Streptococcal M1 Protein-Provoked CXC Chemokine Formation, Neutrophil Recruitment and Lung Damage Are Regulated by Rho-Kinase Signaling.
Zhang, Songen LU ; Rahman, Milladur LU
; Zhang, Su
LU
; Herwald, Heiko
LU
; Qi, Zhongquan
LU
; Jeppsson, Bengt
LU
and Thorlacius, Henrik
LU
(2012)
In Journal of Innate Immunity
4(4).
p.399-408
- Abstract
- Streptococcal toxic shock syndrome is frequently caused by Streptococcus pyogenes of the M1 serotype. The aim of this study was to determine the role of Ras-homologous (Rho)-kinase signaling in M1 protein-provoked lung damage. Male C57BL/6 mice received the Rho-kinase-specific inhibitor Y-27632 before administration of M1 protein. Edema, neutrophil accumulation and CXC chemokines were quantified in the lung 4 h after M1 protein challenge. Flow cytometry was used to determine Mac-1 expression. Quantitative RT-PCR was used to determine gene expression of CXC chemokine mRNA in alveolar macrophages. M1 protein increased neutrophil accumulation, edema and CXC chemokine formation in the lung as well as enhanced Mac-1 expression on neutrophils.... (More)
- Streptococcal toxic shock syndrome is frequently caused by Streptococcus pyogenes of the M1 serotype. The aim of this study was to determine the role of Ras-homologous (Rho)-kinase signaling in M1 protein-provoked lung damage. Male C57BL/6 mice received the Rho-kinase-specific inhibitor Y-27632 before administration of M1 protein. Edema, neutrophil accumulation and CXC chemokines were quantified in the lung 4 h after M1 protein challenge. Flow cytometry was used to determine Mac-1 expression. Quantitative RT-PCR was used to determine gene expression of CXC chemokine mRNA in alveolar macrophages. M1 protein increased neutrophil accumulation, edema and CXC chemokine formation in the lung as well as enhanced Mac-1 expression on neutrophils. Inhibition of Rho-kinase signaling significantly reduced M1 protein-provoked neutrophil accumulation and edema formation in the lung. M1 protein-triggered pulmonary production of CXC chemokine and gene expression of CXC chemokines in alveolar macrophages was decreased by Y-27632. Moreover, Rho-kinase inhibition attenuated M1 protein-induced Mac-1 expression on neutrophils. We conclude that Rho-kinase-dependent neutrophil infiltration controls pulmonary tissue damage in response to streptococcal M1 protein and that Rho-kinase signaling regulates M1 protein-induced lung recruitment of neutrophils via the formation of CXC chemokines and Mac-1 expression. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2431610
- author
- Zhang, Songen
LU
; Rahman, Milladur
LU
; Zhang, Su
LU
; Herwald, Heiko
LU
; Qi, Zhongquan
LU
; Jeppsson, Bengt
LU
and Thorlacius, Henrik
LU
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Innate Immunity
- volume
- 4
- issue
- 4
- pages
- 399 - 408
- publisher
- Karger
- external identifiers
-
- wos:000305819800009
- pmid:22433673
- scopus:84863309800
- pmid:22433673
- ISSN
- 1662-811X
- DOI
- 10.1159/000336182
- language
- English
- LU publication?
- yes
- id
- db3cb0b8-7041-4fe8-8df5-4566e70f6895 (old id 2431610)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22433673?dopt=Abstract
- date added to LUP
- 2016-04-01 10:23:47
- date last changed
- 2022-04-27 21:40:44
@article{db3cb0b8-7041-4fe8-8df5-4566e70f6895,
abstract = {{Streptococcal toxic shock syndrome is frequently caused by Streptococcus pyogenes of the M1 serotype. The aim of this study was to determine the role of Ras-homologous (Rho)-kinase signaling in M1 protein-provoked lung damage. Male C57BL/6 mice received the Rho-kinase-specific inhibitor Y-27632 before administration of M1 protein. Edema, neutrophil accumulation and CXC chemokines were quantified in the lung 4 h after M1 protein challenge. Flow cytometry was used to determine Mac-1 expression. Quantitative RT-PCR was used to determine gene expression of CXC chemokine mRNA in alveolar macrophages. M1 protein increased neutrophil accumulation, edema and CXC chemokine formation in the lung as well as enhanced Mac-1 expression on neutrophils. Inhibition of Rho-kinase signaling significantly reduced M1 protein-provoked neutrophil accumulation and edema formation in the lung. M1 protein-triggered pulmonary production of CXC chemokine and gene expression of CXC chemokines in alveolar macrophages was decreased by Y-27632. Moreover, Rho-kinase inhibition attenuated M1 protein-induced Mac-1 expression on neutrophils. We conclude that Rho-kinase-dependent neutrophil infiltration controls pulmonary tissue damage in response to streptococcal M1 protein and that Rho-kinase signaling regulates M1 protein-induced lung recruitment of neutrophils via the formation of CXC chemokines and Mac-1 expression.}},
author = {{Zhang, Songen and Rahman, Milladur and Zhang, Su and Herwald, Heiko and Qi, Zhongquan and Jeppsson, Bengt and Thorlacius, Henrik}},
issn = {{1662-811X}},
language = {{eng}},
number = {{4}},
pages = {{399--408}},
publisher = {{Karger}},
series = {{Journal of Innate Immunity}},
title = {{Streptococcal M1 Protein-Provoked CXC Chemokine Formation, Neutrophil Recruitment and Lung Damage Are Regulated by Rho-Kinase Signaling.}},
url = {{https://lup.lub.lu.se/search/files/1809660/3688050.pdf}},
doi = {{10.1159/000336182}},
volume = {{4}},
year = {{2012}},
}