title: Lack of lymphoid chemokines CCL19 and CCL21 enhances allergic airway inflammation in mice.
abstract: Lymphoid chemokines CCL19 and CCL21 are crucial for the recruitment of circulating naive T cells into lymph nodes. However, it is not completely known how they contribute to the development of allergic diseases. To determine whether the lack of CCL19 and CCL21 affects allergic airway inflammation, CCL19- and CCL21-deficient [paucity of lymph node T cells (plt/plt)] and wild-type (WT) mice were immunized intra-peritoneally and then challenged intra-nasally with chicken ovalbumin (OVA). Plt/plt mice developed more severe allergic airway inflammation characterized by increased eosinophils and lymphocytes in bronchoalveolar lavage (BAL) and profound inflammation in peribronchiolar and perivascular regions than did WT mice. CD4+ alpha4 integrin+ and CD4+ beta7 integrin+ T cells were significantly increased in the BAL of OVA-immunized and OVA-challenged (OVA/OVA) plt/plt mice compared with OVA/OVA WT mice. Moreover, there were higher levels of IL-4 and IL-13 mRNAs and lower levels of IL-2 and IFN-gamma mRNAs in inflamed lungs of OVA/OVA plt/plt mice compared with OVA/OVA WT mice. Plt/plt mice produced higher levels of total and OVA-specific IgE antibody. Thus, our results suggest that lack of lymphoid chemokines CCL19 and CCL21 enhances allergic airway inflammation by modulating the recruitment of CD4+ T cells into the lung, the balance between Th1 and Th2 cytokines and the IgE production.
authors.affiliation: Department of Environmental Medicine, Faculty of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. xubaohui@gmail.com
authors.forename: Baohui
authors.initials: B
authors.lastname: Xu
authors.forename: Kohji
authors.initials: K
authors.lastname: Aoyama
authors.forename: Mayumi
authors.initials: M
authors.lastname: Kusumoto
authors.forename: Akio
authors.initials: A
authors.lastname: Matsuzawa
authors.forename: Eugene C
authors.initials: EC
authors.lastname: Butcher
authors.forename: Sara A
authors.initials: SA
authors.lastname: Michie
authors.forename: Takami
authors.initials: T
authors.lastname: Matsuyama
authors.forename: Toru
authors.initials: T
authors.lastname: Takeuchi
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D054415:Chemokine CCL19; D054421:Chemokine CCL21; D019742:Chemokines, CC / Q000172:deficiency* / Q000235:genetics; D004804:Eosinophils / Q000378:metabolism / Q000473:pathology; D005260:Female; D015870:Gene Expression; D007073:Immunoglobulin E / Q000097:blood; D039441:Integrin alpha4 / Q000378:metabolism; D039641:Integrin beta Chains / Q000378:metabolism; D007371:Interferon-gamma / Q000235:genetics; D018793:Interleukin-13 / Q000235:genetics; D007376:Interleukin-2 / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D019041:L-Selectin / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D010047:Ovalbumin / Q000276:immunology; D011014:Pneumonia / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: C515461:Ccl19 protein, mouse; C515479:Ccl21c protein, mouse; D054415:Chemokine CCL19; D054421:Chemokine CCL21; D019742:Chemokines, CC; D039641:Integrin beta Chains; D018793:Interleukin-13; D007376:Interleukin-2; C091368:integrin beta7; D019041:L-Selectin; D039441:Integrin alpha4; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma; D010047:Ovalbumin