2001
DOI: 10.1006/pupt.2000.0318
|View full text |Cite
|
Sign up to set email alerts
|

Histamine and Serotonin

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

0
40
0

Year Published

2003
2003
2013
2013

Publication Types

Select...
8
2

Relationship

0
10

Authors

Journals

citations
Cited by 62 publications
(41 citation statements)
references
References 119 publications
0
40
0
Order By: Relevance
“…Although serotonin does not constrict the human airway smooth muscle in vitro, it increases acetylcholine release from airway nerves via 5HT3 and 5HT4 receptors. 35 The activation of the serotoninergic receptors on human airway epithelial cells regulates the release of IL-6 and IL-8. 36 SLC6A4 could play a role in the inflammatory responses of human airway epithelial cells in COPD subjects by changing the concentration of serotonin in the peripheral lungs.…”
Section: Discussionmentioning
confidence: 99%
“…Although serotonin does not constrict the human airway smooth muscle in vitro, it increases acetylcholine release from airway nerves via 5HT3 and 5HT4 receptors. 35 The activation of the serotoninergic receptors on human airway epithelial cells regulates the release of IL-6 and IL-8. 36 SLC6A4 could play a role in the inflammatory responses of human airway epithelial cells in COPD subjects by changing the concentration of serotonin in the peripheral lungs.…”
Section: Discussionmentioning
confidence: 99%
“…In fact, our data suggest that the induction of pulmonary IDO by antigen-specific Th1 cell lines negatively controls their own survival and their inflammatory response, i.e., M-trp implantation reduced Th1 cell death ( Figure 5D) and increased neutrophil infiltration, a marker of pulmonary inflammation ( Figure 5C). IDO can inhibit Th-mediated lung inflammation in multiple ways: (a) it depletes trp availability in the microenvironment (22); (b) it promotes the generation of various toxic trp metabolites, which induce Th cell death (30,31); (c) it generates other compounds, e.g., formylkynurenine, through a reaction that removes oxygen radicals at inflammatory sites (32); and (d) in the case of Th2-mediated lung inflammation, it inhibits the generation of 5-hydroxytryptamine, a potent airway constrictor (33). These unique and synergistic activities of IDO likely collaborate to inhibit Th2-mediated experimental asthma and to attenuate Th1-mediated pulmonary inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…When considering the role of the eosinophil in AHR, we must understand the mechanisms of AHR and then consider where any single cell type would be positioned to cause such effect. While the smooth muscle layers of asthmatic airways can become hypertrophied and more fibrous with time, whether the muscle is intrinsically more hyperresponsive to stimulation remains unclear (34).…”
Section: Tissue Localization and Activation Status Of The Eosinophil mentioning
confidence: 99%