Tags

Type your tag names separated by a space and hit enter

Interleukin-33 from Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model.
PLoS One 2016; 11(6):e0157571Plos

Abstract

BACKGROUND

Interleukin-33 (IL-33) activates group 2 innate lymphoid cells (ILC2), resulting in T-helper-2 inflammation in bronchial asthma. Airway epithelial cells were reported as sources of IL-33 during apoptosis and necrosis. However, IL-33 is known to be from sources other than airway epithelial cells such as leukocytes, and the mechanisms of IL-33 production and release are not fully understood. The aim of this study was to clarify the role of IL-33 production by monocytes in airway inflammation.

METHODS

BALB/c mice were sensitized and challenged with a house dust mite (HDM) preparation. Airway inflammation was assessed by quantifying inflammatory cells in bronchoalveolar lavage (BAL) fluid, and IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) levels in lung. Immunohistochemistry for IL-33 in lung sections was also performed. Ly6c, CD11b, and CD11c expression was examined by flow cytometry. Clodronate liposomes were used in the HDM-airway inflammation model to deplete circulating monocytes.

RESULTS

The IL-33, but not IL-25 or TSLP, level in lung homogenates was markedly increased in HDM mice compared to control mice. IL-33-positive cells in the lungs were identified using immunohistochemistry and were increased in areas surrounding bronchi and vasculature. Furthermore, IL-33 levels were increased in mononuclear cells derived from lungs of HDM mice compared to controls. The expression of Ly6c in mononuclear cells was significantly higher in HDM mice than in controls. Treatment with clodronate liposomes led to inhibition of not only inflammatory cells in BAL fluid, airway hyper reactivity and Th2 cytokines in lung, but also IL-33 in lung.

CONCLUSION

IL-33 from monocytes recruited to the lung may contribute to the pathogenesis of HDM-induced airway inflammation.

Authors+Show Affiliations

Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.Institute of Tokyo Environmental Allergy, Tokyo, Japan.Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.Division of Hematology, Respiratory Medicine and Oncology, Department of Internal Medicine, Faculty of Medicine, Saga University, Saga, Japan.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27310495

Citation

Tashiro, Hiroki, et al. "Interleukin-33 From Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model." PloS One, vol. 11, no. 6, 2016, pp. e0157571.
Tashiro H, Takahashi K, Hayashi S, et al. Interleukin-33 from Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model. PLoS ONE. 2016;11(6):e0157571.
Tashiro, H., Takahashi, K., Hayashi, S., Kato, G., Kurata, K., Kimura, S., & Sueoka-Aragane, N. (2016). Interleukin-33 from Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model. PloS One, 11(6), pp. e0157571. doi:10.1371/journal.pone.0157571.
Tashiro H, et al. Interleukin-33 From Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model. PLoS ONE. 2016;11(6):e0157571. PubMed PMID: 27310495.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-33 from Monocytes Recruited to the Lung Contributes to House Dust Mite-Induced Airway Inflammation in a Mouse Model. AU - Tashiro,Hiroki, AU - Takahashi,Koichiro, AU - Hayashi,Shinichiro, AU - Kato,Go, AU - Kurata,Keigo, AU - Kimura,Shinya, AU - Sueoka-Aragane,Naoko, Y1 - 2016/06/16/ PY - 2016/02/27/received PY - 2016/06/01/accepted PY - 2016/6/17/entrez PY - 2016/6/17/pubmed PY - 2017/7/14/medline SP - e0157571 EP - e0157571 JF - PloS one JO - PLoS ONE VL - 11 IS - 6 N2 - BACKGROUND: Interleukin-33 (IL-33) activates group 2 innate lymphoid cells (ILC2), resulting in T-helper-2 inflammation in bronchial asthma. Airway epithelial cells were reported as sources of IL-33 during apoptosis and necrosis. However, IL-33 is known to be from sources other than airway epithelial cells such as leukocytes, and the mechanisms of IL-33 production and release are not fully understood. The aim of this study was to clarify the role of IL-33 production by monocytes in airway inflammation. METHODS: BALB/c mice were sensitized and challenged with a house dust mite (HDM) preparation. Airway inflammation was assessed by quantifying inflammatory cells in bronchoalveolar lavage (BAL) fluid, and IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) levels in lung. Immunohistochemistry for IL-33 in lung sections was also performed. Ly6c, CD11b, and CD11c expression was examined by flow cytometry. Clodronate liposomes were used in the HDM-airway inflammation model to deplete circulating monocytes. RESULTS: The IL-33, but not IL-25 or TSLP, level in lung homogenates was markedly increased in HDM mice compared to control mice. IL-33-positive cells in the lungs were identified using immunohistochemistry and were increased in areas surrounding bronchi and vasculature. Furthermore, IL-33 levels were increased in mononuclear cells derived from lungs of HDM mice compared to controls. The expression of Ly6c in mononuclear cells was significantly higher in HDM mice than in controls. Treatment with clodronate liposomes led to inhibition of not only inflammatory cells in BAL fluid, airway hyper reactivity and Th2 cytokines in lung, but also IL-33 in lung. CONCLUSION: IL-33 from monocytes recruited to the lung may contribute to the pathogenesis of HDM-induced airway inflammation. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/27310495/Interleukin_33_from_Monocytes_Recruited_to_the_Lung_Contributes_to_House_Dust_Mite_Induced_Airway_Inflammation_in_a_Mouse_Model_ L2 - http://dx.plos.org/10.1371/journal.pone.0157571 DB - PRIME DP - Unbound Medicine ER -