Diesel Exhaust Particle-Treated Human Bronchial Epithelial Cells Upregulate Jagged-1 and OX40 Ligand in Myeloid Dendritic Cells via Thymic Stromal Lymphopoietin

Bleck, Bertram; Tse, David K.; Gordon, Terry; Ahsan, Mohammad R.; Reibman, Joan

doi:10.4049/jimmunol.1000719

Cited by 92 publications

(68 citation statements)

References 79 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, a co-culture of HBECs with DCs in the presence of DEPs promoted the expression of OX40L and TARC in DCs, and activated DCs subsequently increased the proliferation of T cells. These responses were inhibited by TSLP siRNA transfection to HBECs, which indicated that TSLP produced by HBECs plays a role in the activation of DCs (25,26). A recent study demonstrated that microRNA-375 also regulated DEP-induced but not TNF-a-induced TSLP production in HBECs (27).…”

Section: Diesel Exhaust Particlesmentioning

confidence: 98%

“…In an experimental asthma model using Dermatophagoides farinae allergens (Der f), the injection of DEPs with Der f enhanced the production of Th2 cytokines, eosinophil infiltration, and airway remodeling (24). Although it has not yet been clarified whether DEP-induced TSLP influences the exacerbation of these allergic manifestations in vivo, Bleck et al reported that DEPs induced TSLP production in human bronchial epithelial cells (HBECs) (25,26). Furthermore, a co-culture of HBECs with DCs in the presence of DEPs promoted the expression of OX40L and TARC in DCs, and activated DCs subsequently increased the proliferation of T cells.…”

Section: Diesel Exhaust Particlesmentioning

confidence: 99%

See 1 more Smart Citation

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

Segawa

Hirasawa

2014

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. Environmental chemicals, such as cigarette smoke and diesel exhaust, have been reported as risk factors that exacerbate allergic diseases. However, the exacerbation mechanisms induced by these chemicals are not yet fully understood. Thymic stromal lymphopoietin (TSLP) is produced mainly by epithelial cells and plays an important role as a master switch of allergic inflammation because it promotes Th2-type immune responses by inducing the activation of dendritic cells. Chemical compounds, such as formalin, have been shown to bind to proteins and form a new antigen that induces allergic responses. A second group of chemicals that enhance allergic responses to exogenous proteins have also been reported. We recently demonstrated that some of these chemicals induced TSLP production and may potentially augment Th2-type allergic responses. We proposed that TSLP-producing chemical compounds should be recognized as chemical allegro-accelerators.

show abstract

Section: Diesel Exhaust Particlesmentioning

confidence: 98%

Section: Diesel Exhaust Particlesmentioning

confidence: 99%

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

Segawa

Hirasawa

2014

J Pharmacol Sci

View full text Add to dashboard Cite

show abstract

“…Several recent reports have described experiments using human tissue to investigate mechanisms for diesel effects. In experimental in vitro studies using human bronchial epithelial cells in coculture with myeloid DC, it was reported that diesel exhaust particles induced oxidative stress, which up-regulated epithelial production of thymic stromal lymphopoietin, driving myeloid DC to Th2 polarization (26). Incubation of nonatopic human peripheral blood mononuclear cells with diesel exhaust particlederived polyaromatic hydrocarbons resulted in increased IL-13 and decreased IFN-g production and increased chemotaxis of Th2 lymphocytes (27).…”

Section: Discussionmentioning

confidence: 99%

Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers

Noah

Zhou

Zhang³

et al. 2012

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Rationale: Diesel exhaust enhances allergic inflammation, and pollutants are associated with heightened susceptibility to viral respiratory infections. The effects of combined diesel and virus exposure in humans are unknown. Objectives: Test whether acute exposure to diesel modifies inflammatory responses to influenza virus in normal humans and those with allergies. Methods: We conducted a double-blind, randomized, placebocontrolled study of nasal responses to live attenuated influenza virus in normal volunteers and those with allergic rhinitis exposed to diesel (100 mg/m 3 ) or clean air for 2 hours, followed by standard dose of virus and serial nasal lavages. Endpoints were inflammatory mediators (ELISA) and virus quantity (quantitative reverse-transcriptase polymerase chain reaction). To test for exposure effect, we used multiple regression with exposure group (diesel vs. air) as the main explanatory variable and allergic status as an additional factor. Measurements and Main Results: Baseline levels of mediators did not differ among groups. For most postvirus nasal cytokine responses, there was no significant diesel effect, and no significant interaction with allergy. However, diesel was associated with significantly increased IFN-g responses (P ¼ 0.02), with no interaction with allergy in the regression model. Eotaxin-1 (P ¼ 0.01), eosinophil cationic protein (P , 0.01), and influenza RNA sequences in nasal cells (P ¼ 0.03) were significantly increased with diesel exposure, linked to allergy. Conclusions: Short-term exposure to diesel exhaust leads to increased eosinophil activation and increased virus quantity after virus inoculation in those with allergic rhinitis. This is consistent with previous literature suggesting a diesel "adjuvant" effect promoting allergic inflammation, and our data further suggest this change may be associated with reduced virus clearance. Clinical trial registered with www.clinicaltrials.gov (NCT00617110).

show abstract

“…Air pollutants can also generate ROS, which activates NF-κB signalling in the airway epithelium, leading to the secretion of the epithelial cytokines IL-1, IL-25, IL-33, GM-CSF, and TSLP, as well as other mediators. Subsequently a variety of cellular events are promoted and result in allergic sensitization to inhaled allergens [124,125]. O 3 [126], NO 2 [127], and cigarette smoke [128,129] induce epithelial cells to release ROS and RNS.…”

Section: Effect Of Air Pollutants On the Airway Epithelium And Respirmentioning

confidence: 99%

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

López-Rodríguez

Benedé

Barderas

et al. 2017

J Investig Allergol Clin Immunol

View full text Add to dashboard Cite

Airway epithelium is the cellular structure with the greatest surface exposed to a plethora of environmental airborne substances, including microorganisms, respiratory viruses, air pollutants, and allergens. In addition to being a protective physical barrier at the air-liquid interface, the airway epithelium acts as an effective chemical and immunological barrier that plays a crucial role in orchestrating the immune response in the lungs, by supporting the activation, recruitment, and mobilization of immune cells. Airway epithelium dysfunction has been clearly associated with various airway inflammatory diseases, such as allergic asthma. Although it is not fully understood why a person develops respiratory allergy, a growing body of evidence shows that the nature of the host's immune response is strongly determined by the state of the airway epithelium at the time of contact with the inhaled allergen. Our review highlights the physiological state of airway epithelium as a key element in the development of allergy and, particularly, in exacerbation of asthma. We review the role of physiological oxidants as signaling molecules in lung biology and allergic diseases and examine how high exposure to air pollutants (eg, cigarette smoke and diesel particles) can contribute to the increased incidence of respiratory allergy and exacerbation of the disease. Key words: Airway epithelium. Barrier dysfunction. Respiratory allergy. Redox biology. Air pollutants. ResumenEl epitelio pulmonar constituye la barrera celular más susceptible a la acción deletérea de la multitud de agentes que se encuentran en el ambiente, incluidos los alérgenos. Además de prevenir su acceso al organismo, la barrera epitelial de las vías respiratorias juega un papel inmunomodulador crucial, regulando de forma local la acción de las células del sistema inmune subyacentes. Una disfunción epitelial, provocada tanto directa como indirectamente por la acción de los aeroalérgenos, parece ser una de las causas principales de desregulación de la homeostasis pulmonar, causando una respuesta proinflamatoria descontrolada que cada vez más autores atribuyen al origen de las reacciones alérgicas. En esta revisión se quiere destacar el papel de la barrera epitelial pulmonar como regulador de la respuesta inmune en el contexto de la alergia. Las enfermedades crónicas que afectan a las vías respiratorias, tales como el asma alérgica, muestran frecuentemente una función epitelial defectuosa, apoyando así la hipótesis antes mencionada que subyace al origen de la alergia. El impacto de otros contaminantes ambientales -como virus respiratorios, bacterias, humo del tabaco y partículas diésel-sobre la integridad epitelial, así como su influencia en la biología redox pulmonar relacionada con el desarrollo de la respuesta alérgica, también se abordarán en la presente revisión.

show abstract

Diesel Exhaust Particle-Treated Human Bronchial Epithelial Cells Upregulate Jagged-1 and OX40 Ligand in Myeloid Dendritic Cells via Thymic Stromal Lymphopoietin

Cited by 92 publications

References 79 publications

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

Contact Info

Product

Resources

About