The last half century has seen a stable raise in the incidence and prevalence of chronic inflammatory diseases with further increases expected. These diseases are mostly characterized by complex aetiological factors, variable but mostly long latency periods, prolonged course of illness and longterm and costly treatment. The actual therapeutic strategies aim to reduce the signs and the symptoms of the disease and slow down its development. While it is a relief for the affected individual and improved life quality, it is unrealistic, in the long perspective, to handle these huge pandemics by treatment regimes using small molecules or smart medicines. The best strategy is prevention and development of guidelines that sustain health. One way forward would be to find biological biomarkers in order to predict the onset of the disease before the development of the clinical signs. Important advances have been made in predicting the onset of autoimmune disease. For example, it has been shown that the latency period that precedes the development of one major form of rheumatoid arthritis is characterized by immune modifications associated with the presence of rheumatoid factors and as well as anticitrullin antibodies up to 10 years before the onset of the disease (1,2). The association of these biological biomarkers associated with risk factors like smoking and environmental and gene predisposition can contribute to earlier detection of the rheumatoid arthritis and act therapeutically to disable the disease onset (1). Furthermore, regarding another autoimmune pathology, the presence of the autoantibodies against nuclear antigens (antinuclear antibody, anti-Sjogren’s syndrome antigen A, double-stranded DNA) has also high predictive value for the onset of symptoms and systemic lupus erythematosus diagnosis (3). Similarly, huge efforts are invested into the field of neuroscience, trying to find the early predictors, which mean possibilities to intercept before the onset of a full signature of a CNSrelated disease. For example, in the case of autism spectrum disorders (ASD). It has been shown recently by recording the electrophysiological brain responses that neural sensitivity to eye gaze in early infancy would predict the development of the autism spectrum disorders in toddlerhood (4). Target intervention during the key period of the brain development in early infancy may therefore be a possible way to attenuate the full development of ASD once we have reliable biomarkers and indications on how to provide treatment regimes early in life. Necrotizing enterocolitis (NEC) is another devastating pathology with a multifactorial aetiology and an important cause of the morbidity and mortality for the preterm infants (5), and the prediction of this pathology only several days before the onset of clinical symptoms would be of great interest. One of the hypothesis is that alterations in the gut microbiom may play an important role in the aetiopathogenesis of the NEC in the preterm neonates (6). It has been observed that in infants that developed NEC, the microbial diversity differed from healthy preterm infants with an increase in Proteobacteria and a decrease in Firmicutes one week prior to NEC onset, suggesting the potential for early detection and focused intervention (7). A recent study has highlighted in the preterm infants the predominance of Enterococcus faecalis and coagulase-negative staphylococci (8). Infants with NEC were more often colonized with coagulase-negative staphylococci and less often with E. faecalis, suggesting that the presence of the E. faecalis may be associated with a reduced risk of NEC onset. Interestingly, it has been shown Invited Commentary for Stewart et al, The preterm gut microbiota: changes associated with necrotizing enterocolitis and infection, pages 1121–1127. Acta Paediatrica ISSN 0803–5253
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Jun 1, 2013
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Open Access