Phospholipase A2 Is a Circulating Mediator in Typhoid Fever

Keuter, Monique; Dharmana, Edi; Kullberg, Bart Jan; Schalkwijk, Casper G.; Gasem, Muhammad Hussein; Seuren, L.; Djokomoeljanto, R.; Dolmans, W.M.V.; Bosch, H. van den; Meer, J.W.M. van der

doi:10.1093/infdis/172.1.305

Cited by 23 publications

(14 citation statements)

References 11 publications

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“…The serum PLA 2 concentrations in severe inflammatory conditions such as typhoid fever (17) and systemic fungal infections (18) have been reported to be ϳ1-5 g/ml. In normal human tears the concentration of group IIA PLA 2 exceeds 30 g/ml (4).…”

Section: Discussionmentioning

confidence: 99%

Bactericidal Properties of Group IIA and Group V Phospholipases A2

Grönroos

Laine

Janssen

et al. 2001

The Journal of Immunology

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Group V phospholipase A2 (PLA2) is a recently characterized 14-kDa secretory PLA2 of mammalian heart and macrophage-derived cells. Group IIA PLA2, which is structurally close to group V PLA2, has been shown to kill Gram-positive bacteria in vitro and to prevent symptoms of Gram-positive infection in vivo. We studied the antibacterial properties of fully active recombinant rat group IIA and V PLA2s. Both group IIA and V PLA2s were highly bactericidal against Gram-positive bacteria, including methicillin-resistant staphylococci and vancomycin-resistant enterococci. Only high concentrations of group IIA PLA2 showed some bactericidal effect against the Gram-negative bacterium Escherichia coli. Our results confirm that group IIA PLA2 is a potent antibacterial enzyme against Gram-positive bacteria. Moreover, we show here that group V PLA2 is a novel antibacterial mammalian protein, but is less potent than group IIA PLA2. Both enzymes may be considered as future therapeutic agents against bacterial infections.

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Section: Discussionmentioning

confidence: 99%

Bactericidal Properties of Group IIA and Group V Phospholipases A2

Grönroos

Laine

Janssen

et al. 2001

The Journal of Immunology

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“…The concentration of group II PLA2 in sera of PLA2 ϩ mice was somewhat higher (approximately 2,500 g/liter) (16) than that found in humans with severe infectious diseases. These diseases include bacterial infections (240 g/liter) (29), sepsis (880 g/liter) (25), peritonitis (440 g/liter) (25), and typhoid fever (1,440 g/ liter) (13). The PLA2 ϩ mice used in the present study showed no clinical symptoms of inflammation and behaved normally despite the exceedingly high PLA2 catalytic activity (up to 100-fold higher than in PLA2 Ϫ mice) and concentration of group II PLA2 in their sera.…”

Section: Discussionmentioning

confidence: 99%

Resistance of Transgenic Mice Expressing Human Group II Phospholipase A2 toEscherichia coliInfection

Laine

Grass²,

Nevalainen

2000

Infect Immun

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؉ mice and their PLA2-deficient C57BL/6J littermates (PLA2 ؊ mice) were studied after intraperitoneal administration of E. coli. The levels of group II PLA2 in sera of PLA2 ؉ mice increased after the administration of E. coli, and the concentration of group II PLA2 correlated significantly with the catalytic activity of PLA2 in serum. PLA2؉ mice showed lower rates of mortality and less bacterial growth in peritoneal lavage fluid, blood, and spleen and liver tissues than PLA2 ؊ mice. Unlike the observations with staphylococcal infection, serum and peritoneal lavage fluid did not inhibit the growth of E. coli in vitro. The results indicate that expression of the group II PLA2 transgene improves the host defense of mice against E. coli infection.

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“…Probably, the presence of cytokines inhibitors were necessary to counterbalance the high values of proinflammatory cytokines. The same authors studied the influence of blood peripheral 14 kDa group II phospholipase A2 (PLA2) in 12 patients with typhoid fever, after admission and after recovery 30 . On admission, PLA2 levels were high (1444 ± 1560 ng/ml), and decrease gradually to 55 ± 48 ng/ml at 14th day.…”

Section: ) Clinical Manifestations Of Typhoid Fever and Their Pathogmentioning

confidence: 99%

“…Patient with complicated typhoid fever had significantly higher PLA2 levels on admission (2520 ± 48 ng/ml). The authors suggest that PLA2 may be a mediator of seriousness in prolonged inflammatory diseases such as typhoid fever 30 .…”

Section: ) Clinical Manifestations Of Typhoid Fever and Their Pathogmentioning

confidence: 99%

Typhoid fever as cellular microbiological model

Andrade

Júnior

2003

Rev. Inst. Med. trop. S. Paulo

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SUMMARYThe knowledge about typhoid fever pathogenesis is growing in the last years, mainly about the cellular and molecular phenomena that are responsible by clinical manifestations of this disease. In this article are discussed several recent discoveries, as follows: a) Bacterial type III protein secretion system; b) The five virulence genes of Salmonella spp. that encoding Sips (Salmonella invasion protein) A, B, C, D and E, which are capable of induce apoptosis in macrophages; c) The function of Toll R2 and Toll R4 receptors present in the macrophage surface (discovered in the Drosophila). The Toll family receptors are critical in the signalizing mediated by LPS in macrophages in association with LBP and CD14; d) The lines of immune defense between intestinal lumen and internal organs; e) The fundamental role of the endothelial cells in the inflammatory deviation from bloodstream into infected tissues by bacteria. In addition to above subjects, the authors comment the correlation between the clinical features of typhoid fever and the cellular and molecular phenomena of this disease, as well as the therapeutic consequences of this knowledge.

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Phospholipase A2 Is a Circulating Mediator in Typhoid Fever

Abstract: The following full text is a publisher's version. For additional information about this publication click this link.

Cited by 23 publications

References 11 publications

Bactericidal Properties of Group IIA and Group V Phospholipases A2

Bactericidal Properties of Group IIA and Group V Phospholipases A2

Resistance of Transgenic Mice Expressing Human Group II Phospholipase A2 toEscherichia coliInfection

Typhoid fever as cellular microbiological model

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