Necrotizing enterocolitis and the gut-lung axis

Abstract

The recently recognized connection between the gut microbiota and pulmonary disease has been termed the gut-lung axis. However, broader connections link the gut and the lungs and these organ systems are tightly interrelated in both homeostasis and disease. This concept is often ignored in the compartmentalized treatment of pulmonary or gastrointestinal disease. In newborns, the most severe gastrointestinal complication of prematurity, necrotizing enterocolitis, and the most severe pulmonary complication, bronchopulmonary dysplasia, both produce significant systemic morbidity. In this review, we highlight the often neglected pathophysiology of the gut-lung axis contributes to increased risk of bronchopulmonary dysplasia in premature infants with necrotizing enterocolitis.

Keywords: Bronchopulmonary dysplasia; Microbiome; Necrotizing Enterocolitis.

Figure 1.. Dysbiosis of the lung and gut likely contribute to the development of both BPD and NEC.

Multiple, likely interrelated, mechanisms may contribute to the development of both diseases. BPD, bronchopulmonary dysplasia; DC, dendritic cell; ILC3, type 3 innate lymphoid cells; NEC, necrotizing enterocolitis.

Figure 2.. Immune interactions with the intrinsic microbiomes of the gut and lung are critical components of the gut-lung axis.

In addition, to direct transfer of T cells, type 3 innate lymphoid cells (ILC3), metabolites and cytokines, spill over from tissue specific interactions between the microbiota and innate immune cells may also disrupt homeostasis in the opposite organ. AMP, antimicrobial peptides; AT2 alveolar type 2 cell; DC, dendritic cells.