Skip to main content
Journal cover image

Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice.

Publication ,  Journal Article
Grinnan, D; Sung, S-S; Dougherty, JA; Knowles, AR; Allen, MB; Rose, CE; Nakano, H; Gunn, MD; Fu, SM; Rose, CE
Published in: J Allergy Clin Immunol
December 2006

BACKGROUND: Dendritic cells and lymphocytes play a central role in allergic asthma. Chemokines for these cells include the CCR7 agonists secondary lymphoid chemokine/CCL21 and EBV-induced lymphoid chemokine/CCL19, but their role in allergic asthma is poorly understood. OBJECTIVE: We sought to determine the effects of abrogation of lymphoid tissue expression of CCR7 agonists on allergic airway responses. METHODS: Paucity of lymphocyte T cell (plt) mutant mice, deficient in EBV-induced lymphoid chemokine/CCL19 and the lymphoid form of secondary lymphoid chemokine/CCL21, were evaluated in an established ovalbumin (OVA)-induced asthma model (plt-OVA group) and compared with similarly immunized +/+ BALB/c mice (+/+OVA group). RESULTS: APTI responses to methacholine increased similarly in OVA-challenged plt and +/+ mice. However, airway inflammation was strikingly enhanced in plt-OVA mutants over +/+OVA mice and included increased numbers of eosinophils, CD4 and B cells, neutrophils, and total leukocytes in bronchoalveolar lavage fluid and inflammatory cell cuffing around pulmonary arterioles. Enhanced airway inflammation was accompanied by an increase in lung T(H)2 activity, with increased levels of IL-4 and monocyte-derived chemoattractant/CCL22. CONCLUSIONS: Induction of allergic asthma in mutant mice with impaired CCR7 responses results in characteristics that resemble severe asthma in human subjects, including severe bronchial lymphocytosis, eosinophilia, and neutrophilia, but not in enhancement in airway hyperreactivity. CLINICAL IMPLICATIONS: Disruption of chemokines responsible for trafficking of antigen-processing cells and lymphocytes to the draining lymph nodes might lead to enhanced allergic airway responses.

Duke Scholars

Published In

J Allergy Clin Immunol

DOI

ISSN

0091-6749

Publication Date

December 2006

Volume

118

Issue

6

Start / End Page

1234 / 1241

Location

United States

Related Subject Headings

  • T-Lymphocytes
  • Respiratory System
  • Receptors, Chemokine
  • Receptors, CCR7
  • Ovalbumin
  • Neutrophils
  • Monocytes
  • Mice, Mutant Strains
  • Mice, Inbred BALB C
  • Mice
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Grinnan, D., Sung, S.-S., Dougherty, J. A., Knowles, A. R., Allen, M. B., Rose, C. E., … Fu, S. M. (2006). Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice. J Allergy Clin Immunol, 118(6), 1234–1241. https://doi.org/10.1016/j.jaci.2006.07.036
Grinnan, Dan, Sun-Sang Sung, Joseph A. Dougherty, Amy Ryce Knowles, Matthew B. Allen, Charles E. Rose, Hideki Nakano, Michael D. Gunn, Shu Man Fu, and C Edward Rose. “Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice.J Allergy Clin Immunol 118, no. 6 (December 2006): 1234–41. https://doi.org/10.1016/j.jaci.2006.07.036.
Grinnan D, Sung S-S, Dougherty JA, Knowles AR, Allen MB, Rose CE, et al. Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice. J Allergy Clin Immunol. 2006 Dec;118(6):1234–41.
Grinnan, Dan, et al. “Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice.J Allergy Clin Immunol, vol. 118, no. 6, Dec. 2006, pp. 1234–41. Pubmed, doi:10.1016/j.jaci.2006.07.036.
Grinnan D, Sung S-S, Dougherty JA, Knowles AR, Allen MB, Rose CE, Nakano H, Gunn MD, Fu SM. Enhanced allergen-induced airway inflammation in paucity of lymph node T cell (plt) mutant mice. J Allergy Clin Immunol. 2006 Dec;118(6):1234–1241.
Journal cover image

Published In

J Allergy Clin Immunol

DOI

ISSN

0091-6749

Publication Date

December 2006

Volume

118

Issue

6

Start / End Page

1234 / 1241

Location

United States

Related Subject Headings

  • T-Lymphocytes
  • Respiratory System
  • Receptors, Chemokine
  • Receptors, CCR7
  • Ovalbumin
  • Neutrophils
  • Monocytes
  • Mice, Mutant Strains
  • Mice, Inbred BALB C
  • Mice