In adult fecal microbiota Clostridium coccoides subcluster XIVa is NCT-501 nmr the most abundant taxonomic group [16] but in infants it normally constitutes only a subdominant group at much lower counts [25]. Through the peptidoglycan present in their bacterial cell membrane the intestinal Clostridium

species might be able to induce a Th2 cytokine response by binding to the TLR2 of the intestinal dendritic cells [21, 22]. Several studies used DGGE to examine the relationship between the composition of the intestinal microbiota and the development of allergy and eczema [26–28]. In a case-control study, the prevalence of one specific DGGE band (identified as E. coli) was higher in infants with eczema [26]. A reduced fecal microbial diversity Trichostatin A chemical structure was PF-01367338 in vivo observed with DGGE in allergic children [27] or in infants with eczema [28]. Only one study looked at wheezing as outcome using DGGE but did not find a difference in gut microbiota between wheezing and non-wheezing children at the age of 3-5 years [29]. We found a difference in the composition of the fecal microbiota at the age of 3 weeks

but not later (at the age of 6 and 12 months; data not shown), illustrating the importance of a critical time window during the first 6 months of life [3]. Prematurity is a much more complex situation than the normal population observed in our study. A delay of up to 6 months of the intestinal Bacteroides colonization, which occurs in newborns after caesarean section, might even decrease the subsequent risk for asthma in these premature infants according to our findings. However, genetic factors or the underlying disease that provoked the premature delivery itself might significantly increase the subsequent risk for asthma. Future studies on premature newborns and their respiratory disease outcome should not only include the intestinal microbiota but should also correct for confounders like antibiotic use, mode of delivery and underlying disease or genetic mutations. Despite obvious advantages, DGGE also has a limitation. The detection limit of DGGE is estimated to approach 1% aminophylline of the total population or a concentration

of 106 CFU/g feces. This is significantly higher than the detection limit of the culture method we used in our previous study (detection limit ≥ 103 CFU/g feces) [14]. Another limitation of the present study is the fact that no stool sample of the mother was included, so we cannot make any statement on the origin of the Bacteroides and Clostridium strains recovered in these infants. Finally, as in every longitudinal study, missing data is a problem. Since there were no differences in the percentage of children with wheezing, eczema or parental asthma or gender of the infant between children who could or could not be categorized according to API, it seems improbable that the missing data resulted in a systemic bias.