Mycobacterium bovis bacilli Calmette-Guerin regulates leukocyte recruitment by modulating alveolar inflammatory responses.
Andersson, Märta ; Lutay, Nataliya LU ; Hallgren, Oscar ; Westergren-Thorsson, Gunilla LU
; Svensson, Majlis
LU
and Godaly, Gabriela
LU
(2012)
In Innate Immunity
18.
p.531-540
- Abstract
- Leukocyte migration into the epithelial compartment is an important feature in the active phase of mycobacterial infections. In this study, we used the Transwell model to investigate the mechanisms behind mycobacteria-induced leukocyte recruitment and investigated the role of TLR2 and TLR4 in this process. Infection of epithelial cells resulted in significantly increased secretion of the neutrophil chemotactic CXCL8 and IL-6, but no secretion of monocyte chemotactic CCL2 or TNF-α was observed. In contrast to epithelial response, mycobacteria-infected neutrophils and monocytes secreted all these cytokines. Corresponding with epithelial cytokine response, mycobacterial infection of the epithelial cells increased neutrophil diapedesis, but... (More)
- Leukocyte migration into the epithelial compartment is an important feature in the active phase of mycobacterial infections. In this study, we used the Transwell model to investigate the mechanisms behind mycobacteria-induced leukocyte recruitment and investigated the role of TLR2 and TLR4 in this process. Infection of epithelial cells resulted in significantly increased secretion of the neutrophil chemotactic CXCL8 and IL-6, but no secretion of monocyte chemotactic CCL2 or TNF-α was observed. In contrast to epithelial response, mycobacteria-infected neutrophils and monocytes secreted all these cytokines. Corresponding with epithelial cytokine response, mycobacterial infection of the epithelial cells increased neutrophil diapedesis, but decreased monocyte recruitment. However, monocyte recruitment towards mycobacteria infected epithelial cells significantly increased following addition of neutrophil pre-conditioned medium. Mycobacterial infection also increases alveolar epithelial expression of TLR2, but not TLR4, as analyzed by flow cytometry, Western blotting and visualized by confocal microscopy. Blocking of TLR2 inhibited neutrophil recruitment and cytokine secretion, while blocking of TLR4 had a lesser effect. To summarize, we found that primary alveolar epithelial cells produced a selective TLR2-dependent cytokine secretion upon mycobacterial infection. Furthermore, we found that cooperation between cells of the innate immunity is required in mounting proper antimicrobial defence. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2221074
- author
- Andersson, Märta
; Lutay, Nataliya
LU
; Hallgren, Oscar
; Westergren-Thorsson, Gunilla
LU
; Svensson, Majlis
LU
and Godaly, Gabriela
LU
- organization
- publishing date
- 2012
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Innate Immunity
- volume
- 18
- pages
- 531 - 540
- publisher
- SAGE Publications
- external identifiers
-
- wos:000304699600016
- pmid:22058091
- scopus:84861806054
- pmid:22058091
- ISSN
- 1753-4267
- DOI
- 10.1177/1753425911426591
- language
- English
- LU publication?
- yes
- id
- 27a60702-e92f-440c-bad9-5d52878f954f (old id 2221074)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22058091?dopt=Abstract
- date added to LUP
- 2016-04-01 10:21:43
- date last changed
- 2024-01-06 14:45:46
@article{27a60702-e92f-440c-bad9-5d52878f954f,
abstract = {{Leukocyte migration into the epithelial compartment is an important feature in the active phase of mycobacterial infections. In this study, we used the Transwell model to investigate the mechanisms behind mycobacteria-induced leukocyte recruitment and investigated the role of TLR2 and TLR4 in this process. Infection of epithelial cells resulted in significantly increased secretion of the neutrophil chemotactic CXCL8 and IL-6, but no secretion of monocyte chemotactic CCL2 or TNF-α was observed. In contrast to epithelial response, mycobacteria-infected neutrophils and monocytes secreted all these cytokines. Corresponding with epithelial cytokine response, mycobacterial infection of the epithelial cells increased neutrophil diapedesis, but decreased monocyte recruitment. However, monocyte recruitment towards mycobacteria infected epithelial cells significantly increased following addition of neutrophil pre-conditioned medium. Mycobacterial infection also increases alveolar epithelial expression of TLR2, but not TLR4, as analyzed by flow cytometry, Western blotting and visualized by confocal microscopy. Blocking of TLR2 inhibited neutrophil recruitment and cytokine secretion, while blocking of TLR4 had a lesser effect. To summarize, we found that primary alveolar epithelial cells produced a selective TLR2-dependent cytokine secretion upon mycobacterial infection. Furthermore, we found that cooperation between cells of the innate immunity is required in mounting proper antimicrobial defence.}},
author = {{Andersson, Märta and Lutay, Nataliya and Hallgren, Oscar and Westergren-Thorsson, Gunilla and Svensson, Majlis and Godaly, Gabriela}},
issn = {{1753-4267}},
language = {{eng}},
pages = {{531--540}},
publisher = {{SAGE Publications}},
series = {{Innate Immunity}},
title = {{Mycobacterium bovis bacilli Calmette-Guerin regulates leukocyte recruitment by modulating alveolar inflammatory responses.}},
url = {{https://lup.lub.lu.se/search/files/1781426/2363983.pdf}},
doi = {{10.1177/1753425911426591}},
volume = {{18}},
year = {{2012}},
}