Neural control of airway inflammation

Verhein, Kirsten C.; Fryer, A.D.; Jacoby, David B.

doi:10.1007/s11882-009-0071-9

Cited by 28 publications

(26 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Separately, in guinea pigs, a subset of esophageal neurons that express calretinin and ACh have been found to provide excitatory input to tracheal cholinergic ganglia and thus indirectly regulate airway tone (197). Finally, the effects of inflammation (321,332), infection (124), pollutants (252), and other stimuli on airway nerves are being explored, again with the intent of suppressing excessive bronchoconstriction, as well as cough reflexes. Here, an emerging theme is again neurotrophins such as NGF, BDNF, and glial-derived neurotrophic factor that serve to influence airway reactivity (175,176,200) as well as enhance immunity and reactivity in the airway following bacterial infections (38), exposure to house dust mite (and important aspect of allergic asthma) (346), allergen challenge (176), or ozone (322).…”

Section: Neural Controlmentioning

confidence: 99%

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

Prakash

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

179

154

View full text Add to dashboard Cite

Prakash YS. Airway smooth muscle in airway reactivity and remodeling: what have we learned? Am J Physiol Lung Cell Mol Physiol 305: L912-L933, 2013. First published October 18, 2013 doi:10.1152/ajplung.00259.2013.-It is now established that airway smooth muscle (ASM) has roles in determining airway structure and function, well beyond that as the major contractile element. Indeed, changes in ASM function are central to the manifestation of allergic, inflammatory, and fibrotic airway diseases in both children and adults, as well as to airway responses to local and environmental exposures. Emerging evidence points to novel signaling mechanisms within ASM cells of different species that serve to control diverse features, including 1) [Ca 2ϩ ]i contractility and relaxation, 2) cell proliferation and apoptosis, 3) production and modulation of extracellular components, and 4) release of pro-vs. anti-inflammatory mediators and factors that regulate immunity as well as the function of other airway cell types, such as epithelium, fibroblasts, and nerves. These diverse effects of ASM "activity" result in modulation of bronchoconstriction vs. bronchodilation relevant to airway hyperresponsiveness, airway thickening, and fibrosis that influence compliance. This perspective highlights recent discoveries that reveal the central role of ASM in this regard and helps set the stage for future research toward understanding the pathways regulating ASM and, in turn, the influence of ASM on airway structure and function. Such exploration is key to development of novel therapeutic strategies that influence the pathophysiology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis.

show abstract

Section: Neural Controlmentioning

confidence: 99%

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

Prakash

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

179

154

View full text Add to dashboard Cite

show abstract

“…Sensory nerves innervate a range of key structures of the respiratory tract, including the airway epithelium, smooth muscle band, and submucosal glands (Verhein et al, 2009). Afferent sensory nerves located within the airway epithelium serve to detect the presence of noxious stimuli and initiate a reflex bronchoprotective response (Martling, 1987).…”

Section: Introductionmentioning

confidence: 99%

Influence of Influenza A Infection on Capsaicin-Induced Responses in Murine Airways

Taylor

Mann²,

Henry³

2011

J Pharmacol Exp Ther

View full text Add to dashboard Cite

The principal aim of the study was to determine the influence of influenza A virus infection on capsaicin-induced relaxation responses in mouse isolated tracheal segments and clarify the underlying mechanisms. Anesthetized mice were intranasally inoculated with influenza A/PR-8/34 virus (VIRUS) or vehicle (SHAM), and 4 days later tracheal segments were harvested for isometric tension recording and biochemical and histologic analyses. Capsaicin induced dose-dependent relaxation responses in carbachol-contracted SHAM trachea (e.g., 10 M capsaicin produced 66 Ϯ 4% relaxation; n ϭ 11), which were significantly inhibited by capsazepine prostanoid (EP) 2 and EP 4 receptor antagonists, respectively], indicating that capsaicin-induced relaxation involved the TRPV1-mediated release of substance P (SP), activation of epithelial NK 1 receptors, and production of COX products capable of activating relaxant EP 2 /EP 4 receptors. Consistent with this postulate, capsaicin-induced relaxation was associated with the significant release of SP and prostaglandin E 2 (PGE 2 ) from mouse tracheal segments. As expected, influenza A virus infection was associated with widespread disruption of the tracheal epithelium. Tracheal segments from VIRUS mice responded weakly to capsaicin (7 Ϯ 3% relaxation) and were 25-fold less responsive to SP than tracheas from SHAM mice. In contrast, relaxation responses to exogenous PGE 2 and the ␤-adrenoceptor agonist isoprenaline were not inhibited in VIRUS trachea. Virus infection was associated with impaired capsaicin-induced release of PGE 2 , but the release of SP was not affected. In summary, influenza A virus infection profoundly inhibits capsaicin-and SP-induced relaxation responses, most likely by inhibiting the production of PGE 2 .

show abstract

“…Animal studies link prenatal PM with cytokine disruption, increased IgE, impaired lung growth, and airway hyperresponsiveness in offspring (11)(12)(13)(14). Gestational exposure to PM may enhance maternal systemic oxidative stress and proinflammatory cytokine production (15) resulting in placental and endothelial dysfunction, and increased fetal oxidative stress with consequent effects on fetal immune and lung development (7,14,(16)(17)(18).…”

mentioning

confidence: 99%

Prenatal Particulate Air Pollution and Asthma Onset in Urban Children. Identifying Sensitive Windows and Sex Differences

Hsu¹,

Chiu²,

Coull

et al. 2015

Am J Respir Crit Care Med

276

104

View full text Add to dashboard Cite

Rationale: The influence of particulate air pollution on respiratory health starts in utero. Fetal lung growth and structural development occurs in stages; thus, effects on postnatal respiratory disorders may differ based on timing of exposure.Objectives: We implemented an innovative method to identify sensitive windows for effects of prenatal exposure to particulate matter with a diameter less than or equal to 2.5 mm (PM 2.5 ) on children's asthma development in an urban pregnancy cohort.Methods: Analyses included 736 full-term (>37 wk) children. Each mother's daily PM 2.5 exposure was estimated over gestation using a validated satellite-based spatiotemporal resolved model. Using distributed lag models, we examined associations between weekly averaged PM 2.5 levels over pregnancy and physician-diagnosed asthma in children by age 6 years. Effect modification by sex was also examined.Measurements and Main Results: Most mothers were ethnic minorities (54% Hispanic, 30% black), had 12 or fewer years of education (66%), and did not smoke in pregnancy (80%). In the sample as a whole, distributed lag models adjusting for child age, sex, and maternal factors (education, race and ethnicity, smoking, stress, atopy, prepregnancy obesity) showed that increased PM 2.5 exposure levels at 16-25 weeks gestation were significantly associated with early childhood asthma development. An interaction between PM 2.5 and sex was significant (P = 0.01) with sex-stratified analyses showing that the association exists only for boys.Conclusions: Higher prenatal PM 2.5 exposure at midgestation was associated with asthma development by age 6 years in boys. Methods to better characterize vulnerable windows may provide insight into underlying mechanisms.

show abstract

Neural control of airway inflammation

Cited by 28 publications

References 68 publications

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

Influence of Influenza A Infection on Capsaicin-Induced Responses in Murine Airways

Prenatal Particulate Air Pollution and Asthma Onset in Urban Children. Identifying Sensitive Windows and Sex Differences

Contact Info

Product

Resources

About