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The peptide AF-16 abolishes sickness and death at experimental encephalitis by reducing increase of intracranial pressure.

Journal article
Authors Eva Jennische
Tomas Bergström
Maria Johansson
Kristina Nyström
Andrej Tarkowski
Hans-Arne Hansson
Stefan Lange
Published in Brain research
Volume 1227
Pages 189-97
ISSN 0006-8993
Publication year 2008
Published at Institute of Biomedicine
Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Biomedicine, Department of Infectious Medicine
Pages 189-97
Language en
Keywords Administration, Intranasal, Animals, Antidiarrheals, administration & dosage, therapeutic use, Brain, drug effects, pathology, physiopathology, Cells, Cultured, Dose-Response Relationship, Drug, Encephalitis, Herpes Simplex, drug therapy, physiopathology, virology, Herpesvirus 1, Human, genetics, metabolism, Humans, Immunohistochemistry, Intracranial Hypertension, drug therapy, physiopathology, Intracranial Pressure, drug effects, physiology, Male, Neurons, drug effects, pathology, virology, Neuropeptides, administration & dosage, therapeutic use, Peptides, administration & dosage, therapeutic use, Polymerase Chain Reaction, Rats, Rats, Sprague-Dawley, Treatment Outcome
Subject categories Microbiology in the medical area


Elevated intracranial pressure (ICP) is strongly aggravating the injury at brain inflammation, resulting in persistent neurological and psychiatric malfunctions. There is no efficient pharmacological treatment to achieve beneficial ICP reduction. Here, the peptide AF-16, comprising the amino terminal part of the endogenous protein Antisecretory Factor (AF), was used to suppress the raised ICP in experimental herpes simplex encephalitis (HSE) in rats. Intranasal instillation of the peptide AF-16 counteracted the ICP elevation and the prevalence of ICP spikes, abrogated the neurological morbidity, and abolished the mortality in a dose-dependent manner. AF-16, 25 microg twice daily intranasally, rescued all animals with HSE and abrogated neurological malfunction. In contrast, only 10% of the rats survived if treated with the vehicle. A single intranasal dose of 25 microg AF-16 to a rat displaying overt HSE symptoms reduced the ICP to normal levels within an hour. No effects on viral replication or antigen distribution were demonstrable. Thus, AF-16 abolished the prevalence of sickness signs, ICP elevation, neurological malfunctions and completely prevented deaths. We advocate use of AF-16 for suppression of elevated ICP.

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