Complement (C5)-derived chemotactic activity accounts for accumulation of polymorphonuclear leukocytes in cerebrospinal fluid of rabbits with pneumococcal meningitis

Ernst, Joel D.; Hartiala, Kaija; Goldstein, Ira M.; Sande, Merle A.

doi:10.1128/iai.46.1.81-86.1984

Cited by 67 publications

(15 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other not yet characterized factors may also be present and up-regulated in the early stage of Hib meningitis. The contribution of complement factors to the development of CSF pleocytosis has been shown (9). The importance of arachidonic acid pathway metabolites such as leukotrienes and bacterial cell wall products as chemoattractants in bacterial meningitis was shown in rabbits with pneumococcal meningitis (3,20).…”

Section: Discussionmentioning

confidence: 99%

Neutralization of Macrophage Inflammatory Protein 2 (MIP-2) and MIP-1α Attenuates Neutrophil Recruitment in the Central Nervous System during Experimental Bacterial Meningitis

Diab¹,

Abdalla

Li³

et al. 1999

Infect Immun

128

View full text Add to dashboard Cite

Chemokines are low-molecular-weight chemotactic cytokines that have been shown to play a central role in the perivascular transmigration and accumulation of specific subsets of leukocytes at sites of tissue damage. Using in situ hybridization (ISH), we investigated the mRNA induction of macrophage inflammatory protein 2 (MIP-2), MIP-1α, monocyte chemoattractant protein 1 (MCP-1), and RANTES. Challenge of infant rats’ brains with Haemophilus influenzae type b intraperitoneally resulted in the time-dependent expression of MIP-2, MIP-1α, MCP-1, and RANTES, which was maximal 24 to 48 h postinoculation. Immunohistochemistry showed significant increases in neutrophils and macrophages infiltrating the meninges, the ventricular system, and the periventricular area. The kinetics of MIP-2, MIP-1α, MCP-1, and RANTES mRNA expression paralleled those of the recruitment of inflammatory cells and disease severity. Administration of anti-MIP-2 or anti-MIP-1α antibodies (Abs) resulted in significant reduction of neutrophils. Administration of anti-MCP-1 Abs significantly decreased macrophage infiltration. Combined studies of ISH and immunohistochemistry showed that MIP-2- and MIP-1α-positive cells were neutrophils and macrophages. MCP-1-positive cells were neutrophils, macrophages, and astrocytes. Expression of RANTES was localized predominantly to resident astrocytes and microglia. The present study indicates that blocking of MIP-2 or MIP-1α bioactivity in vivo results in decreased neutrophil influx. These data are also the first demonstration that the C-C chemokine MIP-1α is involved in neutrophil recruitment in vivo.

show abstract

Section: Discussionmentioning

confidence: 99%

Neutralization of Macrophage Inflammatory Protein 2 (MIP-2) and MIP-1α Attenuates Neutrophil Recruitment in the Central Nervous System during Experimental Bacterial Meningitis

Diab¹,

Abdalla

Li³

et al. 1999

Infect Immun

128

View full text Add to dashboard Cite

show abstract

“…C5-derived chemotactic activity has been detected in many different types of inflammatory reactions in many species (e.g. Snyderman et al, 1971;Lo et al, 1984;Ernst et al, 1984) including synovial fluid from the rheumatoid joint (Ward & Zvaifler, 1971). Since decomplementation of rabbit and other species has been shown to inhibit many types of inflammatory reactions (Ward & Cochrane, 1965;Willoughby et al, 1969;Cochrane et al, 1970), we suggest that CSa generation can be an important factor controlling the ensuing inflammatory reaction.…”

Section: Discussion Mal Injections Of Zymosan At Different Intervals mentioning

confidence: 99%

Kinetics of the generation and action of chemical mediators in zymosan‐induced inflammation of the rabbit peritoneal cavity

Forrest

Jose

Williams

1986

British J Pharmacology

View full text Add to dashboard Cite

Acute inflammation was induced by intraperitoneal injection of zymosan (yeast cell walls) in the rabbit. Peritoneal inflammation was monitored by the local accumulation of intravenously‐injected Evans blue dye (which binds to plasma albumin) and of polymorphonuclear leukocytes (PMNLs). The zymosan‐induced exudate fluid contained a microvascular permeability‐increasing factor or factors which, unlike histamine and bradykinin, had a long duration of action when tested in rabbit skin and was dependent on circulating PMNLs. Using radioimmunossay, high levels of rabbit C5a, or C5a des Arg, were detected in the exudate fluid and accounted for much of the permeability‐increasing activity, as judged by skin bioassay after separation on Sephadex G‐100. The vasodilator prostaglandin, prostaglandin I2 (PGI2), was generated in the inflammatory reaction, as judged by the presence of high levels of 6‐oxo‐PGF1α detected in the exudate by radioimmunossay. However, in contrast to observations in rabbit skin, inhibition of prostaglandin generation had a relatively small effect on peritoneal oedema formation. C5a and C5a des Arg increase microvascular permeability by a PMNL‐dependent mechanism in the rabbit. However, in response to zymosan, protein leakage was detected considerably earlier than PMNL accumulation. A hypothesis to account for this difference is proposed.

show abstract

“…reference 25), complement components appear to participate in the early phase of recruitment of leukocytes into cerebrospinal fluid(27).…”

mentioning

confidence: 96%

Reduction of inflammation, tissue damage, and mortality in bacterial meningitis in rabbits treated with monoclonal antibodies against adhesion-promoting receptors of leukocytes.

Tuomanen

Saukkonen

Sande

et al. 1989

The Journal of Experimental Medicine

310

142

View full text Add to dashboard Cite

We tested if specific inhibition of recruitment of leukocytes across the blood brain barrier from the vascular compartment to the cerebrospinal fluid (CSF) space reduced tissue damage and improved the outcome of infection in a rabbit model of experimental meningitis. The CD11/CD18 complex of receptors on leukocytes promotes adhesion of these cells to endothelia, a process required for egress of cells into the extravascular space. Intravenous injection of the anti-CD18 mAb IB4 effectively blocked the development of leukocytosis in the CSF of animals challenged intracisternally with living bacteria, bacterial endotoxin, or bacterial cell wall. This effect was associated with protection from blood brain barrier injury as measured by exclusion of serum proteins from CSF in mAb-treated animals. The densities of bacteria in CSF and the degrees of bacterial killing due to ampicillin were not affected by the antibody. Animals receiving the antibody experienced a delay in the development of bacteremia and a significantly reduced inflammatory response during ampicillin-induced bacterial killing. Therapy with mAb IB4 prevented development of brain edema and death in animals challenged with lethal doses of Streptococcus pneumoniae. These studies indicate that the major mechanism of leukocyte migration across the blood brain barrier involves the CD11/CD18 receptors and that inflammatory leukocytes recruited by this mechanism are a major cause of blood brain barrier injury and cerebral edema during meningitis.

show abstract

Complement (C5)-derived chemotactic activity accounts for accumulation of polymorphonuclear leukocytes in cerebrospinal fluid of rabbits with pneumococcal meningitis

Cited by 67 publications

References 18 publications

Neutralization of Macrophage Inflammatory Protein 2 (MIP-2) and MIP-1α Attenuates Neutrophil Recruitment in the Central Nervous System during Experimental Bacterial Meningitis

Neutralization of Macrophage Inflammatory Protein 2 (MIP-2) and MIP-1α Attenuates Neutrophil Recruitment in the Central Nervous System during Experimental Bacterial Meningitis

Kinetics of the generation and action of chemical mediators in zymosan‐induced inflammation of the rabbit peritoneal cavity

Reduction of inflammation, tissue damage, and mortality in bacterial meningitis in rabbits treated with monoclonal antibodies against adhesion-promoting receptors of leukocytes.

Contact Info

Product

Resources

About