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Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model.
PLoS One 2017; 12(1):e0169353Plos

Abstract

BACKGROUND

The proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). However, the mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown.

OBJECTIVES

In this study, we assessed the contribution of IL-17A to eosinophil-related inflammation via the CCL7/CCR3 pathway in experimental allergic rhinitis.

METHODS

IL-17A knockout (KO) and wild-type (WT) BALB/c mice were injected intraperitoneally and challenged intranasally with OVA to induce allergic rhinitis. Various parameters of the allergic response were evaluated, and mRNA and protein levels of CCL7 and CCR3 in nasal tissue and serum were compared between the two groups. The chemotactic response to CCL7 with or without IL-17A in bone marrow-derived eosinophils (bmEos) from BALB/c mice was measured.

RESULTS

In the allergic rhinitis model, IL-17A deficiency significantly decreased nasal symptoms, serum IgE levels, and eosinophil recruitment to the nasal mucosa. CCL7 and CCR3 mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice. BmEos showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence.

CONCLUSION

The suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway.

Authors+Show Affiliations

Department of Otorhinolaryngology-head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea. Research Center for Sensory Organs, and Institute of Allergy, Seoul, Korea.Department of Otorhinolaryngology-head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea.Department of Otorhinolaryngology-head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea.Department of Otorhinolaryngology-head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea. Research Center for Sensory Organs, and Institute of Allergy, Seoul, Korea. Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, Gyeonggido.Department of Otorhinolaryngology-head and Neck Surgery, Seoul National University College of Medicine, Seoul, Korea. Research Center for Sensory Organs, and Institute of Allergy, Seoul, Korea. Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University Bundang Hospital, Seongnam, Gyeonggido. Clinical Immunology, Seoul National University Medical Research Center, Seoul, Korea.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28046055

Citation

Zhang, Yu-Lian, et al. "Role of Interleukin-17A On the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model." PloS One, vol. 12, no. 1, 2017, pp. e0169353.
Zhang YL, Han DH, Kim DY, et al. Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model. PLoS ONE. 2017;12(1):e0169353.
Zhang, Y. L., Han, D. H., Kim, D. Y., Lee, C. H., & Rhee, C. S. (2017). Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model. PloS One, 12(1), pp. e0169353. doi:10.1371/journal.pone.0169353.
Zhang YL, et al. Role of Interleukin-17A On the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model. PLoS ONE. 2017;12(1):e0169353. PubMed PMID: 28046055.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of Interleukin-17A on the Chemotactic Responses to CCL7 in a Murine Allergic Rhinitis Model. AU - Zhang,Yu-Lian, AU - Han,Doo Hee, AU - Kim,Dong-Young, AU - Lee,Chul Hee, AU - Rhee,Chae-Seo, Y1 - 2017/01/03/ PY - 2016/10/13/received PY - 2016/12/15/accepted PY - 2017/1/4/entrez PY - 2017/1/4/pubmed PY - 2017/8/15/medline SP - e0169353 EP - e0169353 JF - PloS one JO - PLoS ONE VL - 12 IS - 1 N2 - BACKGROUND: The proinflammatory cytokine interleukin (IL)-17A is associated with eosinophil infiltration into the nasal mucosa in a mouse model of ovalbumin-induced allergic rhinitis. Chemotaxis of eosinophils is mediated primarily through C-C chemokine receptor type 3 (CCR3). However, the mechanism underlying the IL-17A-mediated enhancement of eosinophil recruitment via chemoattractants/chemokines remains unknown. OBJECTIVES: In this study, we assessed the contribution of IL-17A to eosinophil-related inflammation via the CCL7/CCR3 pathway in experimental allergic rhinitis. METHODS: IL-17A knockout (KO) and wild-type (WT) BALB/c mice were injected intraperitoneally and challenged intranasally with OVA to induce allergic rhinitis. Various parameters of the allergic response were evaluated, and mRNA and protein levels of CCL7 and CCR3 in nasal tissue and serum were compared between the two groups. The chemotactic response to CCL7 with or without IL-17A in bone marrow-derived eosinophils (bmEos) from BALB/c mice was measured. RESULTS: In the allergic rhinitis model, IL-17A deficiency significantly decreased nasal symptoms, serum IgE levels, and eosinophil recruitment to the nasal mucosa. CCL7 and CCR3 mRNA and protein levels were decreased in the nasal mucosa of IL-17A KO mice compared with the WT mice. BmEos showed a significantly increased chemotactic response to -low concentration of CCL7 in the presence of IL-17A compared with its absence. CONCLUSION: The suppression of nasal inflammation due of IL-17A deficiency in allergic rhinitis is partly responsible for the regulation of CCL7 secretion and eosinophil infiltration, which may be regulated via the CCL7/CCR3 pathway. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/28046055/Role_of_Interleukin_17A_on_the_Chemotactic_Responses_to_CCL7_in_a_Murine_Allergic_Rhinitis_Model_ L2 - http://dx.plos.org/10.1371/journal.pone.0169353 DB - PRIME DP - Unbound Medicine ER -