Neonatal capsaicin treatment increases the severity of ozone-induced lung injury.

Sterner-Kock, Anja; Vesely, Keith R.; Stovall, Mary Y.; Schelegle, Edward S.; Green, Jerry F.; Hyde, Dallas M.

doi:10.1164/ajrccm.153.1.8542155

Cited by 33 publications

(35 citation statements)

References 24 publications

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“…There was no significant difference in the number of neutrophils in BAL or in terminal bronchioles of rats treated with SR140333 compared with vehicle-treated rats exposed to ozone. These observations are consistent with our previous observations in rats treated neonatally with capsaicin to ablate C fiber afferents (26). Taken together, these results suggest that substance P is not a critical mediator for neutrophil emigration into airways after ozone injury in the rat.…”

Section: Discussionsupporting

confidence: 93%

“…In a series of experiments, we found that rats depleted of C fibers with neonatal capsaicin treatment did not develop reflex rapid, shallow breathing, epithelial injury of terminal bronchioles was greater, and there was an uncoupling of neutrophil accumulation and other inflammatory responses from repair after ozone exposure. That is, for a given amount of epithelial necrosis, C fiber ablation had no influence on the degree of inflammation, but did modulate epithelial cell turnover and proliferative repair (26,27). Although clearly implicating airway C fibers and the neuropeptides they release in ozoneinduced epithelial injury and repair, interpretation of these observations are complicated by the fact that we do not know how the neonatal ablation of airway C fibers with capsaicin affects the ontogeny of the distal airway epithelium and its response to oxidant stress.…”

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confidence: 96%

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Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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We investigated the importance of neurokinin (NK)-1 receptors in epithelial injury and repair and neutrophil function. Conscious Wistar rats were exposed to 1 ppm ozone or filtered air for 8 hours, followed by an 8-hour postexposure period. Before exposure, we administered either the NK-1 receptor antagonist, SR140333, or saline as a control. Ethidium homodimer was instilled into lungs as a marker of necrotic airway epithelial cells. After fixation, whole mounts of airway dissected lung lobes were immunostained for 5-bromo-29-deoxyuridine, a marker of epithelial proliferation. Both ethidium homodimer and 5-bromo-29-deoxyuridine-positive epithelial cells were quantified in specific airway generations. Rats treated with the NK-1 receptor antagonist had significantly reduced epithelial injury and epithelial proliferation compared with control rats. Sections of terminal bronchioles showed no significant difference in the number of neutrophils in airways between groups. In addition, staining ozone-exposed lung sections for active caspase 3 showed no apoptotic cells, but ethidium-positive cells colocalized with the orphan nuclear receptor, Nur77, a marker of nonapoptotic, programmed cell death mediated by the NK-1 receptor. An immortalized human airway epithelial cell line, human bronchial epithelial-1, showed no significant difference in the number of oxidant stresspositive cells during exposure to hydrogen peroxide and a range of SR140333 doses, demonstrating no antioxidant effect of the receptor antagonist. We conclude that activation of the NK-1 receptor during acute ozone inhalation contributes to epithelial injury and subsequent epithelial proliferation, a critical component of repair, but does not influence neutrophil emigration into airways.

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 96%

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Oslund¹,

Hyde

Putney³

et al. 2008

Am J Respir Cell Mol Biol

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“…controlled inflammatory responses 22,23 . Furthermore, in humans, low levels of soluble L-selectin (that is, minimal shedding) in the early course of disease are negatively correlated with degree of organ injury in adult respiratory distress syndrome 24 .…”

Section: Articlesmentioning

confidence: 99%

Painful stimulation suppresses joint inflammation by inducing shedding of L-selectin from neutrophils

Strausbaugh

Green²,

Lo³

et al. 1999

Nat Med

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Although the inflammatory response is essential for protecting tissues from injury and infection, unrestrained inflammation can cause chronic inflammatory diseases such as arthritis, colitis and asthma. Physiological mechanisms that downregulate inflammation are poorly understood. Potent control might be achieved by regulating early stages in the inflammatory response, such as accumulation of neutrophils at the site of injury, where these cells release chemical mediators that promote inflammatory processes including plasma extravasation, bacteriocide and proteolysis. To access an inflammatory site, neutrophils must first adhere to the vascular endothelium in a process mediated in part by the leukocyte adhesion molecule L-selectin. This adhesion is prevented when L-selectin is shed from the neutrophil membrane. Although shedding of L-selectin is recognized as a potentially important mechanism for regulating neutrophils, its physiological function has not been demonstrated. Shedding of L-selectin may mediate endogenous downregulation of inflammation by limiting neutrophil accumulation at inflammatory sites. Here we show that activation of nociceptive neurons induces shedding of L-selectin from circulating neutrophils in vivo and that this shedding suppresses an ongoing inflammatory response by inhibiting neutrophil accumulation. These findings indicate a previously unknown mechanism for endogenous feedback control of inflammation. Failure of this mechanism could contribute to the etiology of chronic inflammatory disease.

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“…In a series of experiments, we found that rats depleted of C fibers using neonatal capsaicin treatment did not develop rapid shallow breathing, epithelial injury of terminal bronchioles was greater, and there were reductions in epithelial cell turnover and proliferative repair (Sterner-Kock et al 1996;.…”

Section: Introductionmentioning

confidence: 99%

Activation of Calcitonin Gene-Related Peptide Receptor during Ozone Inhalation Contributes to Airway Epithelial Injury and Repair

et al. 2009

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The authors investigated the importance of the neuropeptide, calcitonin gene-related peptide (CGRP), in epithelial injury, repair, and neutrophil emigration after ozone exposure. Wistar rats were administered either a CGRP-receptor antagonist ) or saline and exposed to 8 hours of 1-ppm ozone or filtered air with an 8-hour postexposure period. Immediately after exposure, ethidium homodimer was instilled into lungs as a marker of necrotic airway epithelial cells. After fixation, airway dissected lung lobes were stained for 5'-bromo-2'-deoxyuridine, a marker of epithelial proliferation. Positive epithelial cells were quantified in specific airway generations. Rats treated with CGRP 8-37 had significantly reduced epithelial injury in terminal bronchioles and reduced epithelial proliferation in proximal airways and terminal bronchioles. Bronchoalveolar lavage and sections of terminal bronchioles showed no significant difference in the number of neutrophils emigrating into airways in CGRP 8-37 -treated rats. The airway epithelial cell line, HBE-1, showed no difference in the number of oxidant stress positive cells during exposure to hydrogen peroxide and a range of CGRP 8-37 doses, demonstrating no antioxidant effect of CGRP . We conclude that activation of CGRP receptors during ozone inhalation contributes to airway epithelial injury and subsequent epithelial proliferation, a critical component of repair, but does not influence neutrophil emigration into airways.

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Neonatal capsaicin treatment increases the severity of ozone-induced lung injury.

Cited by 33 publications

References 24 publications

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Activation of Neurokinin-1 Receptors during Ozone Inhalation Contributes to Epithelial Injury and Repair

Painful stimulation suppresses joint inflammation by inducing shedding of L-selectin from neutrophils

Activation of Calcitonin Gene-Related Peptide Receptor during Ozone Inhalation Contributes to Airway Epithelial Injury and Repair

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