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, But Not on Eosinophils1
,§
*
Sections of Pulmonary and Critical Care Medicine and
Immunobiology and
Department of Pathology, Yale University School of Medicine, New Haven, CT 06520;
§
Pathology and Laboratory Medicine Service, Veterans Administration Connecticut Health Care System, West Haven, CT 06516;
¶
Department of Microbiology and Immunology, University of California, San Francisco, CA 94143; and
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Department of Immunology, University of Cape Town, Cape Town, South Africa
Mucus hyperproduction in asthma results from airway inflammation
and contributes to clinical symptoms, airway obstruction, and
mortality. In human asthmatics and in animal models, excess mucus
production correlates with airway eosinophilia. We previously described
a system in which TCR transgenic CD4 Th2 cells generated in vitro were
transferred into recipient mice and activated in the respiratory tract
with inhaled Ag. Th2 cells stimulated airway eosinophilia and a marked
increase in mucus production, while mice that received Th1 cells
exhibited airway inflammation without eosinophilia or mucus. Mucus
could be induced by IL-4-/- Th2 cells at comparable
levels to mucus induced by IL-4+/+ Th2 cells. In the
current studies we dissect further the mechanisms of Th2-induced mucus
production. When IL-4-/- Th2 cells are transferred into
IL-4R
-/- mice, mucus is not induced, and BAL
eosinophilia is absent. These data suggest that in the absence of IL-4,
IL-13 may be critical for Th2-induced mucus production and
eosinophilia. To determine whether eosinophils are important in mucus
production, IL-5-/- Th2 cells were transferred into
IL-5-/- recipients. Eosinophilia was abolished, yet mucus
staining in the epithelium persisted. These studies show definitively
that IL-5, eosinophils, or mast cells are not essential, but signaling
through IL-4R is critically important in Th2 cell stimulation of
mucus production.
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M. Singer, J. Lefort, and B. B. Vargaftig Granulocyte Depletion and Dexamethasone Differentially Modulate Airways Hyperreactivity, Inflammation, Mucus Accumulation, and Secretion Induced by rmIL-13 or Antigen Am. J. Respir. Cell Mol. Biol., January 1, 2002; 26(1): 74 - 84. [Abstract] [Full Text] [PDF]
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A. KANEHIRO, M. LAHN, M. J. MAKELA, A. DAKHAMA, M. FUJITA, A. JOETHAM, R. J. MASON, W. BORN, and E. W. GELFAND Tumor Necrosis Factor-alpha Negatively Regulates Airway Hyperresponsiveness through gamma delta T Cells Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2229 - 2238. [Abstract] [Full Text] [PDF]
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K. Blease, C. Jakubzick, J. M. Schuh, B. H. Joshi, R. K. Puri, and C. M. Hogaboam IL-13 Fusion Cytotoxin Ameliorates Chronic Fungal-Induced Allergic Airway Disease in Mice J. Immunol., December 1, 2001; 167(11): 6583 - 6592. [Abstract] [Full Text] [PDF]
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J. V. FAHY Remodeling of the Airway Epithelium in Asthma Am. J. Respir. Crit. Care Med., November 15, 2001; 164(10): S46 - 51. [Abstract] [Full Text] [PDF]
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D. M. Walter, J. J. McIntire, G. Berry, A. N. J. McKenzie, D. D. Donaldson, R. H. DeKruyff, and D. T. Umetsu Critical Role for IL-13 in the Development of Allergen-Induced Airway Hyperreactivity J. Immunol., October 15, 2001; 167(8): 4668 - 4675. [Abstract] [Full Text] [PDF]
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M. Yang, S. P. Hogan, P. J. Henry, K. I. Matthaei, A. N. J. McKenzie, I. G. Young, M. E. Rothenberg, and P. S. Foster Interleukin-13 Mediates Airways Hyperreactivity through the IL-4 Receptor-Alpha Chain and STAT-6 Independently of IL-5 and Eotaxin Am. J. Respir. Cell Mol. Biol., October 1, 2001; 25(4): 522 - 530. [Abstract] [Full Text] [PDF]
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C. Bandeira-Melo, K. Sugiyama, L. J. Woods, and P. F. Weller Cutting Edge: Eotaxin Elicits Rapid Vesicular Transport-Mediated Release of Preformed IL-4 from Human Eosinophils J. Immunol., April 15, 2001; 166(8): 4813 - 4817. [Abstract] [Full Text] [PDF]
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J. J. Shim, K. Dabbagh, I. F. Ueki, T. Dao-Pick, P.-R. Burgel, K. Takeyama, D. C.-W. Tam, and J. A. Nadel IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils Am J Physiol Lung Cell Mol Physiol, January 1, 2001; 280(1): L134 - L140. [Abstract] [Full Text] [PDF]
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Y. Tesfaigzi, M. J. Fischer, A. J. Martin, and J. Seagrave Bcl-2 in LPS- and allergen-induced hyperplastic mucous cells in airway epithelia of Brown Norway rats Am J Physiol Lung Cell Mol Physiol, December 1, 2000; 279(6): L1210 - L1217. [Abstract] [Full Text] [PDF]
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C.-H. Chen, D.-H. Zhang, J. M. LaPorte, and A. Ray Cyclic AMP Activates p38 Mitogen-Activated Protein Kinase in Th2 Cells: Phosphorylation of GATA-3 and Stimulation of Th2 Cytokine Gene Expression J. Immunol., November 15, 2000; 165(10): 5597 - 5605. [Abstract] [Full Text] [PDF]
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C. M. Lloyd, T. Delaney, T. Nguyen, J. Tian, C. Martinez-A, A. J. Coyle, and J.-C. Gutierrez-Ramos CC Chemokine Receptor (CCR)3/Eotaxin Is Followed by CCR4/Monocyte-derived Chemokine in Mediating Pulmonary T Helper Lymphocyte Type 2 Recruitment after Serial Antigen Challenge In Vivo J. Exp. Med., January 17, 2000; 191(2): 265 - 274. [Abstract] [Full Text] [PDF]
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L. Cohn, R. J. Homer, N. Niu, and K. Bottomly T Helper 1 Cells and Interferon {gamma} Regulate Allergic Airway Inflammation and Mucus Production J. Exp. Med., November 1, 1999; 190(9): 1309 - 1318. [Abstract] [Full Text] [PDF]
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Z. Zhu, B. Ma, R. J. Homer, T. Zheng, and J. A. Elias Use of the Tetracycline-controlled Transcriptional Silencer (tTS) to Eliminate Transgene Leak in Inducible Overexpression Transgenic Mice J. Biol. Chem., June 29, 2001; 276(27): 25222 - 25229. [Abstract] [Full Text] [PDF]
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J. P. Justice, J. Crosby, M. T. Borchers, A. Tomkinson, J. J. Lee, and N. A. Lee CD4+ T cell-dependent airway mucus production occurs in response to IL-5 expression in lung Am J Physiol Lung Cell Mol Physiol, May 1, 2002; 282(5): L1066 - L1074. [Abstract] [Full Text] [PDF]
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