scholarly journals Pulmonary C-fiber degeneration downregulates IFN-γ receptor 1 via IFN-α induction to attenuate RSV-induced airway hyperresponsiveness

Virology ◽  
2017 ◽  
Vol 510 ◽  
pp. 262-272 ◽  
Author(s):  
Zhixu Ye ◽  
Luo Ren ◽  
Zhengzhen Tang ◽  
Yu Deng ◽  
Xiaohong Xie ◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
C Fiber ◽  
Ifn Γ

scholarly journals Interrelationship of IFN-γ, IL-4, pituitary-thyroid and pituitary-adrenocortical systems in cold airway hyperresponsiveness in patients with asthma

Immunologiya ◽  
2021 ◽  
Vol 42 (5) ◽  
pp. 480-489
Author(s):  
A.B. Pirogov ◽  
◽  
A.G. Prihodko ◽  
Ju.M. Perelman ◽  
◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
Ifn Γ

scholarly journals Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness

2010 ◽  
Vol 78 (9) ◽  
pp. 4077-4086 ◽  
Author(s):  
Frank Kirstein ◽  
William G. C. Horsnell ◽  
Natalie Nieuwenhuizen ◽  
Bernhard Ryffel ◽  
Andreas L. Lopata ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Allergic Airway Inflammation ◽  
Gamma Interferon ◽  
Interleukin 4 ◽  
Wild Type ◽  
Receptor Alpha ◽  
Immunological Mechanisms ◽  
Ifn Γ ◽  
Interleukin 4 Receptor

ABSTRACT Infection with the fish parasite Anisakis following exposure to contaminated fish can lead to allergic reactions in humans. The present study examined the immunological mechanisms underlying the development of allergic airway inflammation in mice after different routes of sensitization to Anisakis. Wild-type and interleukin-4 receptor alpha (IL-4Rα)-deficient BALB/c mice were sensitized intraperitoneally with live or heat-killed Anisakis larvae or by intranasal administration of an Anisakis extract and were subsequently challenged intranasally with an Anisakis extract. Both routes of sensitization induced IL-4Rα-dependent allergic airway responses, whereas allergen-specific antibody responses developed only when mice were sensitized intraperitoneally. Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent. Unexpectedly, infection with Anisakis larvae induced AHR in both wild-type and IL-4Rα-deficient mice. IL-4Rα-independent AHR was mediated by gamma interferon (IFN-γ), as evidenced by the fact that in vivo neutralization of IFN-γ abrogated AHR. Together, these results demonstrate that both infection with larvae and inhalational exposure to Anisakis proteins are potent routes of allergic sensitization to Anisakis, explaining food- and work-related allergies in humans. Importantly for diagnosis, allergic airway inflammation can be independent of detectable Anisakis-specific antibodies. Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-γ.

scholarly journals Pulmonary chemoreflex responses are potentiated by tumor necrosis factor-alpha in mice

2013 ◽  
Vol 114 (11) ◽  
pp. 1536-1543 ◽  
Author(s):  
Ruei-Lung Lin ◽  
Yu-Jung Lin ◽  
Marcus J. Geer ◽  
Richard Kryscio ◽  
Lu-Yuan Lee
Keyword(s):  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
C Fiber ◽  
Chemoreflex Sensitivity ◽  
Increased Sensitivity ◽  
Factor Alpha ◽  
Necrosis Factor

Inhalation of tumor necrosis factor-alpha (TNF-α), a proinflammatory cytokine, induces airway hyperresponsiveness, and the underlying mechanism is not fully understood. Hypersensitivity of vagal bronchopulmonary C-fiber afferents is known to contribute to the airway hyperresponsiveness during an airway inflammatory reaction. Because activation of these afferents can elicit pulmonary chemoreflexes, this study was designed to determine if a pretreatment with TNF-α induced airway inflammation and enhanced the pulmonary chemoreflex sensitivity in anesthetized mice; and if so, whether the effect was mediated through activation of either or both of the TNF receptors, p55 and p75. Our results showed that TNF-α instilled into the lung caused an increased sensitivity of pulmonary chemoreflex responses to various chemical stimulants of the vagal bronchopulmonary C-fiber afferents. The increased sensitivity was found 24 h later, persisted at 48 h, and then gradually declined after several days. The TNF-α-induced airway hypersensitivity was accompanied by airway inflammation as shown by a striking elevation of the levels of eosinophils and neutrophils, several potent bronchoactive inflammatory mediators, and proinflammatory cytokines in the bronchoalveolar lavage fluid. Furthermore, the increase in pulmonary chemoreflex response caused by TNF-α was partially abrogated in both p55-null and p75-null mice, but completely abolished in p55/p75-null mice. In conclusion, TNF-α pretreatment induced airway inflammation and a sustained elevation of pulmonary chemoreflex sensitivity, which was mediated through an activation of both types of TNF receptors.

scholarly journals Prostaglandin involvement in lung C-fiber activation by substance P in guinea pigs

2006 ◽  
Vol 100 (6) ◽  
pp. 1918-1927 ◽  
Author(s):  
Dale R. Bergren
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Prostaglandin E ◽  
C Fibers ◽  
Arterial Blood ◽  
C Fiber ◽  
Before And After ◽  
Acid Metabolites ◽  
Series Of Experiments

Airway hyperresponsiveness is a cardinal feature of asthma. Lung C-fiber activation induces central and local defense reflexes that may contribute to airway hyperresponsiveness. Initial studies show that substance P (SP) activates C fibers even though it is produced and released by these same C fibers. SP may induce release of other endogenous mediators. Bradykinin (BK) is an endogenous mediator that activates C fibers. The hypothesis was tested that SP activates C fibers via BK release. Guinea pigs were anesthetized, and C-fiber activity (FA), pulmonary insufflation pressure (PIP), heart rate, and arterial blood pressure were monitored before and after intravenous injection of capsaicin (Cap), SP, and BK. Identical agonist challenges were repeated after infusion of an antagonist cocktail of des-Arg9-[Leu8]-BK (10−3 M, B1 antagonist), and HOE-140 (10−4 M, B2 antagonist). After antagonist administration, BK increased neither PIP nor FA. Increases in neither PIP nor FA were attenuated after Cap or SP challenge. In a second series of experiments, Cap and SP were injected before and after infusion of indomethacin (1 mg/kg iv) to determine whether either agent activates C fibers through release of arachidonic acid metabolites. Indomethacin administration decreased the effect of SP challenge on FA but not PIP. The effect of Cap on FA or PIP was not altered by indomethacin. In subsequent experiments, C fibers were activated by prostaglandin E2 and F2α. Therefore, exogenously applied SP stimulates an indomethacin-sensitive pathway leading to C-fiber activation.

scholarly journals A Th17-polarized cell population that has infiltrated the lung requires cells that convert to IFN-γ production in order to induce airway hyperresponsiveness

2010 ◽  
Vol 22 (6) ◽  
pp. 503-513 ◽  
Author(s):  
Shigeru Ashino ◽  
Daiko Wakita ◽  
Yasuo Shiohama ◽  
Yoichiro Iwakura ◽  
Kenji Chamoto ◽  
...  
Keyword(s):  
Cell Population ◽  
Airway Hyperresponsiveness ◽  
Ifn Γ

scholarly journals Reciprocal Immunomodulatory Effects of Gamma Interferon and Interleukin-4 on Filaria-Induced Airway Hyperresponsiveness

2001 ◽  
Vol 69 (3) ◽  
pp. 1463-1468 ◽  
Author(s):  
Rajeev K. Mehlotra ◽  
Laurie R. Hall ◽  
Musa A. Haxhiu ◽  
Eric Pearlman
Keyword(s):  
Airway Hyperresponsiveness ◽  
Gene Knockout ◽  
Pulmonary Inflammation ◽  
Lung Parenchyma ◽  
Gamma Interferon ◽  
Interleukin 4 ◽  
Interleukin 12 ◽  
Pulmonary Eosinophilia ◽  
Severe Asthmatic ◽  
Ifn Γ

ABSTRACT Tropical pulmonary eosinophilia (TPE) is a severe asthmatic syndrome of lymphatic filariasis, in which an allergic response is induced to microfilariae (Mf) in the lungs. Previously, in a murine model for TPE, we have demonstrated that recombinant interleukin-12 (IL-12) suppresses pulmonary eosinophilia and airway hyperresponsiveness (AHR) by modulating the T helper (Th) response in the lungs from Th2- to Th1-like, with elevated gamma-interferon (IFN-γ) production and decreased IL-4 and IL-5 production. The present study examined the immunomodulatory roles of IL-4 and IFN-γ in filaria-induced AHR and pulmonary inflammation using mice genetically deficient in these cytokines. C57BL/6, IL-4 gene knockout (IL-4−/−), and IFN-γ−/− mice were first immunized with soluble Brugia malayi antigens and then inoculated intravenously with 200,000 live Mf. Compared with C57BL/6 mice, IL-4−/− mice exhibited significantly reduced AHR, whereas IFN-γ−/− mice had increased AHR. Histopathologically, each mouse strain showed increased cellular infiltration into the lung parenchyma and bronchoalveolar space compared with naı̈ve animals. However, consistent with changes in AHR, IL-4−/− mice had less inflammation than C57BL/6 mice, whereas IFN-γ−/− mice had exacerbated pulmonary inflammation with the loss of pulmonary architecture. Systemically, IL-4−/− mice produced significantly higher IFN-γ levels compared with C57BL/6 mice, whereas IFN-γ−/− mice produced significantly higher IL-4 levels. These data indicate that IL-4 is required for the induction of filaria-induced AHR, whereas IFN-γ suppresses AHR.

Gynostemma pentaphyllum Decreases Allergic Reactions in a Murine Asthmatic Model

2008 ◽  
Vol 36 (03) ◽  
pp. 579-592 ◽  
Author(s):  
Wen-Chung Huang ◽  
Ming-Ling Kuo ◽  
Ming-Liang Li ◽  
Rong-Chi Yang ◽  
Chian-Jiun Liou ◽  
...  
Keyword(s):  
Immune Responses ◽  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Low Cost ◽  
Eosinophil Infiltration ◽  
Allergic Reactions ◽  
Herbal Tea ◽  
Gynostemma Pentaphyllum ◽  
Ifn Γ ◽  
Th 1

The increasing incidence of asthma in developing countries emphasizes the importance of identifying more effective treatments that have low cost. Gynostemma pentaphyllum (Thunb.) Makino (Cucurbitaceae), a common herbal tea in China, has been used to treat lung inflammation. Since the Th 2 cytokines are the major mediators in the pathogenesis of asthma, Th 1-biased immune responses caused by G. pentaphyllum might have the potential to relieve asthmatic symptoms. We hypothesized that oral administration of G. pentaphyllum extracts might suppress Th 2 cytokine-induced airway inflammation responses in ovalbumin (OVA)-sensitive mice. BALB/c mice were sensitized with intraperitoneal injection and challenged 3 times with OVA inhalation (IH) (the IH3 model). G. pentaphyllum was orally administered for 7 consecutive days before the end of the OVA challenge. In the IH5 model, 2 more OVA challenges were administered to mimic the encounter with an allergen after drug treatment. G. pentaphyllum extracts significantly attenuated airway hyperresponsiveness (AHR) and inhibited eosinophil infiltration in mice in both models. Serum OVA-specific antibodies were also reduced with the treatment. Decreased Th 2-type cytokines and increased IFN-γ were detected in the cultures of OVA-activated splenocytes from treated mice. Our results suggest that G. pentaphyllum extracts might be beneficial for asthma airway inflammation through the suppression of Th 2 activity.

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