title: Relationship between the induction of inflammatory processes and infectious diseases in patients with ischemic stroke.
abstract: Pro-inflammatory cytokines participate in the induction of ischemic stroke. So far, their participation in the cerebral ischemia was proven for the tumor necrosis factor TNF-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). The release of the pro-inflammatory cytokines into the extracellular space causes the enlargement of the brain damage region, and consequently increases the neurological deficit and negatively affects the survival rate prognoses. That is confirmed by the increased concentration of pro-inflammatory cytokines in blood and the cerebrospinal fluid of patients with brain stroke, as well as by the research on the induced/experimental cerebral ischemia in animals. The pro-inflammatory cytokines participate in the migration of the reactive T lymphocytes to the regions of brain ischemia where they enhance the nerve tissue damage by down-regulation of microcirculation, induce the pro-thrombotic processes and release other neurotoxic cytokines. Also, in the early stage of cerebral ischemia, cytokines activate the axis hypothalamus-pituitary gland-adrenal cortex and increase the cortisol concentration in blood, what results in the decreased resistance to infectious diseases. Administration of the inhibitor of the interleukin-1 receptor (IL-1Ra) inhibits the inflammatory processes in the region of brain ischemia, and subsequently improves the prognosis for the size of the neurological deficit and the survival rate, as well as resistance to infectious diseases.
authors.affiliation: Nerology Department, Regional Polyclinical Hospital in Toruń, Toruń, Poland.
authors.forename: Marek
authors.initials: M
authors.lastname: Cieślak
authors.forename: Andrzej
authors.initials: A
authors.lastname: Wojtczak
authors.forename: Michał
authors.initials: M
authors.lastname: Cieślak
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D002465:Cell Movement; D003141:Communicable Diseases / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D006801:Humans; D006854:Hydrocortisone / Q000276:immunology; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology / Q000382:microbiology; D007155:Immunologic Factors / Q000627:therapeutic use; D007249:Inflammation; D007375:Interleukin-1 / Q000276:immunology*; D015850:Interleukin-6 / Q000276:immunology*; D010913:Pituitary-Adrenal System / Q000276:immunology / Q000382:microbiology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology; D020521:Stroke / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D000893:Anti-Inflammatory Agents; C508600:IL6 protein, human; D007155:Immunologic Factors; D007375:Interleukin-1; D015850:Interleukin-6; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D006854:Hydrocortisone