Inhibition of polymorphonuclear leukocyte function by Legionella pneumophila exoproducts

Sahney, Narendra N.; Lambe, Beverly C.; Summersgill, James T.; Miller, Richard D.

doi:10.1016/0882-4010(90)90085-5

Cited by 18 publications

(10 citation statements)

References 20 publications

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“…Rechnitzer and Kharazmi [34] have shown that low levels of protease had inhibitory effects on the chemotaxis and bactericidal activity of human polymorphonuclear leucocytes (PMNLs), but had no effect on the oxidative burst or phagocytosis by PMNLs and monocytes. In contrast, another study reported that total exoproducts from a proteasede®cient mutant of L. pneumophila were unable to inhibit superoxide anion generation and chemotaxis (by PMNLs), compared with the inhibitory activity demonstrated by total exoproducts from the wild-type strains [35]. These results suggested that the L. pneumophila protease was responsible for the inhibitory effects on the oxidative burst and chemotaxis of PMNLs.…”

Section: Introductioncontrasting

confidence: 46%

Inhibition of oxidative burst and chemotaxis in human phagocytes by Legionella pneumophila zinc metalloprotease

Sahney¹,

Summersgill

Ramirez

et al. 2001

Journal of Medical Microbiology

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Section: Introductioncontrasting

confidence: 46%

Inhibition of oxidative burst and chemotaxis in human phagocytes by Legionella pneumophila zinc metalloprotease

Sahney¹,

Summersgill

Ramirez

et al. 2001

Journal of Medical Microbiology

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“…These data demonstrate that down-regulation of gp91 phox mRNA levels also occurs in vivo. Diverse pathogens, including Legionella pneumophila, Toxoplasma gondii, Chlamydia, Ehrlichia risticii (which infects macrophages), Entamoeba histolytica, and Leishmania, have been shown to inhibit the respiratory burst; however, the mechanism(s) is (are) not known (23)(24)(25)(26)(27)(28). Suppression of NADPH oxidase activity by down-regulating expression of a critical subunit of the enzyme complex by HGE bacteria represents a new mechanism by which microbes circumvent the oxidant-generating respiratory burst.…”

Section: Resultsmentioning

confidence: 99%

Cutting Edge: Infection by the Agent of Human Granulocytic Ehrlichiosis Prevents the Respiratory Burst by Down-Regulatinggp91phox

Banerjee

Anguíta

Roos

et al. 2000

The Journal of Immunology

113

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The agent of human granulocytic ehrlichiosis (HGE) is an emerging tick-borne pathogen that resides in neutrophils and can be cultured in a promyelocytic (HL-60) cell line. In response to microbes, polymorphonuclear leukocytes normally activate the NADPH oxidase enzyme complex and generate superoxide anion (O2−). However, HL-60 cells infected with HGE bacteria did not produce O2− upon activation with PMA. RT-PCR demonstrated that HGE organisms inhibited mRNA expression of a single component of NADPH oxidase, gp91phox, and FACS analysis showed that plasma membrane-associated gp91phox protein was reduced on the infected cells. Infection with HGE organisms also decreased gp91phox mRNA levels in splenic neutrophils in a murine model of HGE, demonstrating this phenomenon in vivo. Therefore, HGE bacteria repress the respiratory burst by down-regulating gp91phox, the first direct inhibition of NADPH oxidase by a pathogen.

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“…This inhibition of macrophage protein kinase C activity also impedes macrophage chemotactic locomotion and interleukin-1 (IL-1) production. Legionella pneumophila se- cretes a compound shown to inhibit the neutrophil oxidative burst (272). Leishmania donovani (114) and Legionella micdadei (271) produce extracellular acidic phosphatases that block ⅐ O 2…”

Section: Defense Strategies Specific For Oxidantsmentioning

confidence: 99%

Role of oxidants in microbial pathophysiology

1997

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Reactive oxidant species (superoxide, hydrogen peroxide, hydroxyl radical, hypohalous acid, and nitric oxide) are involved in many of the complex interactions between the invading microorganism and its host. Regardless of the source of these compounds or whether they are produced under normal conditions or those of oxidative stress, these oxidants exhibit a broad range of toxic effects to biomolecules that are essential for cell survival. Production of these oxidants by microorganisms enables them to have a survival advantage in their environment. Host oxidant production, especially by phagocytes, is a counteractive mechanism aimed at microbial killing. However, this mechanism may be contribute to a deleterious consequence of oxidant exposure, i.e., inflammatory tissue injury. Both the host and the microorganism have evolved complex adaptive mechanisms to deflect oxidant-mediated damage, including enzymatic and nonenzymatic oxidant-scavenging systems. This review discusses the formation of reactive oxidant species in vivo and how they mediate many of the processes involved in the complex interplay between microbial invasion and host defense.

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Inhibition of polymorphonuclear leukocyte function by Legionella pneumophila exoproducts

Cited by 18 publications

References 20 publications

Inhibition of oxidative burst and chemotaxis in human phagocytes by Legionella pneumophila zinc metalloprotease

Inhibition of oxidative burst and chemotaxis in human phagocytes by Legionella pneumophila zinc metalloprotease

Cutting Edge: Infection by the Agent of Human Granulocytic Ehrlichiosis Prevents the Respiratory Burst by Down-Regulatinggp91phox

Role of oxidants in microbial pathophysiology

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