title: Toll-like receptors in rat brains injured by hypoxic-ischaemia or exposed to staphylococcal alpha-toxin.
abstract: Some data suggest that the central nervous system (CNS) is the main target of Staphylococcus alpha-toxin. Since this pathogen cannot penetrate the blood-brain barrier (BBB), the exact mechanism by which alpha-toxin affects the CNS remains unclear. Recent studies on the role of the innate immune system have shed light on how bacterial infections initiate inflammatory responses within the CNS. The aim of this study was to investigate the immunoexpression of Toll-like receptors (TLR 2, TLR 4) in brains of young rats systemically exposed to Staphylococcus alpha-toxin or injured by neonatal hypoxia-ischaemia. The study was carried out on 6-week-old Wistar rats. A group of 6-week-old rats with severe brain injury caused by neonatal hypoxia-ischaemia was also studied separately. In all control rats, the immunoexpression of TLR 2 and TLR 4 was not detected. However, the expression of both TLRs was evident in all brains injured by HI or exposed to alpha-toxin. The immunoexpression was localised in the wall of the small brain vessels, cells of ependyma and leptomeninges. In such vessels the spectrum of ultrastructural lesions was found. The presence of TLR4 detected in the nerve cells of the subcortical gray matter of the brain is particularly of interest, but requires further studies. The presence of TLR 4 antigen in the nerve cells of the subcortical gray matter is particularly of interest. In conclusion, the results show that brain microvessels through TLRs may participate in the immune response of brain affected by bacterial infection as well as injured by non-infection insults.
authors.affiliation: Department of Experimental and Clinical Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warszawa, Poland. maslinskad@cmdik.pan.pl
authors.forename: Danuta
authors.initials: D
authors.lastname: Maślińska
authors.forename: Milena
authors.initials: M
authors.lastname: Laure-Kamionowska
authors.forename: Sławomir
authors.initials: S
authors.lastname: Maśliński
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001427:Bacterial Toxins / Q000633:toxicity*; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D006460:Hemolysin Proteins / Q000633:toxicity*; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis* / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000096:biosynthesis* / Q000187:drug effects; D013211:Staphylococcus aureus; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors
chemical_list: D001427:Bacterial Toxins; D006460:Hemolysin Proteins; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495343:Tlr2 protein, rat; C495347:Tlr4 protein, rat; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; C021091:staphylococcal alpha-toxin