Tachykinins: Effects on Motility and Metabolism of Rat Polymorphonuclear Leucocytes

Roch-Arveiller, M; Regoli, Doménico; Chanaud, Brigitte; LeNoir, Marie; Muntaner, O; Stralzko, S.; Giroud, Jean‐Paul

doi:10.1159/000138225

Cited by 66 publications

(28 citation statements)

References 5 publications

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“…Similar to our results with SR140333, neutrophil recruitment was not affected in a model of thermal injury in rats (48). Roch-Arveiller and colleagues examined the response of rat neutrophils to substance P and found concentration-dependent chemotaxis only at high concentrations (10 26 -10 24 mol/liter) (49).…”

Section: Discussionsupporting

confidence: 88%

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: 88%

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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“…Yet another possibility is that PPT-A gene products may act via the inflammatory cells, such as neutrophils (by inducing chemotaxis) or mast cells (11,29,34,36). Further studies shall be directed at defining the mechanism of action of PPT-A gene products as proinflammatory mediators in the pathogenesis of acute pancreatitis and associated lung injury.…”

Section: Discussionmentioning

confidence: 99%

Preprotachykinin-A gene deletion protects mice against acute pancreatitis and associated lung injury

Bhatia

Slavin

Cao

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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Impaired lung function in severe acute pancreatitis is the primary cause of morbidity and mortality in this condition. Preprotachykinin-A (PPT-A) gene products substance P and neurokinin (NK)-A have been shown to play important roles in neurogenic inflammation. Substance P acts primarily (but not exclusively) via the NK1 receptor. NKA acts primarily via the NK2 receptor. Earlier work has shown that knockout mice deficient in NK1 receptors are protected against acute pancreatitis and associated lung injury. NK1 receptors, however, bind other peptides in addition to substance P, not all of which are derived from the PPT-A gene. To examine the role of PPT-A gene products in acute pancreatitis, the effect of PPT-A gene deletion on the severity of acute pancreatitis and the associated lung injury was investigated. Deletion of PPT-A almost completely protected against acute pancreatitis-associated lung injury, with a partial protection against local pancreatic damage. These results show that PPT-A gene products are critical proinflammatory mediators in acute pancreatitis and the associated lung injury.

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“…(J ttistochem vated teeth after pulp exposure (Byers and 'bylor, 1993) is reported, indicating participation of sensory fibers in the inflammatory defense reactions. Furthermore, CGRP and SP have a chemotactic effect on neutrophils and T-lymphocytes (Foster et al, 1992;Wiedermann et al, 1989;Roch-Arveiller et al, 1986;Marasco et al, 1981) and stimulate macrophage cytokine production (Lott et al, 1988). Intra-articular infusion of SP exacerbates adjuvant-induced arthritis in rats (Levine et al, 1984).…”

Section: Troductionmentioning

confidence: 99%

Recruitment of immunocompetent cells after dentinal injuries in innervated and denervated young rat molars: an immunohistochemical study.

Fristad¹,

Heyeraas²,

Kvinnsland³

et al. 1995

J Histochem Cytochem.

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The dental pulp represents a peripheral end-organ deprived of a collateral nerve supply. After inferior alveolar nerve (IAN) axotomy, rat molar pulp is denervated over a period of at least 6 days. Therefore, rat molar pulp was used as an experimental model to study the effect of sensory nerve fibers on influx of immunocompetent cells after dentinal injury. In the present study we performed a quantitative analysis of CD43+, CD4+, CD11b+, and I-A antigen-expressing cells subjacent to dentinal cavities in denervated and innervated first mandibular molars. For visualization of nerve fibers, antibodies to protein gene product (PGP) 9.5, the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and the sympathetic neuropeptide Y (NPY) were used. Immunohistochemistry was performed by the avidin-biotin-peroxidase method. In the innervated teeth, a correlation between increased sensory nerve density and influx of immunocompetent cells was found. Compared to the contralateral innervated molars, a significant reduction in recruitment of immunocompetent cells was found in the denervated pulp tissue subjacent to the dentinal cavities. The rat molar represents a unique model to illustrate the influence of sensory nerves and neuropeptides on inflammation and recruitment of immunocompetent cells.

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Tachykinins: Effects on Motility and Metabolism of Rat Polymorphonuclear Leucocytes

Cited by 66 publications

References 5 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

Preprotachykinin-A gene deletion protects mice against acute pancreatitis and associated lung injury

Recruitment of immunocompetent cells after dentinal injuries in innervated and denervated young rat molars: an immunohistochemical study.

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