Abstract
In recent years, an aberrant gastrointestinal colonization has been found to be associated with an higher risk for postnatal sepsis, necrotizing enterocolitis (NEC) and growth impairment in preterm infants. As a consequence, the reasons of intestinal dysbiosis in this population of newborns have increasingly become an object of interest. The presence of a link between the gut and lung microbiome's development (gut-lung axis) is emerging, and more data show as a gut-brain cross talking mediated by an inflammatory milieu, may affect the immunity system and influence neonatal outcomes. A revision of the studies which examined gut and lung microbiota in preterm infants and a qualitative analysis of data about characteristic patterns and related outcomes in terms of risk of growing impairment, Necrotizing Enterocolitis (NEC), Bronchopulmonary Dysplasia (BPD), and sepsis have been performed. Microbiota take part in the establishment of the gut barrier and many data suggest its immune-modulator role. Furthermore, the development of the gut and lung microbiome (gut-lung axis) appear to be connected and able to lead to abnormal inflammatory responses which have a key role in the pathogenesis of BPD. Dysbiosis and the gut predominance of facultative anaerobes appear to be crucial to the pathogenesis and subsequently to the prevention of such diseases.
Highlights
All of the microorganisms that inhabit the human body constitutes the so-called human microbiota
The importance of gut microbiome is due to the role it plays as a major interface to the external environment: it contemporarily protects against pathogens and toxins while housing beneficial commensal bacteria which are pivotal to maintain homeostasis, support digestion, protect from injury, regulate intestinal immune function [2]
We limited the search by applying the filter of age “infants” and used the following search terms and logic: “preterm infants microbiota,” “gastrointestinal microbiome AND Necrotizing Enterocolitis OR necrotizing enterocolitis (NEC),” “breastfeeding AND enteral nutrition AND Necrotizing Enterocolitis OR NEC,” “microbiota AND growth retardation,” “intestinal microbiota AND weight gain,” “intestinal microbiota AND growth,” “gut microbiota AND extrauterine growth restriction,” “preterm infants microbiota AND late onset sepsis OR LOS,” “microbiota OR microbiome OR bacteria OR antibiotics OR gut AND lung OR airway OR BPD OR Bronchopulmonary Dysplasia,” and “gut-lung axis.”
Summary
All of the microorganisms that inhabit the human body constitutes the so-called human microbiota. The Human Microbiota Project was launched in 2008 to deepen our understanding of how the microbiome (the whole set of microorganisms, their genomes and the environmental conditions) influences human health and diseases. Microbiota and Preterm Infant’s Outcomes characterizing the complexity of the microbial population to study whether there is an “healthy microbiota” and potential implications of different patterns [1]. Some studies [3, 4] show that at birth infants are nearly sterile but they subsequently acquire microbial colonists. This process progresses in the first 2–3 years of life, until reaching an “adultlike state.”. This process progresses in the first 2–3 years of life, until reaching an “adultlike state.” In at term newborns this evolution appears to be driven by nutritional, immunological, hormonal and prebiotic effect of maternal milk [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
