Oxidative stress and myeloperoxidase activity during bacterial meningitis: Effects of febrile episodes and the BBB permeability

Mirić, Dijana; Katanić, Radoslav; Kisić, Bojana; Zoric, Lepsa; Miric, B.; Mitic, Radoslav; Dragojević, Ilija

doi:10.1016/j.clinbiochem.2009.09.023

Cited by 25 publications

(25 citation statements)

References 36 publications

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“…Upon activation, polymorphonuclear leukocytes would generate substantial reactive oxygen species (ROS) amounts and release MPO [38]. The MPO released in the extracellular space expresses effective pro-oxidant activity [15,39]. Miric et al [15], found, in serum, that the MPO activity and lipid peroxidation remained elevated in patients with bacterial meningitis throughout the course of the disease.…”

Section: Discussionmentioning

confidence: 97%

“…The MPO released in the extracellular space expresses effective pro-oxidant activity [15,39]. Miric et al [15], found, in serum, that the MPO activity and lipid peroxidation remained elevated in patients with bacterial meningitis throughout the course of the disease. However, other ROS sources are probably endothelial cells and activated microglia [40].…”

Section: Discussionmentioning

confidence: 98%

“…These, in turn, trigger a cascade of inflammatory mediators, including others cytokines and chemokines, matrixmetalloproteinases, myeloperoxidase (MPO) and reactive oxygen species (ROS). Moreover, cytokines themselves may contribute to impairment of the BBB and brain damage [15,16]. Case fatality rates have ranged between 5 and 40% and approximately 25-50% of the survivors can suffer serious long-term neurological consequences, such seizures, deafness, blindness, mental retardation and cognitive impairment [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress, Cytokine/Chemokine and Disruption of Blood–Brain Barrier in Neonate Rats After Meningitis by Streptococcus agalactiae

et al. 2011

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We verify the levels of cytokine/chemokine, myeloperoxidase activity, oxidative stress and disruption of BBB in hippocampus and cortex of the neonate Wistar rats after meningitis by S. agalactiae. In the hippocampus the levels were increased of CINC-1 at 6 h and 12 h, IL-1β at 6, 12 and 24 h, IL-6 at 6, 24 and 96 h, IL-10 at 24, 48 and 96 h and TNF-α at 24 h and 96 h. In the cortex the CINC-1 and IL-1β levels were found increased at 6 h. The MPO activity was significantly elevated at 24, 48 and 98 h in hippocampus and at 6, 12, 24, 48 and 96 h in the cortex. The breakdown of BBB started at 12 h.TBARS levels were elevated in the hippocampus at 6, 12, 24, 48, 72 and 96 h and cortex at 72 and 96 h. Protein carbonyls were elevated in the hippocampus and cortex at 6, 24, 48, 72 and 96 h. There was a decrease of SOD activity in hippocampus and in cortex. Catalase activity was elevated in hippocampus at 6 h and in the cortex at 12 and 96 h. Neonatal bacterial infections of the CNS are severe, the interference with the complex network of cytokines/chemokine, other inflammatory mediators and oxidants tend to aggravate the illness and can be involved in the breakdown of the BBB.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress, Cytokine/Chemokine and Disruption of Blood–Brain Barrier in Neonate Rats After Meningitis by Streptococcus agalactiae

et al. 2011

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“…The blood-brain barrier (BBB) of the CNS is the main system that controls leukocyte trafficking from the periphery into the brain [41,42] or convey the cytokines across the BBB (transporters) [42]. Pro-inflammatory cytokines trigger the expression and activation of other inflammatory factors including other cytokines, chemokines and reactive oxygen species, that leads to necrotic and apoptotic neural injury [49,50]. Of these cytokines, TNF-α in particular is shown to be upregulated in CNS inflammatory conditions that involve BBB disruption [51].…”

Section: Translational Neurosciencementioning

confidence: 99%

Tumour necrosis factor - alpha mediated mechanisms of cognitive dysfunction

Baune

Camara²,

Eyre³

et al. 2012

Translational Neuroscience

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Background: Tumour necrosis factor -alpha (TNF-α) is a pro-inflammatory cytokine that combines a plethora of activities in the early stages of an immune response. TNF-α has gained increasing importance given TNF-α upregulation in multiple brain pathologies like neuropsychiatric conditions such as depression, schizophrenia, as well as neuroinflammatory disorder like multiple sclerosis (MS). Aim: The aim of this review is to critically analyse neurobiological, immunological and molecular mechanisms through which TNF-α influences the development of cognitive dysfunction. Principal findings/results: The review presents several lines of original research showing that the immunological properties of TNF-α exacerbate inflammatory responses in the central nervous system such as microglial and endothelial activation, lymphocytic and monocytic infiltration and the expression of downstream pro-inflammatory cytokines and apoptotic factors. Depression, schizophrenia, and MS all manifest symptoms of activated immune response along with cognitive dysfunction, with TNF-α overexpression as a central clinical feature common to these disorders. Furthermore, TNF-α acts negatively on neuroplasticity and the molecular mechanisms of memory and learning (i.e., long-term potentiation and long-term depression). TNF-α also exerts influence over the production of neurotrophins (i.e., nerve growth factor and brain-derived neurotrophic factor), neurogenesis, and dendritic branching. Conclusions/significance: This review outlines that TNF-α and its receptors have a substantial yet underappreciated influence on the development and progression of neuropsychiatric symptoms across several disease entities. An improved understanding of these underlying mechanisms may help develop novel therapeutic targets in the form of drugs specifically targeting downstream products of TNF-α activation within the central nervous system.

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“…Bakteriyel menenjitli hastalarla kontrol grubunu karşılaş-tıran ve serum oksidan değerlerinin yüksek (10,11,(28)(29)(30)(31)(32)(33), antioksidan değerlerinin düşük (11,28,30,33,34) olduğunu bildiren çalışmalar vardır. Çalışmamızda tedavi öncesi serum TOS ve OSİ değerleri, tedavi sonrasına göre anlamlı derecede yüksek bulunurken, TAS değerleri anlamlı derecede dü-şük bulundu.…”

Section: İrdelemeunclassified

Evaluation of S-100B and Oxidative Status before and after Treatment in Children with Bacterial Meningitis

Abuhandan¹,

Çalık²,

Almaz³

et al. 2013

Klimik Dergisi

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ÖzetAmaç: Bakteriyel menenjitli hastaların tedavi öncesi ve sonrası serum ve beyin-omurilik sıvısı (BOS)'nda total oksidan, total antioksidan ve S-100B değerlerinde olası değişikliklerin araştı-rılması amaçlandı. Yöntemler: Bakteriyel menenjit tanısıyla hastaneye yatırılan 25 hasta çalışmaya dahil edildi. Hastalardan yatışın ilk iki saati için-de ve 10 günlük tedavi sonrası kan ve BOS alındı. Tedavi öncesi ve tedavi sonrası serum ve BOS'ta S-100B, total oksidan ve total antioksidan seviyeleri ölçülerek oksidatif stres indeksi (OSİ) hesaplandı. Bulgular: Tedavi öncesi serum total oksidan ve oksidatif stres indeks değerleri, tedavi sonrasına göre istatistiksel olarak anlamlı derecede yüksek bulunurken, total antioksidan ve S-100B değer-leri anlamlı derecede düşük bulundu. Hastaların BOS'unun tedavi öncesi total oksidan ve OSİ değerleri tedavi sonrasına göre anlamlı derecede düşük bulunurken, total antioksidan ve S-100B değerleri için anlamlı bir fark bulunmadı. Sonuçlar: Tedavi sonrası klinik ve bakteriyolojik düzelme sağla-nan bakteriyel menenjitli hastalarda OSİ'de azalma görüldü. Ancak klinik ve bakteriyolojik düzelmeye rağmen S-100B değerleri tedavi sonrası yüksek bulundu. Bu durum akut bakteriyel menenjitli olgularda S-100B'deki biyokimyasal düzelmenin daha uzun bir süreç olacağını düşündürmektedir. Klimik Dergisi 2012; 25(2): 67-70.Anahtar Sözcükler: Çocuk, bakteri, menenjit, oksidatif durum, S-100B. AbstractObjective: The objective of this study is to evaluate the S-100B and oxidative status in serum and cerebrospinal fluid (CSF) of children with bacterial meningitis in both pre-and post-treatment periods. Methods: The study comprised 25 paediatric patients hospitalized with a diagnosis of bacterial meningitis. Blood and CSF were taken within the first 2 hours of hospitalization and on day 10 after treatment. Total oxidant and total antioxidant levels were measured and the oxidative stress index (OSI) was calculated for serum and CSF in both pre-and post-treatment periods. Results: The pre-treatment serum total oxidant levels and OSI values were found to be at significantly higher levels compared to the post-treatment values, while the total antioxidant levels and S-100B values were significantly lower. The pre-treatment CSF total oxidant and OSI values were found to be at a significantly lower level compared to the post-treatment levels, whereas no significance was found in the total antioxidant and S-100B values. Conclusions: Following treatment, clinical and bacteriological improvement was observed together with a reduction in oxidative stress in patients with bacterial meningitis. Despite this clinical and bacteriological improvement, the high post-treatment values of S-100B as a biochemical marker indicate that biochemical improvement after acute bacterial meningitis may require a longer process. Klimik Dergisi 2012; 25(2): 67-70.

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Oxidative stress and myeloperoxidase activity during bacterial meningitis: Effects of febrile episodes and the BBB permeability

Cited by 25 publications

References 36 publications

Oxidative Stress, Cytokine/Chemokine and Disruption of Blood–Brain Barrier in Neonate Rats After Meningitis by Streptococcus agalactiae

Oxidative Stress, Cytokine/Chemokine and Disruption of Blood–Brain Barrier in Neonate Rats After Meningitis by Streptococcus agalactiae

Tumour necrosis factor - alpha mediated mechanisms of cognitive dysfunction

Evaluation of S-100B and Oxidative Status before and after Treatment in Children with Bacterial Meningitis

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