Infantile eczema is an immunological disease that is characterized by itchy and dry skin. Recent studies have suggested that gut microbiota (GM) plays a role in the development and progression of eczema. To further evaluate this potential link, we collected feces from 19 infants with eczema and 14 infants without eczema and analyzed the molecular discrepancies between the two groups using 16S rDNA analysis. Bacteroidaceae and Deinococcaceae were significantly enriched in eczema infants, and Bacteroidaceae was potentially involved in autoimmune diseases by promoting the Th17 (T helper cell 17) secretion of IL-17 (interleukin-17). In the infants without eczema, the co-abundance network featured three core nodes: Clostridiaceae, Veillonellaceae, and Lactobacillaceae, all of which were lacking in the infants with eczema. Furthermore, our data suggested that Enterobacteriaceae was the core of the co-abundance network for the diseased subjects. GM is closely connected to the human immune system, and the dysbiotic GM network plays a role in eczema. This study furthered our understanding of the dynamic GM network and its correlation to the occurrence of eczema.

The imbalanced respiratory microbiota observed in pneumonia causes high morbidity and mortality in childhood. Respiratory metagenomic analysis demands a comprehensive microbial gene catalogue, which will significantly advance our understanding of host–microorganism interactions. We collected 334 respiratory microbial samples from 171 healthy children and 76 children with pneumonia. The respiratory microbial gene catalogue we established comprised 2.25 million non-redundant microbial genes, covering 90.52% of prevalent genes. The major oropharyngeal microbial species found in healthy children were Prevotella and Streptococcus. In children with Mycoplasma pneumoniae pneumonia (MPP), oropharyngeal microbial diversity and associated gene numbers decreased compared with those of healthy children. The concurrence network of oropharyngeal microorganisms in patients predominantly featured Staphylococcus spp. and M. pneumoniae. Functional orthologues, which are associated with the metabolism of various lipids, membrane transport, and signal transduction, accumulated in the oropharyngeal microbiome of children with pneumonia. Several antibiotic resistance genes and virulence factor genes were identified in the genomes of M. pneumoniae and 13 other microorganisms reconstructed via metagenomic data. Although the common macrolide/β-lactam resistance genes were not identified in the assembled M. pneumoniae genome, a single-nucleotide polymorphism (A2063G) related to macrolide resistance was identified in a 23S ribosomal RNA gene. The results of this study will facilitate exploration of unknown microbial components and host–microorganism interactions in studies of the respiratory microbiome. They will also yield further insights into the microbial aetiology of MPP.

Background: In recent years, the morbidity of Mycoplasma pneumoniae pneumonia (MPP) has increased significantly in China. A growing number of studies indicate that imbalanced respiratory microbiota is associated with various respiratory diseases. Methods: We enrolled 119 children, including 60 pneumonia patients and 59 healthy children. Nasopharyngeal (NP) and oropharyngeal (OP) sampling was performed for 16S ribosomal RNA (16S rRNA) gene analysis of all children. Sputum and OP swabs were obtained from patients for pathogen detection. Results: Both the NP and OP microbiota of patients differ significantly from that of healthy children. Diseased children harbor lower microbial diversity and a simpler co-occurrence network in NP and OP. In pneumonia patients, NP and OP microbiota showed greater similarities between each other, suggesting transmission of NP microbiota to the OP. Aside from clinically detected pathogens, NP and OP microbiota analysis has also identified possible pathogens in seven cases with unknown infections. Conclusion: NP and OP microbiota in MPP and non-MPP are definitely similar. Respiratory infection generates imbalanced NP microbiota, which has the potential to transmit to OP. Microbiota analysis also promises to compliment the present means of detecting respiratory pathogens.

Undernutrition (UN) is a worldwide concern affecting morbidity and mortality among children, but the safety and long-term efficacy of its current treatments remain controversial. Recent evidence showing the roles of the gut microbiome (GM) in nutrient absorption indicates its usefulness in alternative interventions to treat UN safely with sustainable amelioration. To enhance our understanding of the GM and childhood undernutrition, we deep sequenced the gut metagenomes of 65 children with moderate or severe undernutrition (UN group) and 61 healthy children (HC group) to identify associated taxa and genes using a two-stage validation scheme. At stage I, 54 UN patients and 51 healthy children were enrolled for the discovery of GM markers in UN children. The accuracy of the markers was then tested in an additional 11 UN patients and 10 healthy children at stage II. Compared to the HC group, the UN group had lower richness in microbial genes (P = 0.005, FDR = 0.005) and species (P = 0.002, FDR = 0.002). The distributions of bacterial genes enable the identification of 16 gene markers with which to discriminate UN patients with high accuracy [averaged areas under the receiver operating curve (AUC) = 0.87], including three Bacteroides uniformis genes that are responsible for the synthesis of iron transporters. We also identified four species markers that enable the UN patients to be confidently discriminated from the HC children (averaged AUC = 0.91), namely Bacteroides ovatus, Bacteroides uniformis, Bacteroides uniformis, and Bacteroides vulgatus. In addition, metabolic comparison showed significantly decreased isobutyric acid (P = 0.005, FDR = 0.017) and increased isovaleric acid (P = 0.006, FDR = 0.017) in UN patients. We also identified notable correlations between microbial species and short-chain fatty acids (SCFAs) and several nutritional indicators, including acetic acid and iron (r = 0.436, P = 0.029), butyric acid and iron (r = 0.422, P = 0.036), butyric acid and lymphocyte (r = −0.309, P = 0.011), and acetic acid and total protein (r = −0.303, P = 0.043). Taken together, the distinct features of gut microbiota in UN patients highlight the taxonomic and functional shift during the development of UN and provide a solid theoretical basis for intervention in childhood undernutrition through gut microbes.

Background: Protracted bacterial bronchitis (PBB) is a chronic purulent bronchitis which could cause recurrent coughing and wheezing in infants. Based on previous reports, main pathogens which caused PBB were identified in the patients, but their impacts on lung microbiota dysbiosis remain unclear. Methods: In this study, bronchoalveolar lavage fluid (BALF) was collected from PBB infants and tracheomalacia (TM) infants younger than 3 years old under the instruction of Shenzhen Children’s Hospital, and 12 samples were randomly selected for 16S rDNA analysis in each group. Based on the results of bacterial composition, the microbiota diversity and co-occurrence network in PBB and TM group were detected and compared. Results: Microbiota diversity was significantly lower in PBB group than it in TM group (P<0.001 for the comparison of Shannon and Simpson indexes). The PBB group was found to harbor 25 accumulated bacterial agents by comparison with TM group, including Haemophilus (P<0.001) and Bacteroides (P<0.001). Whilst, the populations of Lactococcus (P<0.001) and Lactobacillus (P<0.001) were dramatically smaller in PBB group. The co-occurrence network in PBB group also differed from that of TM group. It contained four core nodes in PBB patients, including Haemophilus, Parabacteroides, Porphyromonas, and Cronobacter. Haemophilus was found to be negatively associated with most counterparts, including Clostridium and Bacillus. Conclusions: PBB infants contained discrepant lung genera and co-occurrence network when compared with TM infants. This retrospective study may deepen our understanding of PBB pathogenesis, and it also provided a foundation for bacterial adjunctive therapy of infantile PBB in accordance with clinical treatment.