TLR2 contributes to trigger immune response of pleural mesothelial cells against Mycobacterium bovis BCG and M. tuberculosis infection

Eun Ha Hwanga, Tae Hyoun Kim, Ji Yeon Park, Jung Joo Hong, Dong Hyun Kim, Sang-Jun Ha, Soo Jin Yang, SungJae Shin, Jong Hwan Park

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Mycobacterium tuberculosis is a causative agent leading to pleural effusion, characterized by the accumulation of fluid and immune cells in the pleural cavity. Although this phenomenon has been described before, detailed processes or mechanisms associated with the pleural effusion are still not well understood. Pleural mesothelial cells (PMCs) are specialized epithelial cells that cover the body wall and internal organs in pleural cavity playing a central role in pleural inflammation. Toll-like receptors are expressed in various cell types including mesothelial cells and initiate the recognition and defense against mycobacterial infection. In the present study, we investigated direct immune responses of PMCs against two mycobacterial strains, M. bovis vaccine strain Bacille Calmette-Guérin (BCG) and M. tuberculosis virulent strain H37Rv, and the role of TLR2 in such responses. Infection with BCG and H37Rv increased the production of IL-6, CXCL1, and CCL2 in WT PMCs, which was partially impaired in TLR2-deficient cells. In addition, the activation of NF-κB and MAPKs induced by BCG and H37Rv was suppressed in TLR2-deficient PMCs, as compared with the WT cells. TLR2 deficiency led to the decrease of nitric oxide (NO) production through the delayed gene expression of iNOS in PMCs. TLR2 was also shown to be essential for optimal expression of cellular adhesion molecules such as ICAM-1 and VCAM-1 in PMCs in response to BCG and H37Rv. These findings strongly suggest that TLR2 participates in mycobacteria-induced innate immune responses in PMCs and may play a role in pathogenesis of tuberculosis pleural effusion.

Original languageEnglish
Pages (from-to)80-87
Number of pages8
JournalCytokine
Volume95
DOIs
Publication statusPublished - 2017 Jul 1

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Mycobacterium bovis
Tuberculosis
Vascular Cell Adhesion Molecule-1
Toll-Like Receptors
Intercellular Adhesion Molecule-1
Infection
Gene expression
Interleukin-6
Nitric Oxide
Adhesion
Vaccines
Chemical activation
Molecules
Fluids
Pleural Effusion
Pleural Cavity
Mycobacterium tuberculosis
Mycobacterium
Innate Immunity
Epithelial Cells

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

Cite this

Hwanga, Eun Ha ; Kim, Tae Hyoun ; Park, Ji Yeon ; Hong, Jung Joo ; Kim, Dong Hyun ; Ha, Sang-Jun ; Yang, Soo Jin ; Shin, SungJae ; Park, Jong Hwan. / TLR2 contributes to trigger immune response of pleural mesothelial cells against Mycobacterium bovis BCG and M. tuberculosis infection. In: Cytokine. 2017 ; Vol. 95. pp. 80-87.
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abstract = "Mycobacterium tuberculosis is a causative agent leading to pleural effusion, characterized by the accumulation of fluid and immune cells in the pleural cavity. Although this phenomenon has been described before, detailed processes or mechanisms associated with the pleural effusion are still not well understood. Pleural mesothelial cells (PMCs) are specialized epithelial cells that cover the body wall and internal organs in pleural cavity playing a central role in pleural inflammation. Toll-like receptors are expressed in various cell types including mesothelial cells and initiate the recognition and defense against mycobacterial infection. In the present study, we investigated direct immune responses of PMCs against two mycobacterial strains, M. bovis vaccine strain Bacille Calmette-Gu{\'e}rin (BCG) and M. tuberculosis virulent strain H37Rv, and the role of TLR2 in such responses. Infection with BCG and H37Rv increased the production of IL-6, CXCL1, and CCL2 in WT PMCs, which was partially impaired in TLR2-deficient cells. In addition, the activation of NF-κB and MAPKs induced by BCG and H37Rv was suppressed in TLR2-deficient PMCs, as compared with the WT cells. TLR2 deficiency led to the decrease of nitric oxide (NO) production through the delayed gene expression of iNOS in PMCs. TLR2 was also shown to be essential for optimal expression of cellular adhesion molecules such as ICAM-1 and VCAM-1 in PMCs in response to BCG and H37Rv. These findings strongly suggest that TLR2 participates in mycobacteria-induced innate immune responses in PMCs and may play a role in pathogenesis of tuberculosis pleural effusion.",
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TLR2 contributes to trigger immune response of pleural mesothelial cells against Mycobacterium bovis BCG and M. tuberculosis infection. / Hwanga, Eun Ha; Kim, Tae Hyoun; Park, Ji Yeon; Hong, Jung Joo; Kim, Dong Hyun; Ha, Sang-Jun; Yang, Soo Jin; Shin, SungJae; Park, Jong Hwan.

In: Cytokine, Vol. 95, 01.07.2017, p. 80-87.

Research output: Contribution to journalArticle

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AU - Hwanga, Eun Ha

AU - Kim, Tae Hyoun

AU - Park, Ji Yeon

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AU - Kim, Dong Hyun

AU - Ha, Sang-Jun

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AU - Park, Jong Hwan

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