All-trans retinoic acid (ATRA) prevents lipopolysaccharide-induced neuroinflammation, amyloidogenesis and memory impairment in aged rats

Behairi, Nassima; Belkhelfa, Mourad; Rafa, Hayet; Labsi, Moussa; Deghbar, Nahla; Bouzid, Nora; Mesbah-Amroun, Hamida; Touil-Boukoffa, Chafia

doi:10.1016/j.jneuroim.2016.10.004

Cited by 47 publications

(15 citation statements)

References 57 publications

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“…Peripheral stimulation with LPS induced an increase in IL-1β and IL-6 mRNAs, followed by changes in the expression of APP isoforms in the cerebellum [51]. LPS administration for 7 days increased Aβ 1–42 cerebral expression and triggered AD-like neuronal degeneration [56]. On the other hand, chronic LPS administration increased by about twofold the number of Aβ and APP immunoreactive neurons in the neocortex of APPswe mice [28].…”

Section: Lps-induced Inflammation In Models Of Alzheimer’s Diseasementioning

confidence: 99%

Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration

Batista

Gomes

Candelario‐Jalil

et al. 2019

IJMS

356

233

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A large body of experimental evidence suggests that neuroinflammation is a key pathological event triggering and perpetuating the neurodegenerative process associated with many neurological diseases. Therefore, different stimuli, such as lipopolysaccharide (LPS), are used to model neuroinflammation associated with neurodegeneration. By acting at its receptors, LPS activates various intracellular molecules, which alter the expression of a plethora of inflammatory mediators. These factors, in turn, initiate or contribute to the development of neurodegenerative processes. Therefore, LPS is an important tool for the study of neuroinflammation associated with neurodegenerative diseases. However, the serotype, route of administration, and number of injections of this toxin induce varied pathological responses. Thus, here, we review the use of LPS in various models of neurodegeneration as well as discuss the neuroinflammatory mechanisms induced by this toxin that could underpin the pathological events linked to the neurodegenerative process.

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Section: Lps-induced Inflammation In Models Of Alzheimer’s Diseasementioning

confidence: 99%

Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration

Batista

Gomes

Candelario‐Jalil

et al. 2019

IJMS

356

233

View full text Add to dashboard Cite

show abstract

“…atRA administration prevents LPS-induced neuroinflammation, NO production, amyloidogenesis, and memory impairment in aged rats [ 150 ]. PBMCs from patients with AD in cultures with atRA showed downregulated spontaneous NO production and iNOS expression, which was associated with a reduction in IL-17A production and increased IL-10 release [ 151 ].…”

Section: Immunomodulatory Effect Of Ra During Inflammatory Processmentioning

confidence: 99%

Impact of Retinoic Acid on Immune Cells and Inflammatory Diseases

Oliveira

Teixeira

Sato

2018

Mediators of Inflammation

167

128

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Vitamin A metabolite retinoic acid (RA) plays important roles in cell growth, differentiation, organogenesis, and reproduction and a key role in mucosal immune responses. RA promotes dendritic cells to express CD103 and to produce RA, enhances the differentiation of Foxp3+ inducible regulatory T cells, and induces gut-homing specificity in T cells. Although vitamin A is crucial for maintaining homeostasis at the intestinal barrier and equilibrating immunity and tolerance, including gut dysbiosis, retinoids perform a wide variety of functions in many settings, such as the central nervous system, skin aging, allergic airway diseases, cancer prevention and therapy, and metabolic diseases. The mechanism of RA is interesting to explore as both a mucosal adjuvant and a combination therapy with other effective agents. Here, we review the effect of RA on innate and adaptive immunity with a special emphasis on inflammatory status.

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“…At the same time, both CD and UC are associated with high levels of Th17 cytokines that induce the production of TNF-α, IL-1β, and chemokines [10]. Activation of TNF-α, IL-1β, and TGF-β induces necroptosis, whereas neuroinflammation is involved in amyloidogenesis, memory impairment, and multiple sclerosis [11][12][13]. Therefore, DSS-induced colitis serves as a great model to study complex interactions between microbes and the host in a state of inflammation, as well as provides a platform to test molecules capable of modulating microbiome-to-host crosstalk.…”

Section: Introductionmentioning

confidence: 99%

Fucose Ameliorates Tryptophan Metabolism and Behavioral Abnormalities in a Mouse Model of Chronic Colitis

et al. 2020

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Growing evidence suggests that intestinal mucosa homeostasis impacts immunity, metabolism, the Central Nervous System (CNS), and behavior. Here, we investigated the effect of the monosaccharide fucose on inflammation, metabolism, intestinal microbiota, and social behavior in the Dextran Sulfate Sodium (DSS)-induced chronic colitis mouse model. Our data show that chronic colitis is accompanied by the decrease of the serum tryptophan level and the depletion of the intestinal microbiota, specifically tryptophan-producing E. coli and Bifidobacterium. These changes are associated with defects in the male mouse social behavior such as a lack of preference towards female bedding in an odor preference test. The addition of fucose to the test animals' diet altered the bacterial community, increased the abundance of tryptophan-producing E. coli, normalized blood tryptophan levels, and ameliorated social behavior deficits. At the same time, we observed no ameliorating effect of fucose on colon morphology and colitis. Our results suggest a possible mechanism by which intestinal inflammation affects social behavior in male mice. We propose fucose as a promising prebiotic, since it creates a favorable environment for the beneficial bacteria that promote normalization of serum tryptophan level and amelioration of the behavioral abnormalities in the odor preference test.

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All-trans retinoic acid (ATRA) prevents lipopolysaccharide-induced neuroinflammation, amyloidogenesis and memory impairment in aged rats

Cited by 47 publications

References 57 publications

Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration

Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration

Impact of Retinoic Acid on Immune Cells and Inflammatory Diseases

Fucose Ameliorates Tryptophan Metabolism and Behavioral Abnormalities in a Mouse Model of Chronic Colitis

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