Postnatal exposure to lipopolysaccharide combined with high-fat diet consumption induces immune tolerance without prevention in spatial working memory impairment

Vargas‐Rodríguez, Isaac; Reyes-Castro, Luis A.; Pacheco-López, Gustavo; Lomas-Soria, Consuelo; Zambrano, Elena; Dı́az-Ruiz, Araceli; Dı́az-Cintra, Sofı́a

doi:10.1016/j.bbr.2022.113776

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…Hypothalamus damage often causes cognitive and memory impairments in patients ( Poretti et al, 2004 ; Fjalldal et al, 2013 ). To mimic this clinical phenomenon, many studies have examined the connection between obesity and cognitive impairment, but these obesity models mainly utilized HFD and transgenic methods ( Poon, 2020 ; Vargas-Rodríguez et al, 2022 ); few focused on the hypothalamic injury like the ARC/VMH-lesioned models. So there was little discussion on the potential contribution of the ARC and the VMH themselves to cognitive dysfunction, and the underlying mechanism is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Microglial infiltration mediates cognitive dysfunction in rat models of hypothalamic obesity via a hypothalamic-hippocampal circuit involving the lateral hypothalamic area

Wei

Wang

Zhou

et al. 2022

Front. Cell. Neurosci.

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This study aimed to explore the mechanism underlying cognitive dysfunction mediated by the lateral hypothalamic area (LHA) in a hypothalamic-hippocampal circuit in rats with lesion-induced hypothalamic obesity (HO). The HO model was established by electrically lesioning the hypothalamic nuclei. The open field (OP) test, Morris water maze (MWM), novel object recognition (NOR), and novel object location memory (NLM) tests were used to evaluate changes in cognition due to alterations in the hypothalamic-hippocampal circuit. Western blotting, immunohistochemical staining, and cholera toxin subunit B conjugated with Alexa Fluor 488 (CTB488) reverse tracer technology were used to determine synaptophysin (SYN), postsynaptic density protein 95 (PSD95), ionized calcium binding adaptor molecule 1 (Iba1), neuronal nuclear protein (NeuN), and Caspase3 expression levels and the hypothalamic-hippocampal circuit. In HO rats, severe obesity was associated with cognitive dysfunction after the lesion of the hypothalamus. Furthermore, neuronal apoptosis and activated microglia in the downstream of the lesion area (the LHA) induced microglial infiltration into the intact hippocampus via the LHA-hippocampal circuit, and the synapses engulfment in the hippocampus may be the underlying mechanism by which the remodeled microglial mediates memory impairments in HO rats. The HO rats exhibited microglial infiltration and synapse loss into the hippocampus from the lesioned LHA via the hypothalamic-hippocampal circuit. The underlying mechanisms of memory function may be related to the circuit.

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Section: Discussionmentioning

confidence: 99%

Microglial infiltration mediates cognitive dysfunction in rat models of hypothalamic obesity via a hypothalamic-hippocampal circuit involving the lateral hypothalamic area

Wei

Wang

Zhou

et al. 2022

Front. Cell. Neurosci.

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“…Modern foods not only provide the body with nutrients and satisfy hunger, but also improve physical and mental well-being and prevent nutrition-related diseases [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ]. If consumed regularly, antioxidants improve human health and life quality, inhibit aging, and prevent cancer, cardiovascular diseases, neurological disorders, etc.…”

Section: Introductionmentioning

confidence: 99%

Effect of Lactobacteria on Bioactive Peptides and Their Sequence Identification in Mature Cheese

et al. 2022

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An in silico study that featured the effect of starter cultures on the bioactivity and other health benefits of peptides in semi-hard cheese is presented in this contribution. Model Caciotta-type cheese samples were obtained in laboratory conditions in two variations. Sample A included starter cultures of Lactococcus lactis subsp. lactis and Lactococcus lactis subsp. cremoris. Sample B included starter cultures of Lactococcus lactis subsp. lactis, Lactococcus lactis subsp. cremoris, and a culture of lactobacilli Lacticaseibacillus casei. The in silico method showed that the peptides inhibited angiotensin-converting enzymes (ACE) and ipeptidyl peptidase IV (DPP-4), as well as possessed antioxidant properties. Lactococcus lactis subsp. lactis and Lactococcus lactis subsp. cremoris had a greater effect on the formation of bioactive peptides.

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“…As a consequence, consecutive LPS treatment caused long-term changes in the microglia that months later were sufficient to alter the development of pathology in an experimental mouse model of stroke (focal cortical ischemia) and impede the subsequent development of neuropathology in a spontaneous transgenic mouse model of Alzheimer’s disease-like pathology ( Wendeln et al, 2018 ). Other studies have shown how similar systemic stimuli ( Zhou et al, 2020 ), a high-fat diet ( Vargas-Rodríguez et al, 2022 ), and early life thermal stress ( Ben-Nun et al, 2022 ) can cause long-term changes in microglial responses that can impede their responses to subsequent pro-inflammatory stimuli. The immune tolerance induced in the microglia to these repeated stimuli may be a neuroprotective response to protect the CNS from repetitive or subsequent pro-inflammatory insults ( Lajqi et al, 2020 ; Zhou et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Innate Immune Tolerance in Microglia Does Not Impact on Central Nervous System Prion Disease

Pal

Bradford²,

Mabbott³

2022

Front. Cell. Neurosci.

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Prion diseases such as Creutzfeldt-Jakob disease in humans, bovine spongiform encephalopathy in cattle, and scrapie in sheep, are infectious and chronic neurodegenerative diseases to which there are no cures. Infection with prions in the central nervous system (CNS) ultimately causes extensive neurodegeneration, and this is accompanied by prominent microglial and astrocytic activation in affected regions. The microglia are the CNS macrophages and help maintain neuronal homeostasis, clear dead or dying cells and provide defense against pathogens. The microglia also provide neuroprotection during CNS prion disease, but their pro-inflammatory activation may exacerbate the development of the neuropathology. Innate immune tolerance induced by consecutive systemic bacterial lipopolysaccharide (LPS) treatment can induce long-term epigenetic changes in the microglia in the brain that several months later can dampen their responsiveness to subsequent LPS treatment and impede the development of neuritic damage in a transgenic mouse model of Alzheimer’s disease-like pathology. We therefore reasoned that innate immune tolerance in microglia might similarly impede the subsequent development of CNS prion disease. To test this hypothesis groups of mice were first infected with prions by intracerebral injection, and 35 days later given four consecutive systemic injections with LPS to induce innate immune tolerance. Our data show that consecutive systemic LPS treatment did not affect the subsequent development of CNS prion disease. Our data suggests innate immune tolerance in microglia does not influence the subsequent onset of prion disease-induced neuropathology in mice, despite previously published evidence of this effect in an Alzheimer’s disease mouse model.

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Postnatal exposure to lipopolysaccharide combined with high-fat diet consumption induces immune tolerance without prevention in spatial working memory impairment

Cited by 4 publications

References 27 publications

Microglial infiltration mediates cognitive dysfunction in rat models of hypothalamic obesity via a hypothalamic-hippocampal circuit involving the lateral hypothalamic area

Microglial infiltration mediates cognitive dysfunction in rat models of hypothalamic obesity via a hypothalamic-hippocampal circuit involving the lateral hypothalamic area

Effect of Lactobacteria on Bioactive Peptides and Their Sequence Identification in Mature Cheese

Innate Immune Tolerance in Microglia Does Not Impact on Central Nervous System Prion Disease

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