CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

Bosmann, Markus; Grailer, Jamison; Russkamp, Norman F.; Ruemmler, Robert; Zetoune, Firas S.; Sarma, J. Vidya; Ward, Peter A.

doi:10.1097/shk.0b013e31828f9c92

Cited by 39 publications

(25 citation statements)

References 36 publications

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“…Thus, macrophage depletion is reported to increase mortality[74], lung inflammation [75, 76], and lung bacterial load[73], consistent with the anti-inflammatory effect of alveolar macrophages. However, macrophage depletion decreased BAL levels of the proinflammatory cytokine IL-23[77], revealing a proinflammatory macrophage effect. Concerns have been expressed that the DTR strategy might be associated with non-specific immune effects attributable to depletion of cells other than macrophages[75, 76, 78].…”

Section: Effects Of Macrophage Depletionmentioning

confidence: 99%

Macrophage-epithelial interactions in pulmonary alveoli

Bhattacharya

Westphalen

2016

Semin Immunopathol

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Alveolar macrophages have been investigated for years by approaches involving macrophage extraction from the lung by bronchoalveolar lavage, or by cell removal from lung tissue. Since extracted macrophages are studied outside their natural milieu, there is little understanding of the extent to which alveolar macrophages interact with the epithelium, or with one another to generate the lung’s innate immune response to pathogen challenge. Here, we review new evidence of macrophage-epithelial interactions in the lung and we address the emerging understanding that the alveolar epithelium plays an important role in orchestrating the macrophage driven immune response.

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Section: Effects Of Macrophage Depletionmentioning

confidence: 99%

Macrophage-epithelial interactions in pulmonary alveoli

Bhattacharya

Westphalen

2016

Semin Immunopathol

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“…The infiltration of activated macrophages in liver tissue was assessed by immunohistochemistry staining of established macrophage markers, including F4/80 for mature macrophages, CD11C for classically activated (M1) macrophages, and CD206 for alternatively activated (M2) macrophages (6,21,50) to illustrate the hepatic inflammation response to diabetic pathology (27). Immunohistochemistry was performed as usual (63).…”

Section: Spontaneous Voluntary Activitymentioning

confidence: 99%

CYP2J2 attenuates metabolic dysfunction in diabetic mice by reducing hepatic inflammation via the PPARγ

Chen

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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DW. CYP2J2 attenuates metabolic dysfunction in diabetic mice by reducing hepatic inflammation via the PPAR␥. Am J Physiol Endocrinol Metab 308: E270 -E282, 2015. First published November 11, 2014 doi:10.1152/ajpendo.00118.2014 and arachidonic acid-derived cytochrome P450 (CYP) epoxygenase metabolites have diverse biological effects, including antiinflammatory properties in the vasculature. Increasing evidence suggests that inflammation in type 2 diabetes is a key component in the development of insulin resistance. In this study, we investigated whether CYP epoxygenase expression and exogenous EETs can attenuate insulin resistance in diabetic db/db mice and in cultured hepatic cells (HepG2). In vivo, CYP2J2 expression and the accompanying increase in EETs attenuated insulin resistance, as determined by plasma glucose levels, glucose tolerance test, insulin tolerance test, and hyperinsulinemic euglycemic clamp studies. CYP2J2 expression reduced the production of proinflammatory cytokines in liver, including CRP, IL-6, IL-1␤, and TNF␣, and decreased the infiltration of macrophages in liver. CYP2J2 expression also decreased activation of proinflammatory signaling cascades by decreasing NF-B and MAPK activation in hepatocytes. Interestingly, CYP2J2 expression and exogenous EET treatment increased glucose uptake and activated the insulin-signaling cascade both in vivo and in vitro, suggesting that CYP2J2 metabolites play a role in glucose homeostasis. Furthermore, CYP2J2 expression upregulated PPAR␥, which has been shown to induce adipogenesis, which attenuates dyslipidemias observed in diabetes. All of the findings suggest that CYP2J2 expression attenuates the diabetic phenotype and insulin resistance via inhibition of NF-B and MAPK signaling pathways and activation of PPAR␥. cytochrome P450 epoxygenase 2J2; peroxisome proliferator-activated receptor-␥

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“…Similarly, IL-23 has been shown to induce IL-17A release from peripheral blood mononuclear cells from patients with atherosclerosis (Abbas et al, 2015). Macrophages also have the capacity to produce IL-23 (Bosmann et al, 2013; Abbas et al, 2015), suggesting these cells may use autocrine IL-23 signaling to promote IL-17A production. However, even IL-17A + macrophages were reduced only 50% in IL-23 −/− mice and IL-17 + γδ T cells were unaffected, despite approximately 70% reductions in Il17a mRNA abundance in these mice (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

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

Brand¹,

Mathews²,

Kasahara³

et al. 2016

Journal of Immunotoxicology

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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.

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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

Cited by 39 publications

References 36 publications

Macrophage-epithelial interactions in pulmonary alveoli

Macrophage-epithelial interactions in pulmonary alveoli

CYP2J2 attenuates metabolic dysfunction in diabetic mice by reducing hepatic inflammation via the PPARγ

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

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