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Vagus nerve through α7 nAChR modulates lung infection and inflammation: models, cells, and signals.

Wu H, Li L, Su X - Biomed Res Int (2014)

Bottom Line: Here, we emphasized the research regarding the modulatory effects of CAP on animal models, cell population, and signaling pathways that involved in the pathogenesis of ALI.By comparing the differential effects of CAP on systemic and pulmonary inflammation, we postulated that a pulmonary parasympathetic inflammatory reflex is formed to sense and respond to pathogens in the lung.Work targeting the formation and function of pulmonary parasympathetic inflammatory reflex would extend our understanding of how vagus nerve senses, recognizes, and fights with pathogens and inflammatory responses.

View Article: PubMed Central - PubMed

Affiliation: Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, B104, Life Science Research Building, 320 Yueyang Road, Shanghai 200031, China.

ABSTRACT
Cholinergic anti-inflammatory pathway (CAP) bridges immune and nervous systems and plays pleiotropic roles in modulating inflammation in animal models by targeting different immune, proinflammatory, epithelial, endothelial, stem, and progenitor cells and signaling pathways. Acute lung injury (ALI) is a devastating inflammatory disease. It is pathogenically heterogeneous and involves many cells and signaling pathways. Here, we emphasized the research regarding the modulatory effects of CAP on animal models, cell population, and signaling pathways that involved in the pathogenesis of ALI. By comparing the differential effects of CAP on systemic and pulmonary inflammation, we postulated that a pulmonary parasympathetic inflammatory reflex is formed to sense and respond to pathogens in the lung. Work targeting the formation and function of pulmonary parasympathetic inflammatory reflex would extend our understanding of how vagus nerve senses, recognizes, and fights with pathogens and inflammatory responses.

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The hypothetical model of cholinergic anti-inflammatory pathway.
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fig1: The hypothetical model of cholinergic anti-inflammatory pathway.

Mentions: As Figure 1 shows, in the vagal inflammatory reflex, the sensory neurons may sense the changes of pathogen associated molecular patterns (PAMPs) or damage associated molecule patterns (DAMPs) in the peripheral afferent vagal nerve endings and then feedback to nucleus tractus solitarii (NTS) in the brain stem. After the information is processed in the NTS, the efferent vagus nerve transmits integrated information by action potentials to the celiac ganglion and then delivers in the spleen. Anatomically, the splenic vagus nerve endings are closely in contact with a group of β2 adrenergic receptor- (β2 AR-) expressing T memory lymphocytes (CD4+CD44highCD62Llow) and release norepinephrine (NE), a sympathetic neurotransmitter. NE activates β2 AR in the T lymphocytes, initiates transcription of choline acetyltransferase (ChAT), and synthesizes acetylcholine (ACh). ACh could activate splenic α7 nAChR-expressing macrophages, inhibit NF-κB activity, promote STAT3 phosphorylation [14], and therefore dampen proinflammatory cytokine production (especially TNF-α and HMGB1) [2, 3, 12, 15, 16].


Vagus nerve through α7 nAChR modulates lung infection and inflammation: models, cells, and signals.

Wu H, Li L, Su X - Biomed Res Int (2014)

The hypothetical model of cholinergic anti-inflammatory pathway.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4127262&req=5

fig1: The hypothetical model of cholinergic anti-inflammatory pathway.
Mentions: As Figure 1 shows, in the vagal inflammatory reflex, the sensory neurons may sense the changes of pathogen associated molecular patterns (PAMPs) or damage associated molecule patterns (DAMPs) in the peripheral afferent vagal nerve endings and then feedback to nucleus tractus solitarii (NTS) in the brain stem. After the information is processed in the NTS, the efferent vagus nerve transmits integrated information by action potentials to the celiac ganglion and then delivers in the spleen. Anatomically, the splenic vagus nerve endings are closely in contact with a group of β2 adrenergic receptor- (β2 AR-) expressing T memory lymphocytes (CD4+CD44highCD62Llow) and release norepinephrine (NE), a sympathetic neurotransmitter. NE activates β2 AR in the T lymphocytes, initiates transcription of choline acetyltransferase (ChAT), and synthesizes acetylcholine (ACh). ACh could activate splenic α7 nAChR-expressing macrophages, inhibit NF-κB activity, promote STAT3 phosphorylation [14], and therefore dampen proinflammatory cytokine production (especially TNF-α and HMGB1) [2, 3, 12, 15, 16].

Bottom Line: Here, we emphasized the research regarding the modulatory effects of CAP on animal models, cell population, and signaling pathways that involved in the pathogenesis of ALI.By comparing the differential effects of CAP on systemic and pulmonary inflammation, we postulated that a pulmonary parasympathetic inflammatory reflex is formed to sense and respond to pathogens in the lung.Work targeting the formation and function of pulmonary parasympathetic inflammatory reflex would extend our understanding of how vagus nerve senses, recognizes, and fights with pathogens and inflammatory responses.

View Article: PubMed Central - PubMed

Affiliation: Unit of Respiratory Infection and Immunity, Institut Pasteur of Shanghai, Chinese Academy of Sciences, B104, Life Science Research Building, 320 Yueyang Road, Shanghai 200031, China.

ABSTRACT
Cholinergic anti-inflammatory pathway (CAP) bridges immune and nervous systems and plays pleiotropic roles in modulating inflammation in animal models by targeting different immune, proinflammatory, epithelial, endothelial, stem, and progenitor cells and signaling pathways. Acute lung injury (ALI) is a devastating inflammatory disease. It is pathogenically heterogeneous and involves many cells and signaling pathways. Here, we emphasized the research regarding the modulatory effects of CAP on animal models, cell population, and signaling pathways that involved in the pathogenesis of ALI. By comparing the differential effects of CAP on systemic and pulmonary inflammation, we postulated that a pulmonary parasympathetic inflammatory reflex is formed to sense and respond to pathogens in the lung. Work targeting the formation and function of pulmonary parasympathetic inflammatory reflex would extend our understanding of how vagus nerve senses, recognizes, and fights with pathogens and inflammatory responses.

Show MeSH
Related in: MedlinePlus