Interleukin-1beta plays a role in the activation of peripheral leukocytes after blood-brain barrier rupture in the course of subarachnoid hemorrhage.
Subarachnoid hemorrhage (SAH) develops when extravasated arterial blood enters subarachnoid space and mixes with cerebrospinal fluid. As a result, many pathologies develop, including increase in brain-blood barrier (BBB) permeability and activation of peripheral leukocytes, that in turn augments immuno-inflammatory response, considered as the cause of numerous complications following SAH. In the study, we examined the role of one of major cytokines, interleukin 1-beta (IL-1beta), in the BBB rupture and subsequent migration of leukocytes into central nervous system (CNS) after experimental SAH in adult rats. SAH was produced by injection of 150 uL of autologous arterial blood into cisterna magna. In 50% of animals, IL-1beta activity was inhibited by intracerebroventricular administration of anti-rat IL-1beta antibodies (SAH' groups). Control group consisted of sham-operated rats. Ninety minutes or 24 hrs following surgery, blood samples were taken, then animals were perfused transcardially and whole brains were collected. Three major populations of leukocytes present at brain stem and frontal part of the brain - granulocytes, monocytes/macrophages and lymphocytes - were labeled with appropriate antibodies. S-100B protein concentration in the serum, a marker of BBB permeability, was also measured. Neutralization of IL-1beta activity reduced elevated S-100B level and number of leukocytes found within the CNS, however these changes were not uniformly significant among different subgroups. The results demonstrate an important role of IL-1beta in the BBB damage and leukocyte migration into the CNS subarachnoid hemorrhage.
Department of Physiology, Medical University of Silesia, Katowice, Poland.
Halina
H
Jedrzejowska-Szypułka
Grazyna
G
Straszak
Magdalena
M
Larysz-Brysz
Jacek
J
Karpe
Wiesław
W
Marcol
Edyta
E
Olakowska
Izabella
I
Woszczycka-Korczyńska
Joanna
J
Lewin-Kowalik
D000704:Analysis of Variance; D000818:Animals; D000906:Antibodies / Q000008:administration & dosage; D000943:Antigens, Differentiation / Q000378:metabolism; D001812:Blood-Brain Barrier / Q000503:physiopathology*; D016827:CD8 Antigens / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000187:drug effects; D007276:Injections, Intraventricular / Q000379:methods; D053583:Interleukin-1beta / Q000276:immunology / Q000378:metabolism*; D007962:Leukocytes / Q000145:classification / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D008214:Lymphocytes / Q000502:physiology; D008297:Male; D009414:Nerve Growth Factors / Q000097:blood; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood; D013345:Subarachnoid Hemorrhage / Q000473:pathology* / Q000503:physiopathology*; D013997:Time Factors
D000906:Antibodies; D000943:Antigens, Differentiation; D016827:CD8 Antigens; C409469:CD8 antigen, alpha chain; D053583:Interleukin-1beta; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; C036763:monocyte-macrophage differentiation antigen; D009195:Peroxidase