γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

Mathews, Joel; Williams, Alison S.; Brand, Jeffrey D.; Wurmbrand, Allison P.; Chen, Lucas; Ninin, Fernanda M. C.; Si, Huiqing; Kasahara, David I.; Shore, Stephanie A.

doi:10.1371/journal.pone.0097707

Cited by 25 publications

(53 citation statements)

References 73 publications

(93 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, we also gated on total and activated gd T cells and found that the total numbers of gd T cells, as well as activated gd T cells, were increased in the multiple-dosed mice compared with either the single-dosed or vehicle-only mice (see Figure E2 in the online supplement). Although we did not stain the gd T cells for IL-13 or IL-17A, activated gd T cells can produce both (29,30), and are also a possible source of both IL-13 and IL-17A. …”

Section: Cd3mentioning

confidence: 91%

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Lichtenstein¹,

Molina²,

Donaghey³

et al. 2016

Am J Respir Cell Mol Biol

Self Cite

View full text Add to dashboard Cite

After a single or multiple intratracheal instillations of Stachybotrys chartarum (S. chartarum or black mold) spores in BALB/c mice, we characterized cytokine production, metabolites, and inflammatory patterns by analyzing mouse bronchoalveolar lavage (BAL), lung tissue, and plasma. We found marked differences in BAL cell counts, especially large increases in lymphocytes and eosinophils in multipledosed mice. Formation of eosinophil-rich granulomas and airway goblet cell metaplasia were prevalent in the lungs of multiple-dosed mice but not in single-or saline-dosed groups. We detected changes in the cytokine expression profiles in both the BAL and plasma. Multiple pulmonary exposures to S. chartarum induced significant metabolic changes in the lungs but not in the plasma. These changes suggest a shift from type 1 inflammation after an acute exposure to type 2 inflammation after multiple exposures to S. chartarum. Eotaxin, vascular endothelial growth factor (VEGF), MIP-1a, MIP-1b, TNF-a, and the IL-8 analogs macrophage inflammatory protein-2 (MIP-2) and keratinocyte chemoattractant (KC), had more dramatic changes in multiplethan in single-dosed mice, and parallel the cytokines that characterize humans with histories of mold exposures versus unexposed control subjects. This repeated exposure model allows us to more realistically characterize responses to mold, such as cytokine, metabolic, and cellular changes.

show abstract

Section: Cd3mentioning

confidence: 91%

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Lichtenstein¹,

Molina²,

Donaghey³

et al. 2016

Am J Respir Cell Mol Biol

Self Cite

View full text Add to dashboard Cite

show abstract

“…This laboratory has previously reported that in mice, IL-17A contributes to the PMN recruitment observed following subacute O 3 exposure (0.3 ppm for 24–72 hr), at least in part via effects of IL-17A on expression of G-CSF, a PMN survival factor (Kasahara et al, 2012; Mathews et al, 2014a). Sources of IL-17A in the lung after subacute O 3 include macrophages and γδ T cells (Kasahara et al, 2012; Mathews et al, 2014a).…”

Section: Introductionmentioning

confidence: 99%

“…Sources of IL-17A in the lung after subacute O 3 include macrophages and γδ T cells (Kasahara et al, 2012; Mathews et al, 2014a). IL-23 can promote IL-17A expression in T-cells including γδ T-cells (Gaffen et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…The receptor for IL-23 is widely expressed on immune cells (Parham et al, 2002) and binding of IL-23 to its receptor induces the activation of multiple transcriptional pathways that lead to the expression of IL-17A (Harrington et al, 2006). IL-23 expression is induced in the lungs following subacute O 3 exposure (Mathews et al, 2014a), but its role in subsequent IL-17A expression and PMN recruitment has not been established. IL-1 also has the capacity to increase IL-17A expression in the lungs (Chung et al, 2009; Gasse et al, 2011; Kim et al, 2014), perhaps because IL-1 can induce IL-23 expression (Harris et al, 2008; Shainheit et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Whether DC contribute to the IL-23 and IL-1 induced following O 3 has not been established. However, the observations that DC lie directly adjacent to γδ T-cells in the lungs (Wands et al, 2005) and that γδ T-cells are important sources of IL-17A required for O 3 -induced PMN recruitment (Mathews et al, 2014a) suggest DC may indeed be involved.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Regulation of IL-17A expression in mice following subacute ozone exposure

Brand¹,

Mathews²,

Kasahara³

et al. 2016

Journal of Immunotoxicology

Self Cite

View full text Add to dashboard Cite

Exposure to subacute ozone (O3) causes pulmonary neutrophil recruitment. In mice, this recruitment requires IL-17A. Ozone also causes expression of IL-23 and IL-1, which can induce IL-17A. The purpose of this study was to examine the hypothesis that IL-23 and IL-1 contribute to IL-17A expression and subsequent neutrophil recruitment after subacute O3 exposure. Wild-type, IL-23−/−, and Flt3l−/− mice were exposed to air or 0.3 ppm O3 for 72 hr. Flt3l−/− mice lack conventional dendritic cells (cDC) that can express IL-23 and IL-1. Other wild-type mice were pre-treated with saline or the IL-1R1 antagonist anakinra prior to O3 exposure. After exposure, bronchoalveolar lavage (BAL) was performed and lung tissue harvested. The results indicated that pulmonary Il17a mRNA abundance and IL-17A+ F4/80+ cells were significantly reduced in O3-exposed IL-23−/− vs. in wild-type mice. In contrast, anakinra had no effect on Il23a or Il17a pulmonary mRNA abundance or on BAL concentrations of the neutrophil survival factor G-CSF, but anakinra did reduce BAL neutrophil numbers, likely because anakinra also reduced BAL IL-6. Compared to air, O3 caused a significant increase in DC numbers in wild-type but not in Flt3−/− mice. However, there was no significant difference in Il23a or Il17a mRNA abundance or in BAL neutrophil count in O3-exposed Flt3−/− vs. in wild-type mice. From these results, we conclude that IL-23 but not IL-1 contributes to the IL-17A expression induced by subacute O3 exposure. Induction of IL-23 by O3 does not appear to require cDC.

show abstract

Hypoxia pretreatment enhances the therapeutic potential of mesenchymal stem cells (BMSCs) on ozone-induced lung injury in rats

Abdelrahman

Samy

et al. 2022

Cell Tissue Res

View full text Add to dashboard Cite

Ozone (O3) gas is a double-sided weapon. It provides a shield that protects life on earth from the harmful ultraviolet (UV) rays, but ground-level O3 is considered an urban air pollutant. So, a rat model of chronic O3 inhalation was established to assess the biochemical and morphological alterations in the lung tissue and to investigate the ameliorative effects of bone marrow–derived mesenchymal stem cells (BMSCs) with or without hypoxia pre-treatment. Forty-two adult male albino rats were divided into four groups: control, ozone-exposed, normoxic BMSC-treated, and hypoxic BMSC-treated groups. Lung tissue sections were processed for light and electron microscope examination, immunohistochemical staining for caspase 3, and iNOS. Quantitative real-time PCR for IL-1α, IL-17, TNF-α, and Nrf2 mRNA gene expression were also performed. Chronic O3 exposure caused elevated inflammatory cytokines and decreased antioxidant Nrf2 mRNA expression. Marked morphological alterations with increased collagen deposition and elevated apoptotic markers and iNOS were evident. BMSC treatment showed immunomodulatory (decreased inflammatory cytokine gene expression), antioxidant (increased Nrf2 expression and decreased iNOS), and anti-apoptotic (decreased caspase3 expression) effects. Consequently, ameliorated lung morphology with diminished collagen deposition was observed. Hypoxia pretreatment enhanced BMSC survival by MTT assay. It also augmented the previously mentioned effects of BMSCs on the lung tissue as proved by statistical analysis. Lung morphology was similar to that of control group. In conclusion, hypoxia pretreatment represents a valuable intervention to enhance the effects of MSCs on chronic lung injury.

show abstract

γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα

Cited by 25 publications

References 73 publications

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Regulation of IL-17A expression in mice following subacute ozone exposure

Hypoxia pretreatment enhances the therapeutic potential of mesenchymal stem cells (BMSCs) on ozone-induced lung injury in rats

Contact Info

Product

Resources

About