Neurokinin‐1 receptor activation induces reactive oxygen species and epithelial damage in allergic airway inflammation

Springer, Jochen; Groneberg, David A.; Dinh, Q. Thai; Quarcoo, David; Hamelmann, Eckard; Braun-Dullaeus, Ruediger C.; Geppetti, Pierangelo; Anker, Stefan D.; Fischer, Axel

doi:10.1111/j.1365-2222.2007.02851.x

Cited by 26 publications

(12 citation statements)

References 44 publications

(54 reference statements)

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“…To assess the physiological relevance of the in vitro ROS inhibitor findings, mice were treated with the ROS inhibitor NAc via i.n. administration as previously described (Springer et al, 2007). Similar to the monocyte cell line findings, treatment with NAc completely inhibited the generation of IL-1β in the BALF following influenza infection (Figure 5M).…”

Section: Resultsmentioning

confidence: 99%

The NLRP3 Inflammasome Mediates In Vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

et al. 2009

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SUMMARY NLR genes mediate host immunity to various pathogenic stimuli. However, in vivo evidence for NLR involvement in viral sensing has not been widely investigated and remains controversial. As an ultimate test of the physiologic role of NLRP3 during RNA viral infection, this work explores the in vivo role of NLRP3 inflammasome components during influenza virus infection. Mice lacking Nlrp3, ASC, or Caspase-1, but not Nlrc4, exhibit dramatically increased mortality but reduced immune response following influenza virus exposure. Utilizing analogs of dsRNA (poly(I:C)) and ssRNA (ssRNA40), we demonstrate that NLRP3-mediated response can be activated by RNA species. Mechanistically, NLRP3 inflammasome activation by influenza virus is dependent upon lysosomal maturation and reactive oxygen species. Inhibition of ROS induction eliminated IL-1β production in animals during influenza infection. Together, these data place the NLRP3 inflammasome as an essential component in host defense against influenza infection through the sensing of viral RNA.

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Section: Resultsmentioning

confidence: 99%

The NLRP3 Inflammasome Mediates In Vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

et al. 2009

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“…These responses neutralize, hinder, and expel toxic materials, limiting damage to the delicate alveolar sacs. However, continued exposures can lead to exaggerated responses that compromise respiratory function (20,22). Reactive TIHs can compound pre-existing conditions.…”

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confidence: 99%

“…For example, they are notorious for triggering attacks in individuals with asthma (irritant-induced asthma) (23). The continual respiratory responses might be involved in the development of chronic airway diseases, including bronchitis and occupational asthma, and reactive airway dysfunction syndrome (20)(21)(22)(24)(25)(26)(27)(28)(29). Exaggerated sensory neuronal responses may contribute to the pulmonary edema and adult respiratory distress syndrome (ARDS) seen with high concentration exposure of TIHs (30,31).…”

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confidence: 99%

Sensory Detection and Responses to Toxic Gases: Mechanisms, Health Effects, and Countermeasures

Bessac

Jordt²

2010

Proceedings of the American Thoracic Society

118

112

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The inhalation of reactive gases and vapors can lead to severe damage of the airways and lung, compromising the function of the respiratory system. Exposures to oxidizing, electrophilic, acidic, or basic gases frequently occur in occupational and ambient environments. Corrosive gases and vapors such as chlorine, phosgene, and chloropicrin were used as warfare agents and in terrorist acts. Chemical airway exposures are detected by the olfactory, gustatory, and nociceptive sensory systems that initiate protective physiological and behavioral responses. This review focuses on the role of airway nociceptive sensory neurons in chemical sensing and discusses the recent discovery of neuronal receptors for reactive chemicals. Using physiological, imaging, and genetic approaches, Transient Receptor Potential (TRP) ion channels in sensory neurons were shown to respond to a wide range of noxious chemical stimuli, initiating pain, respiratory depression, cough, glandular secretions, and other protective responses. TRPA1, a TRP ion channel expressed in chemosensory C-fibers, is activated by almost all oxidizing and electrophilic chemicals, including chlorine, acrolein, tear gas agents, and methyl isocyanate, the highly noxious chemical released in the Bhopal disaster. Chemicals likely activate TRPA1 through covalent protein modification. Animal studies using TRPA1 antagonists or TRPA1-deficient mice confirmed the role of TRPA1 in chemically induced respiratory reflexes, pain, and inflammation in vivo. New research shows that sensory neurons are not merely passive sensors of chemical exposures. Sensory channels such as TRPA1 are essential for maintenance of airway inflammation in asthma and may contribute to the progression of airway injury following high-level chemical exposures.

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“…Together, an initial TRPA1 response to respiratory irritants, followed by secondary responses to inflammatory mediators, implicates TRPA1 in sensory processing and augmented dysregulation in airway diseases due to enduring inflammation and lung remodeling (Springer et al, 2007;Li et al, 2008). TRPA1 is also likely to mediate allergen-induced airway inflammation in patients with asthma, as demonstrated using trpa1 2/2 mice or by treatment with the selective TRPA1 inhibitor 2,3,acetamide], which reduces allergen-induced leukocyte infiltration, cytokine and mucus production, and airway hyper-responsiveness Raemdonck et al, 2012).…”

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confidence: 99%

The G Protein–Coupled Receptor–Transient Receptor Potential Channel Axis: Molecular Insights for Targeting Disorders of Sensation and Inflammation

Veldhuis¹,

Poole²,

Grace³

et al. 2014

Pharmacol Rev

137

135

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Neurokinin‐1 receptor activation induces reactive oxygen species and epithelial damage in allergic airway inflammation

Cited by 26 publications

References 44 publications

The NLRP3 Inflammasome Mediates In Vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

The NLRP3 Inflammasome Mediates In Vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA

Sensory Detection and Responses to Toxic Gases: Mechanisms, Health Effects, and Countermeasures

The G Protein–Coupled Receptor–Transient Receptor Potential Channel Axis: Molecular Insights for Targeting Disorders of Sensation and Inflammation

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