Nitric oxide as a mediator of increased microvascular permeability during acute rickettsioses.

Michael E. Woods, Gary Wen, Juan Olano

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Rickettsiae primarily infect the microvascular endothelium, leading to changes in microvascular permeability that result in potentially severe pulmonary and cerebral edema. The mechanisms responsible for these changes are not well understood. One potential mechanism of increased vascular permeability is the anti-rickettsial nitric oxide response described by Walker and colleagues. We hypothesized that anti-rickettsial levels of nitric oxide adversely affects microvascular permeability in vitro. To this end we sought to describe the effects of exogenous nitric oxide on the proliferation of intracellular rickettsiae while monitoring the transendothelial electrical resistance as a measure of endothelial barrier integrity. It was determined that the addition of the NO-donor DETA NONOate at certain levels results in a dose-dependent change in electrical resistance across the monolayer while effectively limiting the number of intracellular rickettsiae in human microvascular endothelial cells. The data presented support the idea that nitric oxide produced by infected endothelial cells may be contributing to the changes in vascular permeability that occur during acute rickettsioses. Future experiments aim to elaborate on these results in a model that more clearly depicts the in vivo response as well as to describe the changes that occur with respect to interendothelial junctions.

Original languageEnglish (US)
Pages (from-to)239-245
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1063
DOIs
StatePublished - Dec 2005

Fingerprint

Capillary Permeability
Rickettsia
Nitric Oxide
Acoustic impedance
Endothelial cells
Electric Impedance
Endothelial Cells
Brain Edema
Pulmonary Edema
Endothelium
Monolayers
Mediator
Permeability
Monitoring
Experiments
Cells
Electrical Resistance

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Nitric oxide as a mediator of increased microvascular permeability during acute rickettsioses. / Woods, Michael E.; Wen, Gary; Olano, Juan.

In: Annals of the New York Academy of Sciences, Vol. 1063, 12.2005, p. 239-245.

Research output: Contribution to journalArticle

@article{569123b3a77349a588e61654981e75cf,
title = "Nitric oxide as a mediator of increased microvascular permeability during acute rickettsioses.",
abstract = "Rickettsiae primarily infect the microvascular endothelium, leading to changes in microvascular permeability that result in potentially severe pulmonary and cerebral edema. The mechanisms responsible for these changes are not well understood. One potential mechanism of increased vascular permeability is the anti-rickettsial nitric oxide response described by Walker and colleagues. We hypothesized that anti-rickettsial levels of nitric oxide adversely affects microvascular permeability in vitro. To this end we sought to describe the effects of exogenous nitric oxide on the proliferation of intracellular rickettsiae while monitoring the transendothelial electrical resistance as a measure of endothelial barrier integrity. It was determined that the addition of the NO-donor DETA NONOate at certain levels results in a dose-dependent change in electrical resistance across the monolayer while effectively limiting the number of intracellular rickettsiae in human microvascular endothelial cells. The data presented support the idea that nitric oxide produced by infected endothelial cells may be contributing to the changes in vascular permeability that occur during acute rickettsioses. Future experiments aim to elaborate on these results in a model that more clearly depicts the in vivo response as well as to describe the changes that occur with respect to interendothelial junctions.",
author = "Woods, {Michael E.} and Gary Wen and Juan Olano",
year = "2005",
month = "12",
doi = "10.1196/annals.1355.037",
language = "English (US)",
volume = "1063",
pages = "239--245",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Nitric oxide as a mediator of increased microvascular permeability during acute rickettsioses.

AU - Woods, Michael E.

AU - Wen, Gary

AU - Olano, Juan

PY - 2005/12

Y1 - 2005/12

N2 - Rickettsiae primarily infect the microvascular endothelium, leading to changes in microvascular permeability that result in potentially severe pulmonary and cerebral edema. The mechanisms responsible for these changes are not well understood. One potential mechanism of increased vascular permeability is the anti-rickettsial nitric oxide response described by Walker and colleagues. We hypothesized that anti-rickettsial levels of nitric oxide adversely affects microvascular permeability in vitro. To this end we sought to describe the effects of exogenous nitric oxide on the proliferation of intracellular rickettsiae while monitoring the transendothelial electrical resistance as a measure of endothelial barrier integrity. It was determined that the addition of the NO-donor DETA NONOate at certain levels results in a dose-dependent change in electrical resistance across the monolayer while effectively limiting the number of intracellular rickettsiae in human microvascular endothelial cells. The data presented support the idea that nitric oxide produced by infected endothelial cells may be contributing to the changes in vascular permeability that occur during acute rickettsioses. Future experiments aim to elaborate on these results in a model that more clearly depicts the in vivo response as well as to describe the changes that occur with respect to interendothelial junctions.

AB - Rickettsiae primarily infect the microvascular endothelium, leading to changes in microvascular permeability that result in potentially severe pulmonary and cerebral edema. The mechanisms responsible for these changes are not well understood. One potential mechanism of increased vascular permeability is the anti-rickettsial nitric oxide response described by Walker and colleagues. We hypothesized that anti-rickettsial levels of nitric oxide adversely affects microvascular permeability in vitro. To this end we sought to describe the effects of exogenous nitric oxide on the proliferation of intracellular rickettsiae while monitoring the transendothelial electrical resistance as a measure of endothelial barrier integrity. It was determined that the addition of the NO-donor DETA NONOate at certain levels results in a dose-dependent change in electrical resistance across the monolayer while effectively limiting the number of intracellular rickettsiae in human microvascular endothelial cells. The data presented support the idea that nitric oxide produced by infected endothelial cells may be contributing to the changes in vascular permeability that occur during acute rickettsioses. Future experiments aim to elaborate on these results in a model that more clearly depicts the in vivo response as well as to describe the changes that occur with respect to interendothelial junctions.

UR - http://www.scopus.com/inward/record.url?scp=33745713628&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33745713628&partnerID=8YFLogxK

U2 - 10.1196/annals.1355.037

DO - 10.1196/annals.1355.037

M3 - Article

C2 - 16481520

AN - SCOPUS:33745713628

VL - 1063

SP - 239

EP - 245

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -