Diesel Exhaust Particle-Exposed Human Bronchial Epithelial Cells Induce Dendritic Cell Maturation and Polarization via Thymic Stromal Lymphopoietin

Bleck, Bertram; Tse, David K.; Lafaille, Maria A. Curotto de; Zhang, Feijie; Reibman, Joan

doi:10.1007/s10875-007-9149-0

Cited by 97 publications

(83 citation statements)

References 32 publications

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“…However, exposure of BM-derived DCs to DEPs did not lead to maturation. This is in line with observations in human monocytederived DCs, in which DEP induce DC maturation through release of the growth factors GM-CSF and thymic stromal lymphopoietin by epithelial cells (12,13). Other DC-activating cytokines that are produced by the epithelium include IL-1b, IL-6, and TNF-a (4).…”

Section: Discussionsupporting

confidence: 85%

“…This could then explain the adjuvant effects of DEP exposure in models published before (2), and in vitro observations indeed suggest that DEP-exposed DCs increase the T cell proliferation (12,13). To our surprise, we observed comparable T cell proliferation in control and DEP-treated mice.…”

Section: Discussionsupporting

confidence: 69%

“…One could therefore speculate that DEP exposure has an impact on several aspects of the DC biology. Indeed, in vitro data demonstrated that DEP exposure induces DC maturation (10,11) via epithelial cell-derived mediators (12,13) and that DEP-exposed DCs induce a Th2 polarization (10,(13)(14)(15).…”

Section: Once Arrived In the Mln Dcs Present The Ags To Naive T Cellmentioning

confidence: 99%

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Diesel Exhaust Particles Stimulate Adaptive Immunity by Acting on Pulmonary Dendritic Cells

Provoost

Maes

Willart

et al. 2009

The Journal of Immunology

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Particulate matter, such as diesel exhaust particles (DEPs), modulate adaptive immune responses in the lung; however, their mechanism of action remains largely unclear. Pulmonary dendritic cells (DCs) are crucial mediators in regulating immune responses. We hypothesized that the immunomodulatory effects of DEPs are caused by alteration of DC function. To test this, we instilled mice with DEPs and examined the pulmonary DC recruitment and maturation, their migration to the mediastinal lymph node (MLN), and the subsequent T cell response. We demonstrated that exposure to DEPs increased DC numbers in the bronchoalveolar lavage and the lungs and that DEPs increased the maturation status of these DCs. DEP exposure also enhanced the DC migration to the MLN. Moreover, we showed that DEPs themselves were transported to the MLN in a CCR7- and DC-dependent manner. This resulted in an enhanced T cell recruitment and effector differentiation in the MLN. These data suggest that DEP inhalation modulates immune responses in the lung via stimulation of DC function.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionsupporting

confidence: 69%

Section: Once Arrived In the Mln Dcs Present The Ags To Naive T Cellmentioning

confidence: 99%

See 1 more Smart Citation

Diesel Exhaust Particles Stimulate Adaptive Immunity by Acting on Pulmonary Dendritic Cells

Provoost

Maes

Willart

et al. 2009

The Journal of Immunology

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“…It seems likely therefore that DC will be among the first cells to sense and respond to inhaled PM, although the importance of bronchial/pulmonary epithelial cells cannot be overlooked. It is possible that exposure to PM disrupts the integrity of pulmonary epithelial cells and thereby releases inflammatory cytokines that activate DC and drive Th2-mediated allergic immunity as suggested by others [57,58] . An attractive mechanism responsible for DC activation by epithelial cells suggests release of granulocyte-macrophage colony-stimulating factor and thymic stromal lymphopoietin (TSLP) on exposure to particulate pollutants that may also involve oxidative stress and the generation of reactive oxygen species in the activation of pulmonary DC [11,42,54,57,59] .…”

Section: Discussionmentioning

confidence: 98%

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

et al. 2010

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The biological effects of acute particulate air pollution exposure in host innate immunity remain obscure and have relied largely on in vitro models. We hypothesized that single acute exposure to ambient or engineered particulate matter (PM) in the absence of other secondary stimuli would activate lung dendritic cells (DC) in vivo and provide information on the early immunological events of PM exposure and DC activation in a mouse model naïve to prior PM exposure. Activation of purified lung DC was studied following oropharyngeal instillation of ambient particulate matter (APM). We compared the effects of APM exposure with that of diesel-enriched PM (DEP), carbon black particles (CBP) and silver nanoparticles (AgP). We found that PM species induced variable cellular infiltration in the lungs and only APM exposure induced eosinophilic infiltration. Both APM and DEP activated pulmonary DC and promoted a Th2-type cytokine response from naïve CD4+ T cells ex vivo. Cultures of primary peribronchial lymph node cells from mice exposed to APM and DEP also displayed a Th2-type immune response ex vivo. We conclude that exposure of the lower airway to various PM species induces differential immunological responses and immunomodulation of DC subsets. Environmental APM and DEP activated DC in vivo and provoked a Th2 response ex vivo. By contrast, CBP and AgP induced altered lung tissue barrier integrity but failed to stimulate CD4+ T cells as effectively. Our work suggests that respirable pollutants activate the innate immune response with enhanced DC activation, pulmonary inflammation and Th2-immune responsiveness.

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“…Thymic stromal lymphopoietin (TSLP) is an epithelial cell-derived cytokine that regulates the Th2 response, 72 -74 and we have described its production in response to exposure to diesel exhaust particles. 75 Thus, the gene for TSLP, located on chromosome 5, is a biologically plausible candidate gene for the study of gene and environment interactions. A locus on 5q23 was associated with cockroach-specific IgE in Costa Rican children in a genome-wide linkage analysis when it was analyzed with sex-stratified linkage analysis.…”

Section: Selected Asthma Genes In the Latino Populationmentioning

confidence: 99%

Genetics and Asthma Disease Susceptibility in the US Latino Population

Reibman¹,

Liu²

2010

Mount Sinai J Medicine

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The US Latino population is heterogeneous with diversity in environmental exposures and socioeconomic status. Moreover, the US Hispanic population derives from numerous countries previously under Spanish rule, and many Hispanics have complex proportions of European, Native American, and African ancestry. Disparities in asthma severity and control are due to complex interactions between environmental exposures, socioeconomic factors, and genetic variations. In addition, diseases within the Latino community may also differ by country of origin. Although US Census data show low asthma rates in the Hispanic population as a whole, there is a lot of variability in the prevalence and morbidity of asthma, with a prevalence of 5.0% in Mexican Americans versus 17.0% in Puerto Ricans. The diversity and population admixture make the study of the genetics of asthma complex in Latino populations. However, an understanding of the genetics of asthma in all populations, including the Latino population, can enhance risk identification, help us Address Correspondence to:Joan Reibman New York University School of Medicine New York, NY Email: joan.reibman@nyumc.org to target pharmacological therapy, and guide environmental regulations, all of which can promote a reduction in health disparities. The inclusion of markers of ancestral diversity and the incorporation of techniques to adjust for stratification now make these studies feasible in complex populations, including the Latino population. To date, studies using linkage analyses, genome-wide associations, or candidate gene analyses have identified an association of asthma or asthma-related phenotypes with candidate genes, including interleukin 13, β-2 adrenergic receptor, a disintegrin and metalloproteinase 33, orosomucoid 1-like 3, and thymic stromal lymphopoietin. As reviewed here, although these genes have been identified in diverse populations, limited studies have been performed in Latino populations, and they have had variable replication. There is a need for the development of registries with well-phenotyped pediatric and adult Latino populations and subgroups for inclusion in the rapidly expanding field of genetic studies, and these studies need to be used to reduce health disparities.

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Diesel Exhaust Particle-Exposed Human Bronchial Epithelial Cells Induce Dendritic Cell Maturation and Polarization via Thymic Stromal Lymphopoietin

Cited by 97 publications

References 32 publications

Diesel Exhaust Particles Stimulate Adaptive Immunity by Acting on Pulmonary Dendritic Cells

Diesel Exhaust Particles Stimulate Adaptive Immunity by Acting on Pulmonary Dendritic Cells

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Genetics and Asthma Disease Susceptibility in the US Latino Population

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