C1 Inhibitor Treatment Improves Host Defense in Pneumococcal Meningitis in Rats and Mice

In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement i...

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Published inThe Journal of infectious diseases Vol. 196; no. 1; pp. 115 - 123
Main Authors Zwijnenburg, Petra J. G., Poll, Tom van der, Florquin, Sandrine, Polfliet, Machteld M. J., van den Berg, Timo K., Dijkstra, Christine D., Roord, John J., Erik Hack, C., Marceline van Furth, A.
Format Journal Article
LanguageEnglish
Published United States The University of Chicago Press 01.07.2007
University of Chicago Press
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Abstract In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement inhibition by C1 inhibitor (C1-inh) is beneficial in animal models of endotoxemia and sepsis. In the present study, we demonstrate classical pathway complement activation during pneumococcal meningitis in rats. We also evaluate the effect of C1-inh treatment on clinical illness, bacterial clearance, and inflammatory responses in rats and mice with pneumococcal meningitis. C1-inh treatment was associated with reduced clinical illness, a lesspronounced inflammatory infiltrate around the meninges, and lower brain levels of proinflammatory cytokines and chemokines. C1-inh treatment increased bacterial clearance, possibly through an up-regulation of CR3. Hence, C1-inh may be a useful agent in the treatment of pneumococcal meningitis.
AbstractList In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement inhibition by C1 inhibitor (C1-inh) is beneficial in animal models of endotoxemia and sepsis. In the present study, we demonstrate classical pathway complement activation during pneumococcal meningitis in rats. We also evaluate the effect of C1-inh treatment on clinical illness, bacterial clearance, and inflammatory responses in rats and mice with pneumococcal meningitis. C1-inh treatment was associated with reduced clinical illness, a less-pronounced inflammatory infiltrate around the meninges, and lower brain levels of proinflammatory cytokines and chemokines. C1-inh treatment increased bacterial clearance, possibly through an up-regulation of CR3. Hence, C1-inh may be a useful agent in the treatment of pneumococcal meningitis.
In spite of antibiotic treatment, pneumococcal meningitis continues to be associated with significant morbidity and mortality. The complement system is a key component of innate immunity against invading pathogens. However, activation of complement is also involved in tissue damage, and complement inhibition by C1 inhibitor (C1-inh) is beneficial in animal models of endotoxemia and sepsis. In the present study, we demonstrate classical pathway complement activation during pneumococcal meningitis in rats. We also evaluate the effect of C1-inh treatment on clinical illness, bacterial clearance, and inflammatory responses in rats and mice with pneumococcal meningitis. C1-inh treatment was associated with reduced clinical illness, a lesspronounced inflammatory infiltrate around the meninges, and lower brain levels of proinflammatory cytokines and chemokines. C1-inh treatment increased bacterial clearance, possibly through an up-regulation of CR3. Hence, C1-inh may be a useful agent in the treatment of pneumococcal meningitis.
Author Marceline van Furth, A.
Erik Hack, C.
van den Berg, Timo K.
Dijkstra, Christine D.
Roord, John J.
Florquin, Sandrine
Poll, Tom van der
Polfliet, Machteld M. J.
Zwijnenburg, Petra J. G.
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Present affiliations: Department of Clinical Genetics, Vrije Universiteit Medical Center, Amsterdam, The Netherlands (P.J.G.Z.); Sanquin Research at CLB, Amsterdam, The Netherlands (T.K.v.d.B.).
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SubjectTerms Animal models
Animals
Bacteria
Bacterial meningitis
Blood
Brain - immunology
Brain - pathology
Brain Chemistry
Central nervous system
Cerebrospinal fluid
Cerebrospinal Fluid - microbiology
Chemokines - analysis
Colony Count, Microbial
Complement Activation
Complement C1 - antagonists & inhibitors
Complement C1 Inhibitor Protein - administration & dosage
Complement C1 Inhibitor Protein - pharmacology
Complement Pathway, Classical
Cytokines
Cytokines - analysis
Disease Models, Animal
Humans
Inoculation
Leukocytes
Macrophage-1 Antigen - biosynthesis
Male
Meninges - pathology
Meningitis, Pneumococcal - immunology
Meningitis, Pneumococcal - microbiology
Meningitis, Pneumococcal - pathology
Mice
Mice, Inbred C57BL
Pneumococcal meningitis
Rats
Rats, Wistar
Streptococcus pneumoniae
Streptococcus pneumoniae - isolation & purification
Title C1 Inhibitor Treatment Improves Host Defense in Pneumococcal Meningitis in Rats and Mice
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