Chest
Original ResearchCritical Care MedicineBile Acid Aspiration in Suspected Ventilator-Associated Pneumonia
Section snippets
Study Setting and Population
This prospective observational study was conducted between June 2006 and October 2006 in one ICU in a university-affiliated medical center. The education program used in this ICU to reduce the incidence of VAP was adopted according to the policy reported by Zack et al.15 We analyzed the levels and influence of bile acids in patients with suspected VAP. All consecutive patients who had received mechanical ventilation in our ICU for at least 4 days were enrolled in the study if they had suspected
Bile Acids and IL-8 in the Airway
Airway secretions were collected from intubated and mechanically ventilated patients with or without suspected VAP. Table 1 shows the characteristics of these patients and the organisms on culture. The concentrations of total bile acids and IL-8 were significantly higher in the suspected VAP group than those without suspected VAP. Figure 1, A, shows the levels of total bile acids in the airway secretions. For further analysis of bile acids in the airways, liquid chromatography-electrospray
Discussion
Aspiration has been considered to be an important risk factor for the development of VAP.19, 20, 21 Placing mechanically ventilated patients in a semirecumbent position is strongly recommended in education programs to prevent VAP15, 22; on the contrary, one well-conducted study23 demonstrated that difference in treatment position angle (28° vs 10°) did not reduce the incidence of VAP. Another view is that aspiration may introduce bacterial pathogens into the respiratory tract. Several studies20
Conclusions
The bile acid levels in the airway are significantly higher in intubated and mechanically ventilated patients with suspected VAP than in those without VAP. The consequence of alveolar epithelial cells exposure to bile acids may be enhanced neutrophilic inflammation through the activation of MAP kinase and subsequent IL-8 production.
Acknowledgment
We thank Dr. Chen for his valuable assistance in the analysis of bile acid components.
References (33)
- et al.
The effect of reflux and bile acid aspiration on the lung allograft and its surfactant and innate immunity molecules SP-A and SP-D
Am J Transplant
(2006) - et al.
Bile acid aspiration and the development of bronchiolitis obliterans after lung transplantation
J Thorac Cardiovasc Surg
(2005) - et al.
The pathophysiologic changes following bile aspiration in a porcine lung model
Chest
(1993) - et al.
Exposure of airway epithelium to bile acids associated with gastroesophageal reflux symptoms: a relation to transforming growth factor-β1 production and fibroblast proliferation
Chest
(2007) - et al.
Characteristics of airway inflammation and bronchodilator reversibility in COPD: a potential guide to treatment
Chest
(2004) - et al.
Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial
Lancet
(1999) - et al.
Gastric colonization by Gram-negative bacilli and nosocomial pneumonia in the intensive care unit patient: evidence for causation
Chest
(1992) - et al.
Gastroduodenal dysfunction and bacterial colonisation of the ventilated lung
Lancet
(1993) - et al.
Reducing ventilator-associated pneumonia rates through a staff education programme
J Hosp Infect
(2004) - et al.
Duodenal reflux induces cyclooxygenase-2 in the esophageal mucosa of rats: evidence for involvement of bile acids
Gastroenterology
(2001)
Endotracheal aspiration in the diagnosis of ventilator-associated pneumonia
Chest
Inhibition of pyocyanin-potentiated IL-8 release by steroids in bronchial epithelial cells
Respir Med
Inhibition of chemokine production from human airway smooth muscle cells by fluticasone, budesonide and beclomethasone
Pulm Pharmacol Ther
Tracheobronchial aspiration of gastric contents in critically ill tube-fed patients: frequency, outcomes, and risk factors
Crit Care Med
Raised bile acid concentrations in SIDS lungs at necropsy
Arch Dis Child
Bile acid pneumonia: a “new” form of neonatal respiratory distress syndrome?
Pediatrics
Cited by (38)
Aspiration of conjugated bile acids predicts adverse lung transplant outcomes and correlates with airway lipid and cytokine dysregulation
2021, Journal of Heart and Lung TransplantationCitation Excerpt :This study has shown particular relevance for TCDCA. The unconjugated form of this primary bile acid, CDCA, has been previously implicated in cellular damage, permeability and increased reactive oxygen species.17-19 The conjugation with taurine adds a sulfonic acid functional group to the molecule, increasing its acidity and solubility.
The profibrotic effects of chronic microaspiration of bile acids on lungs of rats at different stages
2020, International ImmunopharmacologyCitation Excerpt :Thereby, presumably, non-acid components, e.g. bile acids, may be active players in the formation of pulmonary fibrosis. Studies reported that the major components of bile acids (DCA and CDCA) have all been detected in airways of patients with GERD-associated lung diseases [14,15]. Our previous study revealed that microaspiration of bile acids could promote the development of pulmonary fibrosis in vivo [9].
The effect of gastric juice on interleukin-8 production by cystic fibrosis primary bronchial epithelial cells
2013, Journal of Cystic FibrosisCitation Excerpt :In LTx patients, clear correlations between levels of bile acids and IL-8 in BALF have been found [9,10]. Wu et al. demonstrated that exposure of airway epithelial cells in vitro to chenodeoxycholic acid, a major component of bile acids, is capable to induce an increase in IL-8 production [26]. Pepsin itself is inactive at pH 6.5, however, it remains stable to pH 8.0 and can be reactivated when pH is reduced.
Are the enzymatic methods currently being used to measure bronchoalveolar lavage bile salt levels fit for purpose?
2013, Journal of Heart and Lung TransplantationAspiration Pneumonia
2024, Seminars in Respiratory and Critical Care MedicineBile acid-induced lung injury: Update of reverse translational biology
2022, American Journal of Physiology - Lung Cellular and Molecular Physiology
This work was supported by research grants from Taipei Veterans General Hospital (V96C1-065).
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).
- *
These authors made equal contributions to this study.