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Can CRP affect the blood-brain barrier during acute ischemic stroke?

100%

Bielewicz J., Kurzepa J., Czekajska-Chehab E., Kamieniak P., Daniluk B., Bartosik-Psujek H.

Polish Journal of Public Health

2015

vol. 125

issue 2

99-102

Introduction. Ischemic strokes (IS) are one of the main causes of death and disabilities around the globe. Therefore, there is a huge need for researching the pathogenesis of IS. The C-reactive protein (CRP) plays a role during inflammatory processes. Results of some studies conducted on animal models indicate that CRP affects the blood-brain barrier (BBB) stability during IS. The presence of S100BB protein can be considered as an indication of BBB injury. Aim. The purpose of this study was to discover the relationship between CRP and S100BB protein. Material and methods. The study looked at fifty four IS patients, with the disease confirmed by computer tomography (CT). The clinical status was evaluated on the 1st, 3rd, 5th, 10th day and 3 months following the onset of IS. Neurological status was estimated using the National Institute of Health Stroke Scale (NIHSS). Patients’ disability level was determined, using Modified Rankin Scale (mRS) and Barthel Index (BI). The volume of ischemic focus was calculated on the 10th day after the stroke, using CT. The levels of CRP and S100BB were evaluated on 1st, 3rd, 5th and 10th day after the stroke onset with usage of ELISA method. Results. The mean level of CRP and its concentration on the 1st, 3rd, 5th and 10th day directly correlates with a deteriorated clinical status, as measured with the use of NIHSS, BI and mRS on day 10 and 3 months after the onset of IS. We found a correlation with the mean CRP level and bigger volume of ischemic injury. The mean CRP level correlated with the mean level of S100BB protein. In the group of patients with low CRP (0.51-24.68 mg/mL) the level of S100BB and the volume of ischemic focus were lower than in the group with a high level of CRP (24.69-209 mg/mL). Conclusions. CRP can be considered as a predictor of a worse clinical outcome after stroke. The relationship between CRP and S100BB protein can suggest the active role of CRP during IS

Blood-Brain Barrier and Exercise – a Short Review

100%

Nierwińska K., Malecka E., Chalimoniuk M., Żebrowska A., Langfort J.

Journal of Human Kinetics

2008

vol. 19

83-92

Blood-brain barier (BBB) segregates central nervous system (CNS) from the circulating blood. BBB is formed by the brain capillary endothelial cells with complex tight junctions between them as well as by astrocytes and pericytes. BBB is responsible for transport of selected chemicals into and out of the CNS as well as for its protection from fluctuations in plasma composition following meals, during exercise and from circulating agents such as neurotransmitters, xenobiotics and other potentially harmful substances capable to disturb neural function. BBB may be compromised during CNS injury, infection, fever and in some nerodegenerative diseases. The increase of BBB permeability was observed also during exercise as documented by changes of plasma S-100 protein levels, used as a peripheral marker of BBB integrity. Marked change in BBB integrity during exercise may disturb normal brain function and contribute to the development of central fatigue. Moreover, serum S-100β may indicate level of injury in individuals suffering brain injuries during sports. There are also data suggesting that acute effect of physical exercise on serum S100β levels may not be related with CNS injury. Further studies to establish whether training and which type of it may modulate BBB permeability are needed.

Procesy patologiczne w mózgu podczas jego niedokrwienia

45%

Justyna Kacperska M., Jastrzębski K., Głąbiński A.

Aktualności Neurologiczne

2013

vol. 13

issue 1

16-23

Stroke to the present is one of the most common causes of death and permanent disability. Ischemic stroke (ischemic stroke called IS) is not only a dangerous disease because of its high mortality rate, but also because of a disability in patients who do survive, which represents approximately 76% of cases. It is a heterogeneous disease entity, which is a set of symptoms caused by focal ischemia or bleeding into the brain tissue caused by a wide variety of reasons. There are two types of strokes: haemorrhagic and ischemic. Haemorrhagic strokes account for 20% of all strokes, the other 80% are ischemic strokes. Stroke is a systemic disease, mainly resulting from vascular pathology. It plays a huge role in atherosclerosis and the mechanisms involved. The disease process affects the whole of the body, not just the cerebral vessels. From the point of view of pathological, ischemic stroke is the rapidly developing neurodegenerative process that leads to cell death. This disease is beyond the vascular damage, induces cell-molecular immune response to central nervous system and the vascular system, aimed at the development of the inflammatory response. The activated cells of the brain and vascular cells are involved in the synthesis of various molecules, among others. cytokines, chemokines, adhesion molecules and inflammatory enzymes. Continues to grow numerous reports confirming the importance of inflammatory factors in the development of ischemic stroke. In this process, the blood-brain barrier plays an important role. At the cellular level it is the main line of microglia immune surveillance of the central nervous system, which is responsible for the induction of the inflammatory response in stroke. In stroke, a sudden change in the expression of cytokines proceeds, which reveal the neurodegenerative effects of inflammatory cytokines and anti-inflammatory cytokines neuroprotective effect. Processes occurring in the brain during ischemia are very complicated and is not involved in a number of factors.

Udar mózgu (stroke) jest obecnie jedną z najczęstszych przyczyn zgonów i trwałego kalectwa. Udar niedokrwienny mózgu (ischaemic stroke, IS) jest niebezpieczną chorobą nie tylko ze względu na dużą śmiertelność, ale również z powodu niepełnosprawności u pacjentów, którzy go przeżywają (około 76% przypadków). Jest to niejednorodna jednostka chorobowa, będąca zespołem objawów ogniskowych powstałych w wyniku niedokrwienia lub krwotoku do tkanki mózgowej spowodowanych wieloma różnymi przyczynami. Rozróżniamy dwa typy udarów mózgowych: krwotoczne i niedokrwienne. Udary krwotoczne stanowią 15% wszystkich udarów, pozostałe 80% to udary niedokrwienne. Udar mózgu jest chorobą ogólnoustrojową, głównie wynikającą z patologii naczyniowej. Ogromną rolę odgrywa tu miażdżyca i mechanizmy z nią związane. Proces chorobowy dotyczy całego organizmu, a nie tylko naczyń mózgowych. Z punktu widzenia patologii udar niedokrwienny mózgu jest dynamicznie rozwijającym się procesem neurodegeneracyjnym, który prowadzi do śmierci komórek (cell death). Oprócz uszkodzenia naczyniopochodnego choroba ta indukuje komórkowo-molekularną odpowiedź immunologiczną ośrodkowego układu nerwowego i układu naczyniowego, ukierunkowaną na rozwój reakcji zapalnej. Aktywowane komórki mózgu, a także komórki układu naczyniowego zaangażowane są w syntezę różnych molekuł, m.in. cytokin, chemokin, cząsteczek adhezyjnych oraz enzymów prozapalnych. Ciągle rośnie liczba doniesień potwierdzających duże znaczenie czynników zapalnych w rozwoju udaru niedokrwiennego mózgu. W procesie tym znaczącą rolę odgrywa bariera krew-mózg. Na poziomie komórkowym mikroglej stanowi główną linię nadzoru immunologicznego nad ośrodkowym układem nerwowym, odpowiedzialną za indukcję reakcji zapalnej w udarze mózgu. W udarze mózgu następuje gwałtowna zmiana ekspresji cytokin, które ujawniają neurodegeneracyjny efekt cytokin prozapalnych oraz neuroprotekcyjny efekt cytokin antyzapalnych. Procesy zachodzące w mózgu podczas jego niedokrwienia są bardzo skomplikowane i wiele czynników jest w nie zaangażowanych.

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1 Journal of Human Kinetics

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1 Bartosik-Psujek H.

1 Bielewicz J.

1 Chalimoniuk M.

1 Czekajska-Chehab E.

1 Daniluk B.

1 Głąbiński A.

1 Jastrzębski K.

1 Justyna Kacperska M.

1 Kamieniak P.

1 Kurzepa J.

1 Langfort J.

1 Malecka E.

1 Nierwińska K.

1 Żebrowska A.

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Can CRP affect the blood-brain barrier during acute ischemic stroke?

Blood-Brain Barrier and Exercise – a Short Review

Procesy patologiczne w mózgu podczas jego niedokrwienia