Cronobacter sakazakii Infection in Early Postnatal Rats Impaired Contextual-Associated Learning: a Putative Role of C5a-Mediated NF-κβ and ASK1 Pathways

Vinay, Ponnusamy; Karen, Christopher; Balamurugan, Krishnaswamy; Rajan, Koilmani Emmanuvel

doi:10.1007/s12031-020-01622-8

Cited by 6 publications

(10 citation statements)

References 81 publications

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“…Complement C5a levels in cerebrovascular ECs, microglia, and deep neurons increase during sepsis [55]. C5a as a regulatory site influences cronobacter sakazakii related contextual-associated learning through NF-κβ and ASK1 pathways [54]. And the C5a neutralizing antibodies or inhibition of its receptor reduces organ dysfunction and BBB damage [56][57][58].…”

Section: The Complement Systemmentioning

confidence: 99%

“…In the brain, microvascular ECs, microglia, astrocyte, and even neuron are the source of complement proteins under certain conditions [ 51 , 52 ]. Complement activation is a very important factor during sepsis-induced brain dysfunction and may be a potential therapeutic target [ 53 , 54 ]. Complement C5a levels in cerebrovascular ECs, microglia, and deep neurons increase during sepsis [ 55 ].…”

Section: Pathogenesismentioning

confidence: 99%

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Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Pan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Dysregulated host response to infection, which cause life-threatening organ dysfunction, was defined as sepsis. Sepsis can cause acute and long-term brain dysfunction, namely, sepsis-associated encephalopathy (SAE) and cognitive impairment. SAE refers to changes in consciousness without direct evidence of central nervous system infection. It is highly prevalent and may cause poor outcomes in sepsis patients. Cognitive impairment seriously affects the life quality of sepsis patients and increases the medical burden. The pathogenesis of sepsis-induced brain dysfunction is mainly characterized by the interaction of systemic inflammation, blood-brain barrier (BBB) dysfunction, neuroinflammation, microcirculation dysfunction, and brain dysfunction. Currently, the diagnosis of sepsis-induced brain dysfunction is based on clinical manifestation of altered consciousness along with neuropathological examination, and the treatment is mainly involves controlling sepsis. Although treatments for sepsis-induced brain dysfunction have been tested in animals, clinical treat sepsis-induced brain dysfunction is still difficult. Therefore, we review the underlying mechanisms of sepsis-induced brain injury, which mainly focus on the influence of systemic inflammation on BBB, neuroinflammation, brain microcirculation, and the brain function, which want to bring new mechanism-based directions for future basic and clinical research aimed at preventing or ameliorating brain dysfunction.

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Section: The Complement Systemmentioning

confidence: 99%

Section: Pathogenesismentioning

confidence: 99%

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Pan

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Since the pathogenesis of C. sakazakii resulted in several diseases in relation with memory, inflammation on the brain, etc., this study aimed to analyze the impact of C. sakazakii infection on neurotransmission of C.…”

Section: Introductionmentioning

confidence: 99%

“…7 Also in rats, C. sakazakii infection altered the fear memory through serotonin transporters. 8,9 Furthermore, it was reported that the host, C. elegans improved its pathogen recognition system through specific changes associated at the innate immune players such as clec-60, clec-87, lys-7, and ilys-3 against C. sakazakii infection. 10 The intestinally colonized pathogen may also involve in the progression of damages to the nervous system.…”

Section: ■ Introductionmentioning

confidence: 99%

“…10 The intestinally colonized pathogen may also involve in the progression of damages to the nervous system. Since the pathogenesis of C. sakazakii resulted in several diseases in relation with memory, inflammation on the brain, etc., 9 this study aimed to analyze the impact of C. sakazakii infection on neurotransmission of C. elegans. Multiple neurotransmitters generated by the host system utilizing its resources participate in the central nervous system and function together for the cell−cell communication and regulatory mechanisms.…”

Section: ■ Introductionmentioning

confidence: 99%

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Physiological and Metabolite Alterations Associated with Neuronal Signals of Caenorhabditis elegans during Cronobacter sakazakii Infections

Muthubharathi

Balasubramaniam

Mir

et al. 2021

ACS Chem. Neurosci.

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Metabolomic reprogramming plays a crucial role in the activation of several regulatory mechanisms including neuronal responses of the host. In the present study, alterations at physiological and biochemical levels were initially assessed to monitor the impact of the candidate pathogen Cronobacter sakazakii on the nematode host Caenorhabditis elegans. The abnormal behavioral responses were observed in infected worms in terms of hyperosmolarity and high viscous chemicals. The microscopic observations indicated reduction in egg laying and internal hatching of larvae in the host. An increased level of total reactive oxygen species and reduction in antioxidant agents such as glutathione and catalase were observed. These observations suggested the severe effect of C. sakazakii infection on C. elegans. To understand the small molecules which likely mediated neurotransmission, the whole metabolome of C. elegans during the infection of C. sakazakii was analyzed using liquid chromatography−mass spectrometry. A decrease in the quantity of methyl dopamine and palmitoyl dopamine and an increase in hydroxyl dopamine suggested that reduction in dopamine reuptake and dopamine neuronal stress. The disordered dopaminergic transmission during infection was confirmed using transgenic C. elegans by microscopic observation of Dat-1 protein expression. In addition, reduction in arachidonic acid and short-chain fatty acids revealed their effect on lipid droplet formation as well as neuronal damage. An increase in the quantity of stearoyl CoA underpinned the higher accumulation of lipid droplets in the host. On the other hand, an increased level of metabolites such as palmitoyl serotonin, citalopram N-oxide, and N-acyl palmitoyl serotonin revealed serotonin-mediated potential response for neuroprotection, cytotoxicity, and cellular damage. Based on the metabolomic data, the genes correspond to small molecules involved in biosynthesis and transportation of candidate neurotransmitters were validated through relative gene expression.

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Antibiotic treatment during post-natal reverses behavioural and molecular alterations in experimental meningitis survivor rat model

Kamaladevi

Rajan

2023

Neurotoxicology and Teratology

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Cronobacter sakazakii Infection in Early Postnatal Rats Impaired Contextual-Associated Learning: a Putative Role of C5a-Mediated NF-κβ and ASK1 Pathways

Cited by 6 publications

References 81 publications

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment

Physiological and Metabolite Alterations Associated with Neuronal Signals of Caenorhabditis elegans during Cronobacter sakazakii Infections

Antibiotic treatment during post-natal reverses behavioural and molecular alterations in experimental meningitis survivor rat model

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