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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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Related in: MedlinePlus

Different challenge routes of pathogen affect the outcome of acute lung inflammation. Data were pooled from 6 mice in each group. Values are presented as mean ± SD. One-way analysis of variance (ANOVA) with post hoc Bonferroni test was used for statistical analysis (level set at P < 0.05). The committee on Animal Research of Institut Pasteur of Shanghai, Chinese Academy of Sciences approved all the protocol.
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fig2: Different challenge routes of pathogen affect the outcome of acute lung inflammation. Data were pooled from 6 mice in each group. Values are presented as mean ± SD. One-way analysis of variance (ANOVA) with post hoc Bonferroni test was used for statistical analysis (level set at P < 0.05). The committee on Animal Research of Institut Pasteur of Shanghai, Chinese Academy of Sciences approved all the protocol.

Mentions: Alveolar epithelial cells are the main target cells in the epithelial respiratory compartment exposed to noxious substances such as E. coli or acid [45]. Injury to the alveolar epithelial barrier is a major determinant of severity of clinical ALI [46, 47]. Our experiments have demonstrated that, at the same dosage, intratracheal challenge of E. coli could induce much severe lung inflammation than intraperitoneal challenge of E. coli. As Figure 2 shows, mice were divided into three groups: control group received PBS; E. coli pneumonia group received an intratracheal challenge of E. coli (107 cfu); E. coli peritonitis ALI group was given an intraperitoneal challenge of E. coli (107 cfu). All mice were also given I125-albumin intratracheally or intravenously to measure lung wet-to-dry weight ratio and lung epithelial and endothelial permeability as previously reported [5, 48]. At 4 h after challenge, three parameters were markedly higher in the E. coli pneumonia compared to E. coli peritonitis ALI.


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

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

Different challenge routes of pathogen affect the outcome of acute lung inflammation. Data were pooled from 6 mice in each group. Values are presented as mean ± SD. One-way analysis of variance (ANOVA) with post hoc Bonferroni test was used for statistical analysis (level set at P < 0.05). The committee on Animal Research of Institut Pasteur of Shanghai, Chinese Academy of Sciences approved all the protocol.
© Copyright Policy
Related In: Results  -  Collection

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

fig2: Different challenge routes of pathogen affect the outcome of acute lung inflammation. Data were pooled from 6 mice in each group. Values are presented as mean ± SD. One-way analysis of variance (ANOVA) with post hoc Bonferroni test was used for statistical analysis (level set at P < 0.05). The committee on Animal Research of Institut Pasteur of Shanghai, Chinese Academy of Sciences approved all the protocol.
Mentions: Alveolar epithelial cells are the main target cells in the epithelial respiratory compartment exposed to noxious substances such as E. coli or acid [45]. Injury to the alveolar epithelial barrier is a major determinant of severity of clinical ALI [46, 47]. Our experiments have demonstrated that, at the same dosage, intratracheal challenge of E. coli could induce much severe lung inflammation than intraperitoneal challenge of E. coli. As Figure 2 shows, mice were divided into three groups: control group received PBS; E. coli pneumonia group received an intratracheal challenge of E. coli (107 cfu); E. coli peritonitis ALI group was given an intraperitoneal challenge of E. coli (107 cfu). All mice were also given I125-albumin intratracheally or intravenously to measure lung wet-to-dry weight ratio and lung epithelial and endothelial permeability as previously reported [5, 48]. At 4 h after challenge, three parameters were markedly higher in the E. coli pneumonia compared to E. coli peritonitis ALI.

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