YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia

Angelene M. Cantwell, Sarah S. Bubeck, Peter H Dube

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection.Conclusions: Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.

Original languageEnglish (US)
Article number29
JournalBMC Immunology
Volume11
DOIs
StatePublished - Jun 16 2010

Fingerprint

Plague
Pneumonia
Cytokines
Infection
Lung
Yersinia pestis
Spleen
Tumor Necrosis Factor-alpha
Hepatitis D
Interleukins
Liver

ASJC Scopus subject areas

  • Immunology

Cite this

YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia. / Cantwell, Angelene M.; Bubeck, Sarah S.; Dube, Peter H.

In: BMC Immunology, Vol. 11, 29, 16.06.2010.

Research output: Contribution to journalArticle

@article{507f2ec7ee754ca89e38ac4ed0761a4b,
title = "YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia",
abstract = "Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40{\%} of the mice succumbing to infection.Conclusions: Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.",
author = "Cantwell, {Angelene M.} and Bubeck, {Sarah S.} and Dube, {Peter H}",
year = "2010",
month = "6",
day = "16",
doi = "10.1186/1471-2172-11-29",
language = "English (US)",
volume = "11",
journal = "BMC Immunology",
issn = "1471-2172",
publisher = "BioMed Central",

}

TY - JOUR

T1 - YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia

AU - Cantwell, Angelene M.

AU - Bubeck, Sarah S.

AU - Dube, Peter H

PY - 2010/6/16

Y1 - 2010/6/16

N2 - Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection.Conclusions: Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.

AB - Background: Yersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.Results: Here, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection.Conclusions: Altogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.

UR - http://www.scopus.com/inward/record.url?scp=77953519103&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77953519103&partnerID=8YFLogxK

U2 - 10.1186/1471-2172-11-29

DO - 10.1186/1471-2172-11-29

M3 - Article

C2 - 20565713

AN - SCOPUS:77953519103

VL - 11

JO - BMC Immunology

JF - BMC Immunology

SN - 1471-2172

M1 - 29

ER -