The pattern of interleukin-1beta (IL-1beta) and its modulating agents IL-1 receptor antagonist and IL-1 soluble receptor type II in acute meningococcal infections. 1997

M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
Department of Internal Medicine, University Hospital Nijmegen, The Netherlands.

Interleukin-1beta (IL-1beta) is considered an important mediator in the pathogenesis of septic shock or bacterial meningitis. Its activity is specifically modulated by IL-1 receptor antagonist (IL-1Ra) and IL-1 soluble receptor type II (IL-1sRII). We now describe the time-course of IL-1beta and these modulating agents in 59 patients with acute meningococcal infections, the prototype human disease of acute endotoxin exposure. Plasma IL-1beta was increased only in severe shock and normalized within 12 to 24 hours, indicating that patients were admitted in an early stage of cytokine activation. Increased IL-1beta values in cerebrospinal fluid (CSF) were confined to patients with meningitis. Plasma IL-1Ra was elevated in both shock and nonshock patients, extremely high values being measured in severe shock. High concentrations of IL-1Ra in CSF were found in meningitis. Plasma IL-1Ra peaked shortly after IL-1beta and decreased steeply in 1 to 2 days, followed by sustained moderately elevated levels in shock patients. Interestingly, IL-1sRII showed a completely different pattern. At admission, both nonshock and shock patients manifested a similar moderate increase of plasma IL-1sRII. However, during recovery plasma IL-1sRII further increased reaching maximal concentrations 3 to 5 days after admission, 1 to 2 days after normalization of IL-1Ra. In shock patients this increase was more prominent than in nonshock patients. It is hypothesized that this increase in plasma IL-1sRII can be explained by a synergistic effect of dexamethasone and endotoxin. A second interesting observation was that, unlike the pattern in plasma, IL-1sRII levels in CSF paralleled those of IL-1beta and IL-1Ra. This suggests different modulation of IL-1beta activity in the subarachnoid space and the plasma compartment. We conclude that: (1) During the early stage of meningococcal infections IL-1Ra modulates IL-1 activity, whereas during recovery IL-1sRII may be more important. (2) Modulation in CSF and in the plasma compartment are differentially regulated.

UI MeSH Term Description Entries
D007223 Infant A child between 1 and 23 months of age. Infants
D007375 Interleukin-1 A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. IL-1,Lymphocyte-Activating Factor,Epidermal Cell Derived Thymocyte-Activating Factor,Interleukin I,Macrophage Cell Factor,T Helper Factor,Epidermal Cell Derived Thymocyte Activating Factor,Interleukin 1,Lymphocyte Activating Factor
D008297 Male Males
D008585 Meningitis, Meningococcal A fulminant infection of the meninges and subarachnoid fluid by the bacterium NEISSERIA MENINGITIDIS, producing diffuse inflammation and peri-meningeal venous thromboses. Clinical manifestations include FEVER, nuchal rigidity, SEIZURES, severe HEADACHE, petechial rash, stupor, focal neurologic deficits, HYDROCEPHALUS, and COMA. The organism is usually transmitted via nasopharyngeal secretions and is a leading cause of meningitis in children and young adults. Organisms from Neisseria meningitidis serogroups A, B, C, Y, and W-135 have been reported to cause meningitis. (From Adams et al., Principles of Neurology, 6th ed, pp689-701; Curr Opin Pediatr 1998 Feb;10(1):13-8) Meningitis, Neisseria,Neisseria Meningitis,Meningitis, Meningococcal, Serogroup A,Meningitis, Meningococcal, Serogroup B,Meningitis, Meningococcal, Serogroup C,Meningitis, Meningococcal, Serogroup W-135,Meningitis, Meningococcal, Serogroup W135,Meningitis, Meningococcal, Serogroup Y,Meningitis, Meningococcic,Meningococcal Meningitis, Serogroup A,Meningococcal Meningitis, Serogroup B,Meningococcal Meningitis, Serogroup C,Meningococcal Meningitis, Serogroup W-135,Meningococcal Meningitis, Serogroup W135,Meningococcal Meningitis, Serogroup Y,Serogroup A Meningococcal Meningitis,Serogroup B Meningococcal Meningitis,Serogroup C Meningococcal Meningitis,Serogroup W-135, Meningococcal Meningitis,Serogroup W135, Meningococcal Meningitis,Serogroup Y, Meningococcal Meningitis,Meningococcal Meningitis,Meningococcal Meningitis, Serogroup W 135,Neisseria Meningitides,Serogroup W 135, Meningococcal Meningitis
D008589 Meningococcal Infections Infections with bacteria of the species NEISSERIA MENINGITIDIS. Meningococcal Septicemia,Infections, Meningococcal,Meningococcal Disease,Infection, Meningococcal,Meningococcal Diseases,Meningococcal Infection,Septicemia, Meningococcal
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D002675 Child, Preschool A child between the ages of 2 and 5. Children, Preschool,Preschool Child,Preschool Children
D003907 Dexamethasone An anti-inflammatory 9-fluoro-glucocorticoid. Hexadecadrol,Decaject,Decaject-L.A.,Decameth,Decaspray,Dexasone,Dexpak,Hexadrol,Maxidex,Methylfluorprednisolone,Millicorten,Oradexon,Decaject L.A.
D004731 Endotoxins Toxins closely associated with the living cytoplasm or cell wall of certain microorganisms, which do not readily diffuse into the culture medium, but are released upon lysis of the cells. Endotoxin

Related Publications

M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
May 2006, Oncology reports,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
July 1997, Clinical and experimental immunology,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
September 2000, Biochemical and biophysical research communications,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
February 1995, Proceedings of the National Academy of Sciences of the United States of America,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
October 2003, Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
May 1997, Journal of clinical immunology,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
March 2001, The Journal of clinical endocrinology and metabolism,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
July 1995, The Journal of clinical investigation,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
October 1996, American journal of respiratory and critical care medicine,
M van Deuren, and J van der Ven-Jongekrijg, and E Vannier, and R van Dalen, and G Pesman, and A K Bartelink, and C A Dinarello, and J W van der Meer
January 2008, Revista da Sociedade Brasileira de Medicina Tropical,
Copied contents to your clipboard!