Plasma Kallikrein Activation and Inhibition during Typhoid Fever

Colman, Robert W.; Edelman, Robert; Scott, Cheryl F.; Gilman, Robert H.

doi:10.1172/jci108938

Cited by 78 publications

(25 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cluster 2a contains genes coding for intracellular proteins, including transcription factors, secretory granules, and intracellular signaling molecules. A large proportion of the genes in cluster 2b are induced by IFN␥, which is known to be increased during acute typhoid (8,21). This cluster also includes other genes known to be involved in innate immunity (e.g., complement), adaptive immunity, and cell proliferation (22,23).…”

Section: Patterns Of Gene Expression Associated With Temporal Phases Ofmentioning

confidence: 99%

Transcriptional response in the peripheral blood of patients infected with Salmonella enterica serovar Typhi

Thompson

Dunstan

Dolecek

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

We used microarrays and transcriptional profiling of peripheral blood to investigate the host response of 29 individuals who contracted typhoid fever in the Mekong Delta region of Vietnam. Samples were taken over a nine month period encompassing acute disease, convalescence, and recovery. We found that typhoid fever induced a distinct and highly reproducible signature in the peripheral blood that changed during treatment and convalescence, returning in the majority of cases to the ''normal'' profile as measured in healthy uninfected controls. Unexpectedly, there was a strong, distinct signature of convalescence present at day 9 after infection that remained virtually unchanged one month after acute infection and in some cases persisted as long as nine months despite a complete clinical recovery in all patients. Patients who retain the convalescent signature may be genetically or temporarily incapable of developing an effective immune response and may be more susceptible to reinfection, relapse, or the establishment of a carrier state.immune response ͉ microbe-host interaction ͉ transcriptional profiling ͉ typhoid fever

show abstract

Section: Patterns Of Gene Expression Associated With Temporal Phases Ofmentioning

confidence: 99%

Transcriptional response in the peripheral blood of patients infected with Salmonella enterica serovar Typhi

Thompson

Dunstan

Dolecek

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Measurement of the zymogens, cofactors, altered inhibitors, and enzyme-inhibitor complexes in clinical samples have documented that changes of these proteins occur in sepsis (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia. In vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons.

Pixley

Cadena²,

Page³

et al. 1993

J. Clin. Invest.

271

153

View full text Add to dashboard Cite

The hypotension and disseminated intravascular coagulation (DIC) in bacteremia is thought to be mediated by the combined actions of cytokines, prostaglandins, and complement. The contact system, via the release of bradykinin and the activation of Factor XI, has been postulated to be contributing to the observed hypotension and DIC. Using a mAb to Factor XII (C6B7), we blocked the activation of the contact system in an established experimental baboon model in which Escherichia coli was infused to produce lethal bacteremia with hypotension. The untreated group (n = 5) displayed contact activation, manifested by a significant decrease in high molecular weight kininogen (HK) and a significant increase in a2macroglobulin-kallikrein complexes (a2M-Kal). The C6B7-treated group (n = 5) showed an inactivation of Factor XII and the changes in HK and a2M-Kal complexes were prevented. Both groups developed DIC manifested by a decrease in platelet, fibrinogen, and Factor V levels. The untreated group developed irreversible hypotension. The treated group experienced an initial hypotension that was reversed and extended the life of the animals. This study suggests that irreversible hypotension correlates with prolonged activation of the contact system, and specific antibody therapy can modulate both the pathophysiological and biochemical changes. (J. Clin. Invest. 1993.91:61-68.) Key words: septic shock * bradykinin * prekallikrein * high molecular weight kininogen * a2-macroglobulin Introduction Activation of the kallikrein-kinin system concomitant with hypotension has been demonstrated to occur in humans ( 1, 2) and in a lethal baboon model (3) during gram-negative bacteremia. The consequences ofcontact activation include the generation of kallikrein, which releases bradykinin from high molecular weight kininogen (HK),' and the generation of Factor

show abstract

“…Kallikrein antiserum was used at a final concentration of 1.6%. Electrophoresis was performed for 16 h at 14°C at 50 V. The plates were soaked and stained as previously described (16 plasma was added to 50 Al of a mixture containing 0.1% inosithin in 0.15 M NaCl and 10 mg/ml kaolin. 50 ,ul of prekallikrein-deficient plasma was introduced and the mixture wvas then incubated for 1 min at 37°C before recalcification with 50 ,ul of 0.025 M CaC12.…”

Section: Introductionmentioning

confidence: 99%

Function and Immunochemistry of Prekallikrein-High Molecular Weight Kininogen Complex in Plasma

Scott¹,

Colman²

1980

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

A B S T R A C T Plasma from individuals with high molecular weight (HMW) kininogen deficiency has been reported to be deficient in prekallikrein as measured by radial immunodiffusion, prekallikrein coagulant activity, and/or kaolin-activated arginine esterase activity. Addition of HMW kininogen increased the apparent prekallikrein activity in native normal plasma (as measured by esterase activity) but not in normal plasma in which inhibitors were inactivated. The apparent prekallikrein antigen concentration (as measured by radial immunodiffusion or electroimmunodiffusion) increased upon addition of HMW kininogen. Immunoelectrophoresis as well as gel filtration of normal plasma revealed the presence of free prekallikrein (17-38% of the total) in addition to the HMW kininogen-prekallikrein complex previously reported.This study emphasizes the influence of HMW kininogen on both functional and immunologic determinations of prekallikrein.

show abstract

Plasma Kallikrein Activation and Inhibition during Typhoid Fever

Abstract: A B S T R A C T As an ancillary part of a typhoid fever vaccine study, 10

Cited by 78 publications

References 37 publications

Transcriptional response in the peripheral blood of patients infected with Salmonella enterica serovar Typhi

Transcriptional response in the peripheral blood of patients infected with Salmonella enterica serovar Typhi

The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia. In vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons.

Function and Immunochemistry of Prekallikrein-High Molecular Weight Kininogen Complex in Plasma

Contact Info

Product

Resources

About