Epithelial responses in airway inflammation and immunity

Summary The epithelium is thought to serve an important barrier function in the airways. However, growing evidence now supports the notion that the respiratory epithelium plays a key role in host responses to infectious and allergenic stimuli. The epithelium functions to produce a variety of proinflammatory cytokines during the inflammatory response. More recently, the epithelium has been shown to express a variety of receptors that can recognize microorganisms, such as toll-like receptors (TLRs), as well as complement and acute phase proteins. Additionally, the cell surface of epithelial cells have also been shown to express a variety of costimulatory molecules which may be involved in regulating the activation of antigen-specific T cells in the airways. This paper reviews the novel ways by which the epithelium may function in both the innate and adaptive immune responses of the airways.

[1]  A. Lane,et al.  Toll-like receptors are expressed in sinonasal mucosa , 2003 .

[2]  Lieping Chen,et al.  Expression of the costimulatory molecule B7-H2 (inducible costimulator ligand) by human airway epithelial cells. , 2003, American journal of respiratory cell and molecular biology.

[3]  R. Medzhitov,et al.  Linking Toll-like receptors to IFN-α/β expression , 2003, Nature Immunology.

[4]  R. Ye,et al.  Serum amyloid A induces IL-8 secretion through a G protein-coupled receptor, FPRL1/LXA4R. , 2003, Blood.

[5]  R. Schleimer,et al.  Airway epithelial cell activation and toll-like receptors (TLR) , 2003 .

[6]  Lieping Chen,et al.  Airway epithelial cells express multiple members of the B7 family , 2003 .

[7]  J. Hoffmann,et al.  Toll signaling: the TIReless quest for specificity , 2003, Nature Immunology.

[8]  T. Akazawa,et al.  TICAM-1, an adaptor molecule that participates in Toll-like receptor 3–mediated interferon-β induction , 2003, Nature Immunology.

[9]  S. Akira,et al.  Toll-like receptors. , 2003, Annual review of immunology.

[10]  S. Akira,et al.  Cutting Edge: A Novel Toll/IL-1 Receptor Domain-Containing Adapter That Preferentially Activates the IFN-β Promoter in the Toll-Like Receptor Signaling1 , 2002, The Journal of Immunology.

[11]  M. Wills-Karp,et al.  Complement factor 3 mediates particulate matter-induced airway hyperresponsiveness. , 2002, American journal of respiratory cell and molecular biology.

[12]  C. Walker,et al.  Toll-like receptors as potential therapeutic targets for multiple diseases , 2002, Nature Reviews Drug Discovery.

[13]  B. Harten,et al.  Human keratinocytes express functional CD14 and toll-like receptor 4. , 2002, The Journal of investigative dermatology.

[14]  Jiahuai Han,et al.  Glucocorticoids Synergistically Enhance NontypeableHaemophilus influenzae-induced Toll-like Receptor 2 Expression via a Negative Cross-talk with p38 MAP Kinase* , 2002, The Journal of Biological Chemistry.

[15]  Sankar Ghosh,et al.  Negative Regulation of Toll-like Receptor-mediated Signaling by Tollip* , 2002, The Journal of Biological Chemistry.

[16]  Mary Collins,et al.  The B7 family of ligands and its receptors: new pathways for costimulation and inhibition of immune responses. , 2002, Annual review of immunology.

[17]  S. Akira,et al.  Lipopolysaccharide Stimulates the MyD88-Independent Pathway and Results in Activation of IFN-Regulatory Factor 3 and the Expression of a Subset of Lipopolysaccharide-Inducible Genes1 , 2001, The Journal of Immunology.

[18]  Ruslan Medzhitov,et al.  Toll-like receptors and innate immunity , 2001, Nature Reviews Immunology.

[19]  C. Akdis,et al.  Role of IL-10 in allergen-specific immunotherapy and normal response to allergens. , 2001, Microbes and infection.

[20]  P. Perrin,et al.  Costimulation of memory T-cells by ICOS: a potential therapeutic target for autoimmunity? , 2001, Clinical immunology.

[21]  M. Abreu,et al.  Decreased Expression of Toll-Like Receptor-4 and MD-2 Correlates with Intestinal Epithelial Cell Protection Against Dysregulated Proinflammatory Gene Expression in Response to Bacterial Lipopolysaccharide1 , 2001, The Journal of Immunology.

[22]  S. Akira,et al.  Toll-like receptors: critical proteins linking innate and acquired immunity , 2001, Nature Immunology.

[23]  G. Zhu,et al.  B7-H3: A costimulatory molecule for T cell activation and IFN-γ production , 2001, Nature Immunology.

[24]  A. Robeva,et al.  Serum Amyloid A (apoSAA) Expression Is Up-Regulated in Rheumatoid Arthritis and Induces Transcription of Matrix Metalloproteinases , 2001, The Journal of Immunology.

[25]  J. Zabner,et al.  Expression of the Complement Anaphylatoxin C3a and C5a Receptors on Bronchial Epithelial and Smooth Muscle Cells in Models of Sepsis and Asthma1 , 2001, The Journal of Immunology.

[26]  G. Cunnane.  Amyloid precursors and amyloidosis in inflammatory arthritis. , 2001, Current opinion in rheumatology.

[27]  G. Berger,et al.  Acute Sinusitis: A Histopathological and Immunohistochemical Study , 2000, The Laryngoscope.

[28]  G. Grevers,et al.  Involvement of inferior turbinate mucosa in chronic sinusitis – localization of T‐cell subset , 2000, Allergy.

[29]  D. Podolsky,et al.  Differential Alteration in Intestinal Epithelial Cell Expression of Toll-Like Receptor 3 (TLR3) and TLR4 in Inflammatory Bowel Disease , 2000, Infection and Immunity.

[30]  G. Zhu,et al.  Costimulation of T cells by B7-H2, a B7-like molecule that binds ICOS , 2000 .

[31]  Bao Lu,et al.  A role for the C3a anaphylatoxin receptor in the effector phase of asthma , 2000, Nature.

[32]  S. M. Propst,et al.  Proinflammatory and Th2-Derived Cytokines Modulate CD40-Mediated Expression of Inflammatory Mediators in Airway Epithelia: Implications for the Role of Epithelial CD40 in Airway Inflammation , 2000, The Journal of Immunology.

[33]  S. Lehar,et al.  The CD28-related molecule ICOS is required for effective T cell-dependent immune responses. , 2000, Immunity.

[34]  F. Martinon,et al.  Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor , 2000, Nature Cell Biology.

[35]  N. Papadopoulos,et al.  Rhinovirus infection induces major histocompatibility complex class I and costimulatory molecule upregulation on respiratory epithelial cells. , 2000, The Journal of infectious diseases.

[36]  G. Diamond,et al.  The innate immune response of the respiratory epithelium , 2000, Immunological reviews.

[37]  S. Urieli-Shoval,et al.  Expression and function of serum amyloid A, a major acute-phase protein, in normal and disease states , 2000, Current opinion in hematology.

[38]  G. Zhu,et al.  B7-H1, a third member of the B7 family, co-stimulates T-cell proliferation and interleukin-10 secretion , 1999, Nature Medicine.

[39]  W. Gong,et al.  A Seven-transmembrane, G Protein–coupled Receptor, FPRL1, Mediates the Chemotactic Activity of Serum Amyloid A for Human Phagocytic Cells , 1999, The Journal of experimental medicine.

[40]  R. Schleimer,et al.  Inhibition of VCAM-1 expression in human bronchial epithelial cells by glucocorticoids. , 1999, American journal of respiratory cell and molecular biology.

[41]  J. Brieva,et al.  T lymphocytes that infiltrate nasal polyps have a specialized phenotype and produce a mixed TH1/TH2 pattern of cytokines. , 1998, The Journal of allergy and clinical immunology.

[42]  P. Brandtzaeg,et al.  Phenotypic distribution of T cells in human nasal mucosa differs from that in the gut. , 1998, American journal of respiratory cell and molecular biology.

[43]  J. Rotter,et al.  Association between serum amyloid A proteins and coronary artery disease: evidence from two distinct arteriosclerotic processes. , 1997, Circulation.

[44]  C. Janeway,et al.  A human homologue of the Drosophila Toll protein signals activation of adaptive immunity , 1997, Nature.

[45]  R. Djukanović,et al.  Identification of neutrophil chemotactie factors in bronchoalveolar lavage fluid of asthmatic patients , 1997, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[46]  M. Leach,et al.  Interleukin-10 Is a Natural Suppressor of Cytokine Production and Inflammation in a Murine Model of Allergic Bronchopulmonary Aspergillosis , 1997, The Journal of experimental medicine.

[47]  R. Schleimer,et al.  Phenotyping and cytokine regulation of the BEAS-2B human bronchial epithelial cell: demonstration of inducible expression of the adhesion molecules VCAM-1 and ICAM-1. , 1997, American journal of respiratory cell and molecular biology.

[48]  A. Whitehead,et al.  Expression and Regulation of Constitutive and Acute Phase Serum Amyloid A mRNAs in Hepatic and Non‐Hepatic Cell Lines , 1996, Scandinavian journal of immunology.

[49]  T. Hugli,et al.  C3a is a chemotaxin for human eosinophils but not for neutrophils. I. C3a stimulation of neutrophils is secondary to eosinophil activation , 1995, The Journal of experimental medicine.

[50]  T. Out,et al.  ELISA of complement C3a in bronchoalveolar lavage fluid. , 1992, Journal of immunological methods.

[51]  R. Strunk,et al.  Pulmonary alveolar type II epithelial cells synthesize and secrete proteins of the classical and alternative complement pathways. , 1988, The Journal of clinical investigation.

[52]  W. J. Matthews,et al.  Complement biosynthesis by human bronchoalveolar macrophages. , 1983, Clinical immunology and immunopathology.