Background: Gut microbiota plays a critical role in many important physiological processes and is linked with various pulmonary infectious diseases. The relationship between pulmonary tuberculosis (PTB) and gut microbiota has been poorly studied. The present study aimed to characterize gut microbiota in pediatric patients with PTB.Methods: A case-controlled study was executed for the characterization of gut microbiota in pediatric PTB patients. Fecal samples were collected from the PTB patients and healthy controls upon admission. In addition, a one-month follow-up assessment was performed to investigate alterations in the gut microbiota post anti-tuberculosis treatment. 16SrDNA sequencing analysis of fecal DNA was completed on the Illumina MiSeq platform.Results: Compared with healthy controls, the gut microbiota of pediatric patients with PTB was characterized by decreased microbial diversity. PTB patients further presented an up-regulation of the pro-inflammatory bacteriaPrevotella,the opportunistic pathogenEnterococcus,as well as a reduction of beneficial bacteria includingRuminococcaceae,Bifidobacteriaceaeandprausnitzii.One-month after anti-tuberculosis therapy, the richness of gut microbiota in PTB patients was distinctly depleted.Conclusions: The gut microbiota of pediatric patients with PTB was significantly distinct from healthy controls. Additionally, the richness of gut microbiota in PTB patients decreased after one-month anti-tuberculosis treatment. It is hypothesized that the homeostasis of gut microbiota in PTB patients may affect the pathogenies of PTB by de-regulation of the hosts’ immune status through the gut-lung axis.

Background: In recent years, the impact of Helicobacter pylori (H pylori) on the gut microbiota has attracted more attention; however, the relationship in pediatric population rarely was reported.Methods: Endoscopic gastric mucosal biopsy specimens from 55 children with gastrointestinal symptoms were collected, 37 of them were H pylori‐positive (23 nonpeptic ulcer and 14 peptic ulcer) and 18 were H pylori‐negative. In addition, 11 specimens were collected from H pylori‐positive children who performed second endoscopy in 4 weeks after therapy. Microbial abundance and compositions were analyzed by 16S ribosomal RNA amplification and microbial functions were predicted using the software PICRUSt.Results: The gastric microbiota of H pylori‐positive children were mainly dominated by Helicobacter in genus (95.43%). The microbiota richness and diversity of H pylori‐positive children were lower than that of H pylori‐negative children. No difference was found in microbiota structure between H pylori‐positive children with or without peptic ulcer. The richness and compositions after therapy were closer to the characteristics of H pylori‐negative children. For predicted functions, higher abundance in pathways of infection diseases, cancer and lower abundance in the pathways of amino acid, lipid, and carbohydrate metabolism were found in H pylori‐positive group than H pylori‐negative group.Conclusion: The characteristics of gastric microbiota were affected by H pylori infection rather than disease states, and the richness and diversity of gastric species were inverse correlation with H pylori infection in children. Eradication therapy was helpful to restore shifted gastric microbiota.

To investigate the situation of antibiotic consumption and to assess the inappropriate use on pediatric inpatients of different types hospitals in Sichuan, China. A cross-sectional survey of antibiotic prescriptions among hospitalized children aged 1month -14years were conducted from April 2018 to June 2018 in southwestern China. Antibiotic prescriptions were extracted from electronic records during hospitalization of each inpatient in five different types hospitals. In this study, the antibiotic prescription rate of hospitalized children was 66.9% (1176/1758). Compared with tertiary children hospital (TC) (46.1%), general hospitals and non-tertiary children hospitals has higher rate of antibiotic prescription (almost 85%) (P < .001). 93.4% of inpatients received parenteral antibiotic. Overall, the most common antibiotics were Cefoperazone and enzyme inhibitor, Cefixime and Azithromycin. Lower respiratory tract infection (LRTI) was the leading reason for antibiotic consumption in pediatric wards (56.8%), followed by upper respiratory tract infection (URTI) (22.2%). For children with LRTI, Cephalosporins were heavy prescribed, especially broad-spectrum third-generation Cephalosporins (60.3%). The antibiotic prescription proportion of URTI in general hospitals and non-tertiary children hospitals (more than 18%) was higher than TC (8.1%) (P < .001). There was inappropriate use of antibiotic in hospitalized children including overuse of parenteral administration, overprescribing of antibiotic on URTI and misuse of third-generation Cephalosporins in pediatric inpatients with LRTI. Compared with tertiary freestanding children hospital, the irrational antibiotic prescription of general hospitals and non-tertiary children hospitals were more serious. Management strategy should be implementer on quality improvement of antibiotic use.

Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disease. Recently, an increasing number of studies have shown that Toll-like receptor 4 (TLR4), widely distributed on the surface of a variety of epithelial cells (ECs) and immune sentinel cells in the gut, plays a vital role in developing IBS.Objectives: We sought to synthesize the existing literature on TLR4 in IBS and inform further study.Methods: We conducted a systematic search of the PubMed, Embase (Ovid), Scopus, Web of Science, MEDLINE, and Cochrane Library databases on June 8, 2024, and screened relevant literature. Critical information was extracted, including clinical significance, relevant molecular mechanisms, and therapeutic approaches targeting TLR4 and its pathways.Results: Clinical data showed that aberrant TLR4 expression is associated with clinical manifestations such as pain and diarrhea in IBS. Aberrant expression of TLR4 is involved in pathological processes such as intestinal inflammation, barrier damage, visceral sensitization, and dysbiosis, which may be related to TLR4, NF-κB, pro-inflammatory effects, and CRF. Several studies have shown that many promising therapeutic options (i.e., acupuncture, herbs, probiotics, hormones, etc.) have been able to improve intestinal inflammation, visceral sensitization, intestinal barrier function, intestinal flora, defecation abnormalities, and depression by inhibiting TLR4 expression and related pathways.Conclusion: TLR4 plays a crucial role in the development of IBS. Many promising therapeutic approaches alleviate IBS through TLR4 and its pathways. Strategies for targeting TLR4 in the future may provide new ideas for treating IBS.

Rationale: Facial paralysis as the initial clinical presentation of infant leukemia (IL) is rare, and the rate of its misdiagnosis is high. Identifying the clinical characteristics of IL with facial paralysis as the initial symptom is necessary to improve the understanding of the causes of facial paralysis and IL. Patient concerns: A 10-month-old infant had facial paralysis and recurrent fever. He was misdiagnosed as having bacterial meningitis for >2 months. Diagnoses: The infant was diagnosed as having acute monocytic leukemia (M5) with central infiltration based on examinations of the bone marrow and cerebrospinal fluid by flow cytometry. Interventions: Before the diagnosis of leukemia, the patient was given meropenem, ceftriaxone, vancomycin, and ampicillin successively for anti-infective treatment for 2 months, and dexamethasone for several days. But he gave up further treatment after confirmed diagnosis. Outcomes: Our patient discontinued treatment and discharged. From literature review, there were 6 cases (including this case) of IL with facial paralysis as the initial symptom. 80% of patients were misdiagnosis and treated with a corticosteroid in the early stage, and the mortality was 33.3%. Lessons: The clinical symptoms of IL with facial paralysis are not typical, with a high rate of misdiagnosis. When the cause of facial paralysis is unknown or the advance treatment effect is poor, tumor diseases should be considered. Corticosteroids should be carefully administered to children with facial paralysis.

Tuberous sclerosis complex (TSC) is a rare autosomal dominant disorder. The TSC1 and TSC2 genes have been identified as pathogenic genes. In this report, we are discussing a novel frameshift mutation and a novel missense mutation in the TSC2 gene. The two cases discussed in this study met the latest diagnostic criteria for TSC published by the International Tuberculosis Sclerosis Complex Consensus Conference in 2012. High-throughput sequencing and multiplex ligation-dependent probe amplification (MLPA) were used to examine tuberous sclerosis complex (TSC)-related genes (TSC1 and TSC2) and their splicing regions using peripheral blood DNA from two probands in two families with TSC and to identify the genetic mutation sites. Amplification primers were designed for the mutation sites, and polymerase chain reaction and Sanger sequencing were used to verify the peripheral blood DNA sequences from the probands and their parents. Proband 1 had the c.1228 (exon 12)_c.1229 (exon 12) insG (p.L410RfsX11) heterozygous mutation in the TSC2 gene (chr16), which was a new frameshift mutation. Proband 2 had the c.4925G>A (exon 38) (p.G1642D) heterozygous mutation in the TSC2 gene (chr16), which was a new missense mutation. These two novel mutations may be pathogenic mutations for TSC, and their association with the disease needs to be further verified by mutant protein function cell model and animal model.