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Antigenic Challenge (antigenic + challenge)

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Selected Abstracts

Role of 5-HT2A, 5-HT4 and 5-HT7 receptors in the antigen-induced airway hyperresponsiveness in guinea-pigs

CLINICAL & EXPERIMENTAL ALLERGY, Issue 2 2010
P. Segura
Summary Background A possible role of 5-hydroxytryptamine (5-HT) in the origin of antigen-induced airway hyperresponsiveness (AI-AHR) has been scarcely investigated. Objective To explore the participation of different 5-HT receptors in the development of AI-AHR in guinea-pigs. Methods Lung resistance was measured in anaesthetized guinea-pigs sensitized to ovalbumin (OVA). Dose,response curves to intravenous (i.v.) acetylcholine (ACh) were performed before and 1 h after antigenic challenge and expressed as the 200% provocative dose (PD200). Organ bath experiments, confocal microscopy and RT-PCR were additionally used. The 5-HT content in lung homogenates was measured by HPLC. Results Antigenic challenge significantly decreased PD200, indicating the development of AI-AHR. This hyperresponsiveness was abolished by a combination of methiothepin (5-HT1/5-HT2/5-HT5/5-HT6/5-HT7 receptors antagonist) and tropisetron (5-HT3/5-HT4 antagonist). Other 5-HT receptor antagonists showed three different patterns of response. Firstly, WAY100135 (5-HT1A antagonist) and ondansetron (5-HT3 antagonist) did not modify the AI-AHR. Secondly, SB269970 (5-HT7 antagonist), GR113808 (5-HT4 antagonist), tropisetron or methiothepin abolished the AI-AHR. Thirdly, ketanserin (5-HT2A antagonist) produced airway hyporresponsiveness. Animals with bilateral vagotomy did not develop AI-AHR. Experiments in tracheal rings showed that pre-incubation with LP44 or cisapride (agonists of 5-HT7 and 5-HT4 receptors, respectively) induced a significant increase of the cholinergic contractile response to the electrical field stimulation. In sensitized lung parenchyma strips, ketanserin diminished the contractile responses to ACh. Sensitization was associated with a ninefold increase in the 5-HT content of lung homogenates. Confocal microscopy showed that sensitization enhanced the immunolabelling and co-localization of nicotinic receptor and 5-HT in airway epithelium, probably located in pulmonary neuroendocrine cells (PNECs). RT-PCR demonstrated that neither sensitization nor antigen challenge modified the 5-HT2A receptor mRNA levels. Conclusions Our results suggested that 5-HT was involved in the development of AI-AHR to ACh in guinea-pigs. Specifically, 5-HT2A, 5-HT4 and 5-HT7 receptors seem to be particularly involved in this phenomenon. Participation of 5-HT might probably be favoured by the enhancement of the PNECs 5-HT content observed after sensitization. Cite this as: P. Segura, M. H. Vargas, G. Córdoba-Rodríguez, J. Chávez, J. L. Arreola, P. Campos-Bedolla, V. Ruiz, L. M. García-Hernández, C. Méndez and L. M. Montaño, Clinical & Experimental Allergy, 2010 (40) 327, 338. [source]

Naturally occurring polyphenolic antioxidants modulate IgE-mediated mast cell activation

IMMUNOLOGY, Issue 4 2000
S.-S. Chen
Summary Reactive oxygen species (ROS) are known to modulate activities of a host of kinases, phosphatases and transcription factors. Rutin and chlorogenic acid (CGA) are the major polyphenolic antioxidants present in the small molecular fraction of smokeless tobacco leaf extracts, as ascertained by reverse-phase high-pressure liquid chromatography (HPLC) and mass spectrometry. Levels of intracellular ROS in resting versus antigen,immunoglobulin E (IgE)-challenged murine mast cells were measured at 510 nm by fluorescence-activated cell sorting (FACS) using carboxy-dichlorofluorescein (DCFH-DA). Enhanced ROS production was observed in IgE-sensitized mast cells following antigenic challenge. Rutin and CGA reduced ROS levels in antigen,IgE-activated mast cells. Concomitantly, they also profoundly inhibited histamine release by these activated mast cells. In contrast, rutin and CGA augmented the inducible cytokine messages, i.e. interleukin (IL)-10, IL-13, interferon-, (IFN-,), IL-6 and tumour necrosis factor-, (TNF-,) in IgE-sensitized mast cells following antigen challenge. This study indicates that tobacco polyphenolic antioxidants that quench intracellular ROS, differentially affect two effector functions of antigen,IgE-activated mast cells. This model system may be employed to determine the molecular target of polyphenols. The potential role of these polyphenolic antioxidants on IgE-mediated allergy in vivo depends on a balance of their differential effects on mast cell activation. [source]

Role of 5-HT2A, 5-HT4 and 5-HT7 receptors in the antigen-induced airway hyperresponsiveness in guinea-pigs

Inhibitory effect of 1,8-cineole on guinea-pig airway challenged with ovalbumin involves a preferential action on electromechanical coupling

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2009
Vasco PD Bastos
Summary 11,8-Cineole is a terpenoid constituent of essential oils with anti-inflammatory properties. It reduces the neural excitability, functions as an antinociceptive agent and has myorelaxant actions in guinea-pig airways. The aim of the present study was to investigate the mechanism underlying the myorelaxant effects of 1,8-cineole in guinea-pig isolated trachea from either naïve guinea-pigs or ovalbumin (OVA)-sensitized animals subjected to antigenic challenge. 2Isometric recordings were made of the tone of isolated tracheal rings. Rings with an intact epithelium relaxed beyond basal tone in the presence of 1,8-cineole (6.5 × 10,6 to 2 × 10,2 mol/L) in a concentration-dependent manner (P < 0.001, anova) with a pD2 value of 2.23 (95% confidence interval 2.10,2.37). Removal of the epithelium or pretreatment of intact tissue for 15 min with 50 µmol/L NG -nitro- l -arginine methyl ester, 5 mmol/L tetraethylammonium, 0.5 µmol/L tetrodotoxin or 5 µmol/L propranolol did not alter the potency (pD2) or the maximal myorelaxant effect (Emax) of 1,8-cineole. 31,8-Cineole also significantly decreased the Schultz-Dale contraction induced by OVA, mainly in preparations from OVA-sensitized animals submitted to antigen challenge. 1,8-Cineole decreased tracheal hyperresponsiveness to KCl and carbachol caused by antigen challenge and almost abolished the concentration,response curves to KCl, whereas it had little effect on the concentration,response curves to carbachol. Under Ca2+ -free conditions and in the presence of 10,4 mol/L acetylcholine, neither 1,8-cineole (6.5 × 10,3 mol/L) nor verapamil (1 × 10,5 mol/L) affected Ca2+ -induced contractions, but they almost abolished Ba2+ -induced contractions. 4In conclusion, the findings of the present study show that 1,8-cineole is a tracheal myorelaxant that acts preferentially on contractile responses elicited electromechanically. [source]

Inflammatory nerve responses in the dental pulp

ENDODONTIC TOPICS, Issue 1 2007
INGE FRISTAD
Tooth pulp has a dense innervation and a rich vascular supply to maintain homeostasis and to preserve the integrity of the tissue. Function, trauma, and antigenic challenges make teeth and supporting tissues susceptible to tissue injury and inflammation, partially due to the lack of collateral blood and nerve supply and to their low compliance. This review focuses on dental nerve functions and adaptive changes in the pulpal nerve supply following inflammation and peripheral injury. Overviews of dental innervation and its development and of the peptidergic innervation of oral tissues are presented, followed by a discussion of peripheral and central changes after local insults to teeth and peripheral nerve injuries. The functional implications of these adaptive changes are considered. Received 13 February 2009; accepted 3 September 2009. [source]

Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar rats

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2001
Torbjørn Breivik
Abstract Background: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. Objective: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. Method: New-born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. Results: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth. Conclusions: This study supports our resent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression. Zusammenfassung Hintergrund: Es hatte gezeigt werden können, dass die Unfähigkeit des Gehirns auf einen bakteriellen oder antigenen Reiz mit einer angemessenen neuroendokrinen Antwort zu reagieren, eine wichtige Rolle für die Empfänglichkeit für infektiöse und entzündliche Erkrankungen einschliesslich Parodontitis spielt. Die Gabe von Glutamat nach der Geburt führt zu irreversiblen Schäden der Neurone des Nucleus arcuatus des Hypothalamus. Zielzetzung: Untersuchung der Auswirkungen von Glutamatgaben bei neugeborenen Wistar-Ratten auf die Entstehung und das Fortschreiten natürlich vorkommender und ligaturinduzierter Parodontitis im Erwachsenenalter. Material und Methoden: Bei 24 neugeborenen Wistar-Ratten wurden einmal täglich 2 mg/g L-Mononatriumglutamat und bei 20 Kontrolltieren statt dessen Kochsaltzlösung vom 4. Lebenstag an 4 Tage lang subkutan injiziert. Am rechten zweiten Oberkiefermolaren wurden bei den 12 Wochen alten Ratten eine experimentelle ligaturinduzierte Parodontitis ausgelöst. Der kontralaterale 2. Molar des Oberkiefers diente als Kontrolle und um natürlich vorkommende Parodontitis zu untersuchen. Das Fortschreiten der parodontalen Zerstörung wurde histometrisch erfasst. Ergebnisse: Die Ergebnisse zeigten, dass die Ratten mit den glutamatinduzierten Läsionen statistisch signifikant stärkere parodontale Zerstörungen sowohl an den Zähnen mit wie auch an denen ohne Ligaturen im Vergleich zur Kontrollgruppe aufwiesen. Schlussfolgerungen: Eine unangemessene neuroendokrinoimmunologische Regulation des Gehirns scheint eine Rolle bei der Empfänglichkeit für und das Fortschreiten von Parodontitis zu haben. Résumé Origine: L'incapacitéàétablir une réponse neuroendocrinienne cervicale efficace pour des défis bactériens ou antigèniques joue un rôle important dans la susceptibilité et la progression des maladies infectieuses et inflammatoires, dont les parodontites. But: Cette étude a été imaginée pour déterminer les effets de l'administration de glutamate à des rats Wistar nouveau-nés sur le développement et la progression de maladies parodontales naturelles et induites par des ligatures chez le rat adulte. On sait que l'administration de glutamate en postnatal endommage de façon permanente les neurones du noyau d'arc hypothalamique. Méthodes: Les rats nouveaus-nés furent traités une fois par jour par administration sous cutanée de 2 mg/g de monosodium-L-glutamate (MSG) pendant 5 jours. Les animaux contrôles recevaient une dose similaire de sérum physiologique. La parodontite expérimentale par ligature était réalisée à l'âge de 12 semaines, sur la deuxième molaire supérieure droite. La dent controlatérale servait de contrôle et à la mise en évidence de maladie parodontale naturelle. La progression de la maladie fut évaluée par histométrie. Résultats: Les résultats montrent que les rats atteints de lésions dues au glutamate développent plus de destructions parodontales (par ligatures ou sans ligatures) par rapport aux rats contrôles atteints de lésions simulées. Conclusion: Cette étude supporte nos récentes découvertes qui indiquent qu'une régulation immunitaire neuroendocrinienne cervicale inappropriée peut jouer un rôle dans la susceptibilité et la progression des maladies parodontales. [source]