Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease

Atsushi Sumida, Yoshinori Hasegawa, Masakazu Okamoto, Naozumi Hashimoto, Kazuyoshi Imaizumi, Hiroshi Yatsuya, Toyoharu Yokoi, Kenzo Takagi, Kaoru Shimokata, Tsutomu Kawabe

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background: Inflammatory response in pulmonary fibrosis closely resembles a T-helper (Th) 2 immune response. For recruitment to an inflammatory lesion, the majority of Th1 cells express CXC chemokine receptor 3, recognizing monokine induced by interferon-gamma (Mig), interferon γ-inducible protein of 10 kD (IP-10), and interferon-inducible T-cell α chemoattractant (I-TAC). Th2 cells express CC chemokine receptor 4, recognizing thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). We investigated the Th1/Th2 chemokine production patterns by lung fibroblasts and their evaluation in bronchoalveolar lavage (BAL) fluid of interstitial lung disease. Methods: The production pattern of Th1/Th2 chemokines by lung fibroblasts was examined in ELISA and quantitative reverse transcriptase polymerase chain reactions. Th1/Th2 chemokine levels in BAL fluid of idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP) were examined to evaluate the clinical relevance of Th1/Th2 chemokines. Results: The lung fibroblasts were polarized to produce Th1-type chemokines by the pro-inflammatory cytokine, tumor necrosis factor (TNF)-α and the anti-fibrotic cytokine, interferon (IFN)-γ. However, the induction patterns of chemokines by these two cytokines were different, i.e., involving predominant induction of IP-10 and I-TAC by TNF-α and induction of Mig by IFN-γ. Although Mig, IP-10, and I-TAC were produced within the BAL fluid of patients, TARC and MDC were at significantly low levels. Conclusions: Our results suggest that lung fibroblasts tend to induce a Th1-type immune response under normal conditions, and that a Th2-type immune response does not play a significant role in smoldering inflammation around the established lesions in IPF and NSIP.

Original languageEnglish
Pages (from-to)503-510
Number of pages8
JournalArchives of Medical Research
Volume39
Issue number5
DOIs
Publication statusPublished - 01-07-2008
Externally publishedYes

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Interstitial Lung Diseases
Chemokines
Fibroblasts
Lung
Chemotactic Factors
Bronchoalveolar Lavage Fluid
Chemokine CCL22
Chemokine CCL17
Interferons
Idiopathic Pulmonary Fibrosis
Cytokines
T-Lymphocytes
Interferon-gamma
CCR4 Receptors
CXCR3 Receptors
Tumor Necrosis Factor-alpha
Chemokine CXCL10
Monokines
Th2 Cells
Th1 Cells

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Sumida, A., Hasegawa, Y., Okamoto, M., Hashimoto, N., Imaizumi, K., Yatsuya, H., ... Kawabe, T. (2008). Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease. Archives of Medical Research, 39(5), 503-510. https://doi.org/10.1016/j.arcmed.2008.02.005
Sumida, Atsushi ; Hasegawa, Yoshinori ; Okamoto, Masakazu ; Hashimoto, Naozumi ; Imaizumi, Kazuyoshi ; Yatsuya, Hiroshi ; Yokoi, Toyoharu ; Takagi, Kenzo ; Shimokata, Kaoru ; Kawabe, Tsutomu. / Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease. In: Archives of Medical Research. 2008 ; Vol. 39, No. 5. pp. 503-510.
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Sumida, A, Hasegawa, Y, Okamoto, M, Hashimoto, N, Imaizumi, K, Yatsuya, H, Yokoi, T, Takagi, K, Shimokata, K & Kawabe, T 2008, 'Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease', Archives of Medical Research, vol. 39, no. 5, pp. 503-510. https://doi.org/10.1016/j.arcmed.2008.02.005

Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease. / Sumida, Atsushi; Hasegawa, Yoshinori; Okamoto, Masakazu; Hashimoto, Naozumi; Imaizumi, Kazuyoshi; Yatsuya, Hiroshi; Yokoi, Toyoharu; Takagi, Kenzo; Shimokata, Kaoru; Kawabe, Tsutomu.

In: Archives of Medical Research, Vol. 39, No. 5, 01.07.2008, p. 503-510.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Th1/Th2 Immune Response in Lung Fibroblasts in Interstitial Lung Disease

AU - Sumida, Atsushi

AU - Hasegawa, Yoshinori

AU - Okamoto, Masakazu

AU - Hashimoto, Naozumi

AU - Imaizumi, Kazuyoshi

AU - Yatsuya, Hiroshi

AU - Yokoi, Toyoharu

AU - Takagi, Kenzo

AU - Shimokata, Kaoru

AU - Kawabe, Tsutomu

PY - 2008/7/1

Y1 - 2008/7/1

N2 - Background: Inflammatory response in pulmonary fibrosis closely resembles a T-helper (Th) 2 immune response. For recruitment to an inflammatory lesion, the majority of Th1 cells express CXC chemokine receptor 3, recognizing monokine induced by interferon-gamma (Mig), interferon γ-inducible protein of 10 kD (IP-10), and interferon-inducible T-cell α chemoattractant (I-TAC). Th2 cells express CC chemokine receptor 4, recognizing thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). We investigated the Th1/Th2 chemokine production patterns by lung fibroblasts and their evaluation in bronchoalveolar lavage (BAL) fluid of interstitial lung disease. Methods: The production pattern of Th1/Th2 chemokines by lung fibroblasts was examined in ELISA and quantitative reverse transcriptase polymerase chain reactions. Th1/Th2 chemokine levels in BAL fluid of idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP) were examined to evaluate the clinical relevance of Th1/Th2 chemokines. Results: The lung fibroblasts were polarized to produce Th1-type chemokines by the pro-inflammatory cytokine, tumor necrosis factor (TNF)-α and the anti-fibrotic cytokine, interferon (IFN)-γ. However, the induction patterns of chemokines by these two cytokines were different, i.e., involving predominant induction of IP-10 and I-TAC by TNF-α and induction of Mig by IFN-γ. Although Mig, IP-10, and I-TAC were produced within the BAL fluid of patients, TARC and MDC were at significantly low levels. Conclusions: Our results suggest that lung fibroblasts tend to induce a Th1-type immune response under normal conditions, and that a Th2-type immune response does not play a significant role in smoldering inflammation around the established lesions in IPF and NSIP.

AB - Background: Inflammatory response in pulmonary fibrosis closely resembles a T-helper (Th) 2 immune response. For recruitment to an inflammatory lesion, the majority of Th1 cells express CXC chemokine receptor 3, recognizing monokine induced by interferon-gamma (Mig), interferon γ-inducible protein of 10 kD (IP-10), and interferon-inducible T-cell α chemoattractant (I-TAC). Th2 cells express CC chemokine receptor 4, recognizing thymus- and activation-regulated chemokine (TARC) and macrophage-derived chemokine (MDC). We investigated the Th1/Th2 chemokine production patterns by lung fibroblasts and their evaluation in bronchoalveolar lavage (BAL) fluid of interstitial lung disease. Methods: The production pattern of Th1/Th2 chemokines by lung fibroblasts was examined in ELISA and quantitative reverse transcriptase polymerase chain reactions. Th1/Th2 chemokine levels in BAL fluid of idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP) were examined to evaluate the clinical relevance of Th1/Th2 chemokines. Results: The lung fibroblasts were polarized to produce Th1-type chemokines by the pro-inflammatory cytokine, tumor necrosis factor (TNF)-α and the anti-fibrotic cytokine, interferon (IFN)-γ. However, the induction patterns of chemokines by these two cytokines were different, i.e., involving predominant induction of IP-10 and I-TAC by TNF-α and induction of Mig by IFN-γ. Although Mig, IP-10, and I-TAC were produced within the BAL fluid of patients, TARC and MDC were at significantly low levels. Conclusions: Our results suggest that lung fibroblasts tend to induce a Th1-type immune response under normal conditions, and that a Th2-type immune response does not play a significant role in smoldering inflammation around the established lesions in IPF and NSIP.

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