The Emerging Role of the Microbiota in the ICU

Nora Suzanne Wolff; Floor Hugenholtz; Willem Joost Wiersinga

Disclosures

Crit Care. 2018;22(78) 

In This Article

The Evolving Role of the Lung Microbiota in Critical Illness

Healthy lungs were long thought to be sterile, until recent studies showed that bacteria can be cultured from healthy lungs.[42] The lung environment is less advantageous for bacteria to grow and flourish when compared to the intestine, leading to a less dense bacterial community compared to the gut. A lack of nutrients, the bidirectional movement of the lung, the aerobic environment, and the coating of alveoli with a lipid-rich surfactant that has bacteriostatic effects all contribute to this harsh environment for bacteria.[42,43] Furthermore, obtaining a sample from the lung is far more invasive than obtaining a stool sample to study the microbiome. Contamination from the sampling device or from the upper respiratory tract is another point to take into consideration.

In a healthy lung, the microbiota is delicately balanced by the reproduction rate of present bacteria and the immigration and elimination rate of bacteria. Under normal circumstances, the reproduction rate of bacteria remains low and the immigration and elimination high. However, in critical illness, sedatives and endotracheal intubation can decrease the mucociliary clearance and cough reflex, leading to decreased microbial elimination. Furthermore, mechanical ventilation can cause an increase in alveolar edema, which can lead to an increase in available nutrients in the lung and areas where the oxygen levels are lower, allowing bacteria to thrive.[1]

In healthy lungs, it is thought that most of the bacteria come from the oral microbiota. The lung microbiota most closely resembles the microbiota of the oropharynx, more so than that of the nasopharynx, gastrointestinal tract or inhaled air.[42] The healthy oropharynx contains benign Veillonella spp. and Prevotella spp., and, therefore, these are also found in healthy lungs. During critical illness, the oropharynx can become overpopulated with pathogenic proteobacteria, such as Pseudomonas aeruginosa and Klebsiella pneumoniae. Furthermore, in critical illness the stomach and small intestine can become the primary source of bacterial migration to the lung.[1,42]

ARDS and pneumonia are thought to cause alveolar injury and as a consequence induce changes in the microbiome. The alveoli become covered with protein-rich fluids and the bactericidal surfactant from the alveoli becomes inactivated, making the alveoli a more hospitable environment for bacteria.[1] Furthermore, Dickson et al.[44] proposed a theory regarding the existence of a positive feedback loop between the growth of certain bacterial species in the lung and the local inflammatory response; as the bacterial population grows, it starts to limit itself due to nutrient shortage while it also provokes an increased inflammatory response. This inflammatory response can consequently lead to endothelial and epithelial injury, releasing fluids that are rich in proteins and nutrients, thus stimulating bacterial growth. Further bacterial growth will increase the local inflammation, thus creating a positive feedback loop. This suggests that in some cases the body's inflammatory response may be making the infection worse.

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