Oxidative stress and S-100B protein in children with bacterial meningitis

Hamed, Sherifa A.; Hamed, Enas A.; Zakary, Madeha M.

doi:10.1186/1471-2377-9-51

Cited by 53 publications

(29 citation statements)

References 40 publications

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“…In the present study, the significantly higher level of expression of S100B in brain tissues in the B7-H3 plus SP group compared with that in the SP group indicates that B7-H3 aggravates SP infection-induced neurological damage, since elevated S100B expression reflects an ongoing cellular injury (specifically of astrocytes) (17,18). Furthermore, persistent increases in S100B may have a neurotoxic effect by inducing apoptosis, causing the release of proinflammatory cytokines as well as nitric oxide from astroglial cells, and exhibiting detrimental effects on neurons (13,19). Consistent with the dynamic changes of S100B expression, a greater amount of neuronal apoptosis and/or loss in the brain tissues, and a worse clinical status were observed from 18 to 72 h after SP infection.…”

Section: Discussionmentioning

confidence: 99%

“…S100B belongs to the multi-genic family of Ca 2+ -binding proteins and is abundant in astrocytes, where it is found diffusely in the cytoplasm and is associated with membranes and cytoskeleton constituents (12). Extensive evidence indicates that S100B in high levels (micromolar) may contribute to the severity of and neurological damage during bacterial meningitis (13,14). As a biomarker that indicates damage or dysfunction of the CNS (15), S100B levels could be used as an additional monitoring parameter in CNS infection (16).…”

Section: Discussionmentioning

confidence: 99%

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B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

Chen

Wang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Despite the application of antibiotics, Streptococcus pneumoniae (SP)-induced meningitis continues to be a life-threatening disease with a high fatality rate and an elevated risk of serious neurological sequelae, particularly in developing countries. In this study, the contribution of the co-stimulatory molecule B7 homolog 3 (B7-H3) to the pathogenesis of experimental SP-induced meningitis was investigated. Mice were challenged with the intracerebroventricular injection of serotype 3 SP with or without B7-H3. The clinical status of mice with SP-induced meningitis was examined by body weight loss and spontaneous motor activity with neurological scoring. Coronal brain sections were analyzed by counting Nissl-positive neurons and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells. Protein expression of neuron-specific enolase (NSE) and S100B in brain tissues was examined with immunohistochemical staining. All experiments were performed in a randomized and blinded setting. By the intracerebroventricular injection of SP suspension, a murine model of pneumococcal meningitis was successfully established. In this SP-induced meningitis model, B7-H3 deteriorated the clinical status, as manifested by a decreased neurological score and increased body weight loss. Following the B7-H3 challenge, the number of Nissl-positive cells decreased and TUNEL-stained positive cells increased in the brain tissues of mice with SP meningitis, which demonstrates the enhancement of neuronal necrosis and apoptosis, respectively. Protein expression of NSE was decreased, while that of S100B was increased. These in vivo findings indicate that B7-H3 aggravates brain injury during the pathological process of experimental SP-induced meningitis. IntroductionDespite treatment with effective antibiotics, Streptococcus pneumoniae (SP) meningitis remains a serious infectious disease of the central nervous system (CNS) with mortality rates between 16 and 37% (1) and neurological sequelae in up to 30% of survivors (2). Therefore, further study of the pathological mechanisms of SP meningitis and the identification of new means of intervention has a great clinical significance. SP-induced meningitis can cause disruption of the blood-brain barrier (BBB), and most severely it can result in brain damage, which affects the prognosis of patients with SP meningitis. Emerging studies have demonstrated that necrosis and apoptosis of brain neurons occur while brain damage is taking place. Neuron-specific enolase (NSE) and S100B have been confirmed to be specific markers of brain damage (3). B7 homolog 3 (B7-H3) is a newly identified member of the B7 superfamily, which serves a key function in the regulation of immune responses (4). Our previous study (5) found an abnormally high expression level of soluble B7-H3 (sB7H3) protein in children with bacterial meningitis. In a murine model of SP-induced meningitis, we also demonstrated that B7-H3 further augmented the inflammatory response, exacerbated BBB disruption, a...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

Chen

Wang

et al. 2015

Experimental and Therapeutic Medicine

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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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“…Выявлена положительная корреляция между кон центрацией S100B в СМЖ и активацией перекисного окисле ния липидов, а также между соотношением S100B и степенью тяжести течения менингита [48]. Обнаружена положительная корреляция между сывороточным S100B с общим содержани ем тиолов в сыворотке, что предположительно указывает на то, что повреждение астроцитов может увеличивать образование S100B в соответствии с тяжестью окислительного стресса [49,50].…”

Section: белок S100b при сепсисеunclassified

“…Это приводит к гиперфер ментемии (усилению активности катепсина Д, кислой фосфа тазы в тканях головного мозга и в крови) и накоплению токсических веществ (молекул средней массы) в крови (так называемой, токсемии) [52]. В настоящее время воспаление [53], глутамат [32] и окислительный стресс [54] рассматрива ются в качестве важных стимуляторов для выброса S100B [48].…”

Section: белок S100b при сепсисеunclassified

Diagnostic Value of S100B Protein in Critical Conditions

Белобородова¹,

Dmitrieva²,

Черневская³

2011

rmt

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Медицина критических состояний нуждается в прямых лабораторных индикаторах повреждения клеток нервной сис темы, опережающих клинические и радиологические методы оценки. Возможность количественной оценки степени повреж дений мозга путем измерения уровня белка S100B в различных биологических жидкостях (ликвор, кровь, амниотическая жид кость, моча, слюна), является чрезвычайно привлекательной, особенно -у новорожденных высокого риска с перинатальны ми повреждениями головного мозга. Как будет показано ниже, концентрация белка S100B в различных биологических жидко стях достоверно коррелирует со степенью повреждения мозга. Можно утверждать, что белок S100B удовлетворяет основным критериям маркера повреждения головного мозга в перина тальной медицине, что подтверждается следующими фактами: -благодаря современным технологиям, S100B легко измерить количественно, используя минимальный объем ис следуемого образца; -S100B обнаруживается во многих биологических жидкостях, с хорошей воспроизводимостью результатов; -по данным многочисленных исследований, S100В известен в качестве раннего лабораторного признака мозговых повреждений различного генеза.Фракция глиальных белков мозга, продуцирующихся главным образом астроцитами, была открыта в 1965 году и на звана S100 [1]. Название «S100» связано со способностью бел ка растворяться в 100% растворе сульфата аммония при рН 7,2. Церебральный S100 представляет собой комбинацию двух тес но связанных белков семейства: S100A1 (S100α) и S100B (S100β). В настоящее время, по крайней мере, 20 белков отне сено к семейству S100 -это внутриклеточные кальций сен сорные и кальций связывающие белки с молекулярным весом 10-12 килодальтон. Для некоторых членов семейства S100 по казана возможность связывания с ионами цинка и меди, что косвенно указывает на участие в регуляции их биологической активности не только кальция. Чаще всего в пределах клетки белки S100 существуют как димеры (гомодимеры). Основная часть белков S100 (до 85-90% от общего содержания в нерв ной ткани) сосредоточена в астроцитах; 10-15% расположены в нейронах, минимальное их количество определяется в олиго дендроцитах. Белки S100 синтезируются глиальными клетка ми, а затем транспортируются в нейроны.Благодаря способности к регуляции активности ряда бел ков, S100A1 и S100B вовлечены в трансдукцию сигналов, кон тролирующих активность ферментов энергетического обмена в клетках мозга [2], кальциевый гомеостаз [3], клеточный цикл, функции цитоскелета, транскрипцию, пролиферацию и дифференцировку клеток, их подвижность, секреторные про цессы, структурную организацию биомембран [4]. Таким обра зом, различные изоформы и конформеры белков S100 пред ставляют наиболее универсальные из известных макромолекул, которые участвуют в регуляции практически всех основных мембранных, цитоплазматических и ядерных метаболических процессов, связанных с обеспечением меха низмов восприятия и интеграции поступающей в нервную си стему информации, принимают участие в ответе генов раннего реагирования, в реализации генетических программ апоптоза и антиапоптоз...

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Oxidative stress and S-100B protein in children with bacterial meningitis

Cited by 53 publications

References 40 publications

B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

B7 homolog 3 aggravates brain injury in a murine model of Streptococcus pneumoniae-induced meningitis

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

Diagnostic Value of S100B Protein in Critical Conditions

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