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1.
J Neuroimmunol ; 120(1-2): 129-37, 2001 Nov 01.
Article in English | MEDLINE | ID: mdl-11694327

ABSTRACT

Children presenting with acute systemic illnesses that lack specific clinical or serological defining features may be diagnosed as having a chronic infection, an atypical systemic vasculitis or a connective tissue disease, but often turn out to have occult neoplasias. Cytokines have been implicated in causing many of the systemic effects in such cases. In this study, we describe the case of a 9-year-old boy presenting at an interval of 18 months with a marked acute-phase response due to a recurrent atypical meningioma with rhabdoid transformation of the tentorium cerebelli. Resection of the recurrent tumor was curative. We evaluated in detail the local and systemic production of cytokines released by the primary and the recurrent tumor. Blood and CSF samples were taken pre-, intra-, and postoperatively, and the production of IL-6, IL-1beta, and TNF-alpha was measured by enzyme-linked immunosorbent assays (ELISA). The level of IL-6 in CSF was about 150-fold increased before tumor resection, normalizing postoperatively. On the contrary, the levels of IL-1beta and TNF-alpha in CSF and of IL-6, IL-1beta, and TNF-alpha in serum were pre-, intra-, and postoperatively within normal limits. Cytokine production was also evaluated immunohistochemically, and confirmed strong IL-6 and TNF-alpha expression in the primary and the recurrent tumor, while expression of IL-1beta was lacking. The scattered MHC class II- and leukocyte common antigen (LCA)-expressing inflammatory cells, which were infiltrating exclusively the tumoral stroma, had no detectable cytokine immunoreactivity. We conclude that chronic IL-6 and TNF-alpha production by the tumor cells in this patient was responsible for the severe systemic illness with which he presented.


Subject(s)
Cytokines/metabolism , Dura Mater/pathology , Fever of Unknown Origin/etiology , Meningeal Neoplasms/metabolism , Meningioma/metabolism , Neoplasm Recurrence, Local/metabolism , Rhabdoid Tumor/metabolism , Acute Disease , Child , Cranial Fossa, Posterior/pathology , Cytokines/blood , Cytokines/cerebrospinal fluid , Desmin/metabolism , Dura Mater/ultrastructure , Enzyme-Linked Immunosorbent Assay , Fever of Unknown Origin/pathology , Fever of Unknown Origin/physiopathology , Fibroblast Growth Factors/metabolism , Humans , Immunohistochemistry , Interleukin-1/blood , Interleukin-1/cerebrospinal fluid , Interleukin-1/metabolism , Interleukin-6/blood , Interleukin-6/cerebrospinal fluid , Interleukin-6/metabolism , Magnetic Resonance Imaging , Male , Meningeal Neoplasms/cerebrospinal fluid , Meningeal Neoplasms/pathology , Meningioma/cerebrospinal fluid , Meningioma/pathology , Microscopy, Electron , Neoplasm Recurrence, Local/cerebrospinal fluid , Neoplasm Recurrence, Local/pathology , Pyrogens/blood , Pyrogens/cerebrospinal fluid , Pyrogens/metabolism , Rhabdoid Tumor/cerebrospinal fluid , Rhabdoid Tumor/pathology , Treatment Outcome , Tumor Necrosis Factor-alpha/cerebrospinal fluid , Tumor Necrosis Factor-alpha/metabolism , Vimentin/metabolism
2.
Brain Res Bull ; 32(1): 75-81, 1993.
Article in English | MEDLINE | ID: mdl-8319107

ABSTRACT

Previously it was reported that a control saline solution infused into the anterior hypothalamic, preoptic area (AH/POA) can induce an intense fever from an unknown source. To avoid such fevers, cerebral dialysis has been proposed as an alternative procedure, although in nearly all experiments on the febrile response, a nonpyrogenic solution is injected, not dialyzed, directly into the AH/POA. The purpose of this study was to determine the: a) possible conditions whereby a control solution can cause an experimental fever; b) putative organisms which may comprise the source of a centrally induced fever; and c) procedures whereby such fevers can be avoided. In twelve adult male Sprague-Dawley rats, an intracerebral cannula for microinjections and a Minimitter temperature transmitter were implanted within the AH/POA and intraperitoneal cavity, respectively. Following recovery, the thermoreactivity of each site in the AH/POA was verified by a microinjection of norepinephrine which typically lowers body temperature (Tb) by 0.5-1.0 degrees C. Two artificial cerebrospinal fluid (CSF) test solutions were used: one exposed to the ambient conditions of the laboratory, and a second prepared under pathogen-free conditions, including filtration, to exclude biological contaminants. A rise in temperature of 0.8-1.0 degrees C within 1.0 h after microinjection, which increased to as high as 3.5 degrees C within 4 h, typically was produced by the contaminated artificial CSF solution. The filtered CSF did not evoke a consistent or reliable rise in Tb of the rats.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Fever/physiopathology , Mycoses/physiopathology , Preoptic Area/physiology , Trichosporon , Animals , Body Temperature , Brain Mapping , Male , Microinjections , Preoptic Area/microbiology , Preoptic Area/physiopathology , Pyrogens/cerebrospinal fluid , Rats , Rats, Sprague-Dawley , Time Factors
3.
Br J Pharmacol ; 66(4): 565-72, 1979 Aug.
Article in English | MEDLINE | ID: mdl-380709

ABSTRACT

1 A study has been made of the possible entry of 51Cr-bacterial endotoxin and [5,6,8,11,12,14,15(n)-3H]-prostaglandin E2 ([3H5-PGE2) into the CNS of the anaesthetized cat. 2 No radioactivity was detected in perfusates of the preoptic-anterior hypothalamus or in the cerebrospinal fluid (c.s.f.) in vivo, or in brain tissue post mortem following intracarotid infusion of 51Cr-bacterial endotoxin. 3 Intracarotid administration of [3H]-PGE2 resulted in the entry of radioactivity into the CNS of endotoxin pretreated cats. Chromatographic analysis indicated the radioactivity in c.s.f. to be associated with PGE2 and a metabolite similar to 13, 14-dihydro-15-keto PGE2. 4 Intracarotid administration of 13, 14-dihydro-15-keto [5,6,8,11,12,14(n)-3H]-PGE2 resulted in the presence of the compound in the CNS of the anaesthetized cat after pretreatment with bacterial endotoxin. 5 It is concluded that PGE2 and possibly 13,14-dihydro-15-keto PGE2 but not bacterial endotoxin may enter the CNS from the cerebral circulation to elicit the febrile response to bacterial endotoxin in cats.


Subject(s)
Blood-Brain Barrier , Brain/drug effects , Endotoxins/metabolism , Prostaglandins E/metabolism , Pyrogens/metabolism , Animals , Brain/metabolism , Cats , Endotoxins/cerebrospinal fluid , Female , Prostaglandins E/cerebrospinal fluid , Pyrogens/cerebrospinal fluid , Radioisotope Dilution Technique , Shigella flexneri
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