Background 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. Results 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. Conclusions 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.

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2)‐induced multisystem inflammatory syndrome in children (MIS‐C) is a life‐threatening illness that has been reported in the United States and Europe. It affects multiple organ systems and often requires patient admission to an intensive care unit. Although some features of MIS‐C overlap with Kawasaki disease, MIS‐C is more common among older children and adolescents, more often affects cardiovascular and gastrointestinal systems, and more frequently presents with elevated inflammatory markers. Rapid and complete clinical recovery is possible in nearly all patients following immunomodulation therapy. Thus far, MIS‐C pathophysiology and long‐term prognosis are not sufficiently clear; further studies are needed.

Streptococcus pyogenes is a bacterial pathogen that causes a wide spectrum of clinical diseases exclusively in humans. The distribution of emm type, antibiotic resistance and virulence gene expression for S. pyogenes varies temporally and geographically, resulting in distinct disease spectra. In this study, we analyzed antibiotic resistance and resistance gene expression patterns among S. pyogenes isolates from pediatric patients in China and investigated the relationship between virulence gene expression, emm type, and disease categories. Forty-two representative emm1.0 and emm12.0 strains (n = 20 and n = 22, respectively) isolated from patients with scarlet fever or obstructive sleep apnea-hypopnea syndrome were subjected to whole-genome sequencing and phylogenetic analysis. These strains were further analyzed for susceptibility to vancomycin. We found a high rate and degree of resistance to macrolides and tetracycline in these strains, which mainly expressed ermB and tetM. The disease category correlated with emm type but not superantigens. The distribution of vanuG and virulence genes were associated with emm type. Previously reported important prophages, such as φHKU16.vir, φHKU488.vir, Φ5005.1, Φ5005.2, and Φ5005.3 encoding streptococcal toxin, and integrative conjugative elements (ICEs) such as ICE-emm12 and ICE-HKU397 encoding macrolide and tetracycline resistance were found present amongst emm1 or emm12 clones from Shenzhen, China.

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.

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Background The microtubule-dependent molecular motor protein Kinesin Family Member 2A (KIF2A) is down-regulated in asthmatic human airway epithelium. However, little is known about the roles of KIF2A as well as the possible underlying mechanisms in asthma. Methods House dust mite (HDM) extract was administered to establish a murine model of asthma. The expression of KIF2A, IL-33 and the autophagy pathways were detected. The plasmid pCMV-KIF2A was used to overexpress KIF2A in the airway epithelial cells in vitro and in vivo. IL-4, IL-5, IL-33 and other cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues homogenates were measured. Results In response to the challenge of house dust mite (HDM) in vitro and in vivo, airway epithelial cells displayed decreased production of KIF2A. Meanwhile, autophagy and IL-33 were increased in HMD-treated epithelial cells. Mechanistically, KIF2A decreased autophagy via suppressing mTORC1 pathway in HDM-treated epithelial cells, which contributed to the reduced production of IL-33. Moreover, in vivo KIF2A transfection reduced IL-33 and autophagy in the lung, leading to the attenuation of allergic asthma. Conclusion KIF2A suppressed mTORC1-mediated autophagy and decreased the production of epithelial-derived cytokine IL-33 in allergic airway inflammation. These data indicate that KIF2A may be a novel target in allergic asthma.

MicroRNA (miRNA) mimics or antagomirs hold great promise for asthma treatment compared with glucocorticoids as mainstay therapy for asthma. But the role of miRNA in regulating asthmatic inflammation is largely unclear. We previously reported that miR-3162-3p in the peripheral blood of children with asthma was obviously upregulated compared to that in healthy children. This study aimed to elucidate the role of miR-3162-3p in pulmonary inflammation in normal and asthmatic mice as well as preliminarily explore the potential of miR-3162-3p antagomir in asthma treatment. A noninvasive whole-body plethysmograph measured airway responsiveness. Both qRT-PCR and Western blot were used to detect the expression of miRNA, mRNA, or protein. Cells in bronchoalveolar lavage fluid were counted by platelet counting and Wright's staining. Inflammatory infiltration and mucus secretion were identified by hematoxylin and eosin and periodic acid-Schiff staining, respectively. Cytokines in the lungs were detected by ELISA. The miR-3162-3p mimic intraperitoneally administered to normal mice decreased β-catenin levels in the lungs without obviously altering the lung histology and cytokine levels. Antagonizing miR-3162-3p in ovalbumin-induced asthmatic mice effec-Juman Liua, Yinhui Chena, and Feng Zhang contributed equally to this work. Edited by: H.-U. Simon, Bern.

IntroductionThe current study aims to investigate the etiology spectrum and the clinical characteristics of bronchiectasis in Chinese children.MethodsThe study is designed as a multicenter retrospective study. 193 cases were enrolled in 13 centers in China between 2008 and 2017. The inclusive cases must meet the clinical as well as the HRCT criteria. Only if both two radiologists confirmed the diagnosis, the case could be enrolled. The cases that could not provide clinical and imageology data were excluded. The data were entered into the specialized system and then analyzed.ResultsOne hundred sixty‐nine cases (87%) were found to have the underlying etiology. Post‐infective (46%), primary immunodeficiency (14%), and PCD (13%) were the common causes. All cases came from 28 provinces in Mainland China. The median age of symptom onset was 5.8 (2.0, 8.9) years. The median age of diagnosis was 8.4 (4.5, 11.6) years. The main symptoms were cough, sputum expectoration, and fever during the exacerbation. Nineteen percent of patients suffered from limited exercise tolerance. Clubbing was found in 17% of cases. Nearly 30% of patients presented growth limitations. On the HRCT findings, 126 cases had diffused bronchiectasis, and bilateral involvement was found in 94 cases. The lower lobes and right middle lobes were most commonly involved. Approximately 30% of cultures of sputum and bronchoalveolar lavage were positive.ConclusionA majority of cases could be found the underlying etiology. Post‐infective, primary immunodeficiency, and PCD were the most common causes. Some clinical figures might indicate a specific etiology.