intracranial atherosclerotic disease (ICAD) are causes of such deficits in CKD5D. Chronic inflammation from renal failure elevates risk for these diseases through oxidative stress and vascular dysfunction. The adverse impact on the carotid and intracranial vasculatures contributes to the multifactorial pathophysiology of stroke. Eleven plasma biomarker levels in patients with CKD5D (n = 97) and healthy controls (n = 17-50) were measured using sandwich enzyme-linked immunosorbent assay (ELISA) method. Of the 97 patients with CKD5D, 24 had CCAD, 19 had ICAD, and 23 had acute stroke. Elevations in NACHT, LRR, and PYD domains-containing protein 3 (NALP3) levels in patients with CKD5D (+)CCAD (1.80 ± 0.11 ng/mL) compared to patients with (−)CCAD (1.55 ± 0.08 ng/mL) were statistically significant ( P = .0299). Differences in D-dimer levels were also found to be statistically significant ( P = .0258) between CKD5D (+)stroke (1.83 ± 0.42 μg/mL) and (−)stroke (0.89 ± 0.13 μg/mL) groups. The ages of the (+) neurovascular disease groups were found to be significantly elevated compared to the (−) neurovascular disease groups ( P = .0002 carotid AD; P < .0001 ICAD; P = .0157 stroke). D-dimer levels were positively correlated with age in CKD5D ( P = .0375). With the possible exception of NALP3 for CCAD, profiling levels of specific biomarkers for risk stratification of neurovascular diseases in the CKD5D population warrants further investigation.

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“…Brain tissue preparation, immunohistochemistry, and image acquisition and analysis were performed as previously described. 13 , 14 , 15 Commercially available antisera raised against COX‐2 (goat anti‐COX‐2; M‐19 sc‐1747, lot# F2512, Santa Cruz Biotechnology, Heidelberg, Germany) diluted 1:750, the microglia‐macrophage‐specific ionized calcium‐binding adaptor molecule (Iba‐1; rabbit anti‐Iba‐1; 019‐19741, Wako Chemicals GmbH, Neuss, Germany) diluted 1:1000 and rat immunoglobulin G (IgG; biotinylated goat anti IgG, BA‐9401, Vector Laboratories, Burlingame, CA, USA) diluted 1:2000 and the intermediate filament glial fibrillary acidic protein GFAP (mouse anti‐GFAP mAb, clone GA5, MAB360, Merck Millipore, Fontenay sous Bois, France) diluted 1:500 were used.…”

Section: Methodsmentioning

confidence: 99%

“…Based on its overall well‐known profile of effects compared to other anesthetics, our previous work employed isoflurane anesthesia to assess with MRI cerebral blood flow and perfusion as well as water diffusion in experimental models of bacterial sepsis‐associated neurological dysfunction. 13 , 14 , 15 For the sepsis model consisting of the peripheral administration of bacterial lipopolysaccharide (LPS), it has been shown, among different anesthetics tested, that the early LPS‐induced changes in hemodynamics under isoflurane anesthesia were closest to those observed in awake rats. 16 But isoflurane anesthesia does reduce LPS‐induced systemic as well as brain cell production of the pro‐inflammatory cytokine interleukin‐1β 17 , 18 , 19 , 20 and increases survival.…”

Section: Introdutionmentioning

confidence: 99%

Magnetic resonance imaging under isoflurane anesthesia alters cortical cyclooxygenase‐2 expression and glial cell morphology during sepsis‐associated neurological dysfunction in rats

Dhaya

Griton

Konsman

2021

Anim Models and Exp Med

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Bacterial lipopolysaccharide-induced systemic inflammation alters perfusion of white matter-rich regions without altering flow in brain-irrigating arteries: Relationship to blood-brain barrier breakdown?

Cited by 12 publications

References 64 publications

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Blood-Brain Barrier Disruption by Lipopolysaccharide and Sepsis-Associated Encephalopathy

Biomarker Profiling of Neurovascular Diseases in Patients with Stage 5 Chronic Kidney Disease

Magnetic resonance imaging under isoflurane anesthesia alters cortical cyclooxygenase‐2 expression and glial cell morphology during sepsis‐associated neurological dysfunction in rats

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