Background

In adults the microbial community of the gut (microbiota) influences a diverse range of health outcomes from obesity, diabetes, asthma and allergy to seemingly ‘remote’ diseases like Parkinson's disease.1 In preterm infants, establishment of the gut microbiota is also of importance for key morbidities like late onset sepsis (LOS) and necrotising enterocolitis (NEC), both significant causes of mortality.2 Many episodes of LOS are with gut derived organisms3 and changes in the intestinal barrier contribute to both LOS and NEC. The gut microbiota are key to developing barrier function, integrity, and mucosal and systemic immune function. They also ‘educate’ the gut associated lymphoid tissue, allowing the establishment of a ‘tolerant’ state between microbiota and the immune system, affecting intestinal function including tight junction structure and immune function.4–6 Patterns of initial colonisation affect host metabolic function: fat deposition, circulating leptin levels, and insulin resistance.6

In the preterm gut structural and immunological immaturity contribute to inflammatory necrosis and abnormal bacterial colonisation (dysbioses). This may result in decreased microbial diversity and an increased inflammatory response exacerbated by an immature innate immune response that increases the risk of diseases like NEC or LOS. An improved understanding of the microbiota of infants cared for in neonatal intensive care, and how this is affected by current practices may allow clinicians to promote more ‘healthy’ gut microbiota patterns, and may be associated with reductions in mortality and improvements in long term outcomes.7