Dendritic Cell-Nerve Clusters Are Sites of T Cell Proliferation in Allergic Airway Inflammation

Veres, Tibor Z.; Shevchenko, Marina; Krasteva, Gabriela; Spies, Emma; Prenzler, Frauke; Rochlitzer, Sabine; Tschernig, Thomas; Krug, Norbert; Kummer, Wolfgang; Braun, Armin

doi:10.2353/ajpath.2009.080800

Cited by 54 publications

(49 citation statements)

References 22 publications

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“…It may also be that ozone has subtle effects on tissue leukocytes near airways or recruited to airways that could indirectly affect AHR through interaction with neural signaling. In a mouse model of allergic airways, dendritic cells have been found to have close proximity to airway nerves (38,39), but the functional significance is unknown. In the guinea pig, eosinophils have been shown to interfere with termination of airway neuromuscular signaling (40), but, to our knowledge, this mechanism has not been shown in other species.…”

Section: Discussionmentioning

confidence: 99%

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

Auten¹,

Gilmour

Krantz

et al. 2012

Am J Respir Cell Mol Biol

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Air pollutant exposure is linked with childhood asthma incidence and exacerbations, and maternal exposure to airborne pollutants during pregnancy increases airway hyperreactivity (AHR) in offspring. To determine if exposure to diesel exhaust (DE) during pregnancy worsened postnatal ozone-induced AHR, timed pregnant C57BL/6 mice were exposed to DE (0.5 or 2.0 mg/m 3 ) 4 hours daily from Gestation Day 9-17, or received twice-weekly oropharyngeal aspirations of the collected DE particles (DEPs). Placentas and fetal lungs were harvested on Gestation Day 18 for cytokine analysis. In other litters, pups born to dams exposed to air or DE, or to dams treated with aspirated diesel particles, were exposed to filtered air or 1 ppm ozone beginning the day after birth, for 3 hours per day, 3 days per week for 4 weeks. Additional pups were monitored after a 4-week recovery period. Diesel inhalation or aspiration during pregnancy increased levels of placental and fetal lung cytokines. There were no significant effects on airway leukocytes, but prenatal diesel augmented ozone-induced elevations of bronchoalveolar lavage cytokines at 4 weeks. Mice born to the high-concentration dieselexposed dams had worse ozone-induced AHR, which persisted in the 4-week recovery animals. Prenatal diesel exposure combined with postnatal ozone exposure also worsened secondary alveolar crest development. We conclude that maternal inhalation of DE in pregnancy provokes a fetal inflammatory response that, combined with postnatal ozone exposure, impairs alveolar development, and causes a more severe and long-lasting AHR to ozone exposure.Keywords: diesel; fetal inflammation; ozone; airway hyperreactivity Increasing asthma prevalence among children in industrialized nations has stimulated a number of investigations focused on early life exposures to air pollutants (1). Maternal exposures to a variety of inhaled atmospheric pollutants, including side and mainstream tobacco smoke, diesel exhaust (DE), and ozone, have been linked in epidemiologic studies to asthma and other respiratory diseases in children (2-4). Animal models aimed at deciphering the mechanisms by which maternal exposures during pregnancy are linked to childhood asthma have largely focused on pathways relevant to allergic asthma (5).In addition to allergic sensitization, in utero exposure to air pollutants may also affect nonspecific pulmonary responses, such as airway hyperreactivity (AHR) (6). It has already been shown that fetal pulmonary inflammatory challenges are linked with impaired postnatal alveolar development (7-9), which affects airway stability and AHR (10). Previous studies have shown that maternal exposure to DE during pregnancy modified mouse placental cytokines relevant to airway inflammation (11), and lowered the threshold for AHR in ovalbuminsensitized offspring (12).We have previously shown that a standardized urban particulate delivered by oropharyngeal aspiration during pregnancy induced placental inflammatory cytokine expression and worsened neonatal ozone-induced...

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Section: Discussionmentioning

confidence: 99%

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

Auten¹,

Gilmour

Krantz

et al. 2012

Am J Respir Cell Mol Biol

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“…Specimen preparation and analyses were performed as described previously (37). SI Materials and Methods provides a detailed description of experimental procedures.…”

Section: Methodsmentioning

confidence: 99%

“…The antibody staining was performed as previously described (37). Image stacks for the quantitative analysis were scanned with an XYZ-resolution of 1,024 × 1,024 × 53, with dimensions of 318.2 μm × 318.2 μm × 30 μm, respectively, starting from the luminal side of the tracheal epithelium.…”

Section: Methodsmentioning

confidence: 99%

Cholinergic chemosensory cells in the trachea regulate breathing

Krasteva

Canning²,

Hartmann

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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249

323

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In the epithelium of the lower airways, a cell type of unknown function has been termed "brush cell" because of a distinctive ultrastructural feature, an apical tuft of microvilli. Morphologically similar cells in the nose have been identified as solitary chemosensory cells responding to taste stimuli and triggering trigeminal reflexes. Here we show that brush cells of the mouse trachea express the receptors (Tas2R105, Tas2R108), the downstream signaling molecules (α-gustducin, phospholipase C β2 ) of bitter taste transduction, the synthesis and packaging machinery for acetylcholine, and are addressed by vagal sensory nerve fibers carrying nicotinic acetylcholine receptors. Tracheal application of an nAChR agonist caused a reduction in breathing frequency. Similarly, cycloheximide, a Tas2R108 agonist, evoked a drop in respiratory rate, being sensitive to nicotinic receptor blockade and epithelium removal. This identifies brush cells as cholinergic sensors of the chemical composition of the lower airway luminal microenvironment that are directly linked to the regulation of respiration.airway sensory innervation | respiratory epithelium | jugular-nodose ganglion | bitter-tasting substances

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“…Following antigen uptake in the airways [11], DCs migrate to the draining lymph nodes in order to present antigenic information to specialised lymphocytes, which organise an inflammatory response against the encountered antigen [10]. In addition, DCs can also present antigens locally to lymphocytes within the lung parenchyma [9,12].…”

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confidence: 99%

Acute effects of tobacco smoke on human airway dendritic cellsin vivo

Lommatzsch¹,

Bratke²,

Knappe³

et al. 2009

Eur Respir J

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Airway dendritic cells (DCs) play a key role in smoke-related lung diseases; however, the acute effects of tobacco smoke on human airway DCs in vivo are unknown.A total of 16 smokers underwent bronchoalveolar lavage at two time-points: directly after a 4-h period of nonsmoking (no smoke exposure); and directly after a 4-h period during which eight cigarettes were smoked (acute smoke exposure). Using flow cytometry, myeloid DCs (mDCs) and plasmacytoid DCs (pDCs), as well as function-associated surface molecules on mDCs, were analysed in bronchoalveolar lavage fluid (BALF) and in blood.The numbers of macrophages, lymphocytes, neutrophils, eosinophils and pDCs were unchanged in BALF following acute smoke exposure, as compared to no smoke exposure. In contrast, there was a strong increase in mDC number in BALF and a concomitant decrease in mDC number in blood following acute smoke exposure. In addition, acute smoke exposure led to an increase in the expression of the surface molecules blood dendritic cell antigen 1 and 4 and a decrease in the expression of the lung homing receptor, CC chemokine receptor 5, on mDCs in BALF.Acute tobacco smoke inhalation results in an immediate and selective recruitment of mDCs into human airways, which might reflect the very early reaction of the adaptive immune system to smoke exposure.

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Dendritic Cell-Nerve Clusters Are Sites of T Cell Proliferation in Allergic Airway Inflammation

Cited by 54 publications

References 22 publications

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

Cholinergic chemosensory cells in the trachea regulate breathing

Acute effects of tobacco smoke on human airway dendritic cellsin vivo

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