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Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation.
J Allergy Clin Immunol 2008; 122(6):1208-14JA

Abstract

BACKGROUND

Both active and passive smoking are considered to be risk factors for asthma development. However, the precise mechanisms involved remain elusive. Recently, thymic stromal lymphopoietin (TSLP) has been shown to play a key role in the development of T(H)2-type allergic inflammation in patients with asthma.

OBJECTIVE

The aim of this study was to investigate whether there was a causal relationship between cigarette smoke exposure and TSLP expression in the lung.

METHODS

We examined the effects of repeated intranasal exposure of cigarette smoke extract (CSE) on TSLP mRNA and protein expression in the mouse lung by means of real-time PCR, Western blotting, and immunohistochemistry. We also examined the effects of intranasal exposure of CSE plus ovalbumin (OVA) on T(H)2-type immune responses and lung pathology.

RESULTS

Repeated exposure of CSE induced TSLP mRNA and protein expression, which was inhibited by treatment with antioxidative N-acetylcysteine and by TNF-alpha receptor I deficiency. In addition, the intranasal exposure of CSE simultaneously with OVA induced OVA-specific T(H)2-type immune responses and airway inflammation, which were inhibited by the blockade of the TSLP activity.

CONCLUSION

CSE induced TSLP expression in the mouse lung in an oxidative stress-dependent and TNF-alpha receptor I-dependent manner, and when challenged simultaneously with an antigen, CSE promoted the development of airway inflammation in association with T(H)2-type immune responses.

Authors+Show Affiliations

Department of Immunology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18926564

Citation

Nakamura, Yuki, et al. "Cigarette Smoke Extract Induces Thymic Stromal Lymphopoietin Expression, Leading to T(H)2-type Immune Responses and Airway Inflammation." The Journal of Allergy and Clinical Immunology, vol. 122, no. 6, 2008, pp. 1208-14.
Nakamura Y, Miyata M, Ohba T, et al. Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation. J Allergy Clin Immunol. 2008;122(6):1208-14.
Nakamura, Y., Miyata, M., Ohba, T., Ando, T., Hatsushika, K., Suenaga, F., ... Nakao, A. (2008). Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation. The Journal of Allergy and Clinical Immunology, 122(6), pp. 1208-14. doi:10.1016/j.jaci.2008.09.022.
Nakamura Y, et al. Cigarette Smoke Extract Induces Thymic Stromal Lymphopoietin Expression, Leading to T(H)2-type Immune Responses and Airway Inflammation. J Allergy Clin Immunol. 2008;122(6):1208-14. PubMed PMID: 18926564.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to T(H)2-type immune responses and airway inflammation. AU - Nakamura,Yuki, AU - Miyata,Masanori, AU - Ohba,Tetsuro, AU - Ando,Takashi, AU - Hatsushika,Kyosuke, AU - Suenaga,Fumiko, AU - Shimokawa,Naomi, AU - Ohnuma,Yuko, AU - Katoh,Ryohei, AU - Ogawa,Hideoki, AU - Nakao,Atsuhito, Y1 - 2008/10/16/ PY - 2008/02/07/received PY - 2008/07/22/revised PY - 2008/09/15/accepted PY - 2008/10/18/entrez PY - 2008/10/18/pubmed PY - 2009/1/24/medline SP - 1208 EP - 14 JF - The Journal of allergy and clinical immunology JO - J. Allergy Clin. Immunol. VL - 122 IS - 6 N2 - BACKGROUND: Both active and passive smoking are considered to be risk factors for asthma development. However, the precise mechanisms involved remain elusive. Recently, thymic stromal lymphopoietin (TSLP) has been shown to play a key role in the development of T(H)2-type allergic inflammation in patients with asthma. OBJECTIVE: The aim of this study was to investigate whether there was a causal relationship between cigarette smoke exposure and TSLP expression in the lung. METHODS: We examined the effects of repeated intranasal exposure of cigarette smoke extract (CSE) on TSLP mRNA and protein expression in the mouse lung by means of real-time PCR, Western blotting, and immunohistochemistry. We also examined the effects of intranasal exposure of CSE plus ovalbumin (OVA) on T(H)2-type immune responses and lung pathology. RESULTS: Repeated exposure of CSE induced TSLP mRNA and protein expression, which was inhibited by treatment with antioxidative N-acetylcysteine and by TNF-alpha receptor I deficiency. In addition, the intranasal exposure of CSE simultaneously with OVA induced OVA-specific T(H)2-type immune responses and airway inflammation, which were inhibited by the blockade of the TSLP activity. CONCLUSION: CSE induced TSLP expression in the mouse lung in an oxidative stress-dependent and TNF-alpha receptor I-dependent manner, and when challenged simultaneously with an antigen, CSE promoted the development of airway inflammation in association with T(H)2-type immune responses. SN - 1097-6825 UR - https://www.unboundmedicine.com/medline/citation/18926564/Cigarette_smoke_extract_induces_thymic_stromal_lymphopoietin_expression_leading_to_T_H_2_type_immune_responses_and_airway_inflammation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(08)01686-2 DB - PRIME DP - Unbound Medicine ER -