Pediatrics and Neonatology最新文献

Background: Mild Th1 and Th17 immune responses in childhood against Helicobacter pylori are presumed to be responsible for H. pylori colonization and mucosal atrophy reduction. However, the mechanism remains unclear. In this study, we aimed to investigate the childhood-specific immune responses observed after H. pylori infection by analyzing galectin expression in the gastric mucosa. We focused on galectin-1 (Gal-1) and galectin-9 (Gal-9), which function to suppress Th1 and Th17 immune responses.

Methods: We analyzed changes in the expression of Gal-1 and Gal-9 in the gastric mucosa of pediatric patients with H. pylori infection. Ten pediatric patients with and ten patients without H. pylori infection who underwent biopsy to assess the cause of chronic abdominal symptoms using esophagogastroduodenoscopy were evaluated. Gal-1 and Gal-9 expression in the biopsy tissues of the gastric antrum and corpus was analyzed by immunohistochemical staining.

Results: Gal-1 expression was significantly increased in the stromal cells of the corpus owing to H. pylori infection. No alterations in Gal-1 expression due to H. pylori infection were observed in the antral tissue. Helicobacter pylori infection considerably increased Gal-9 expression in all tissues. According to previous reports, the increased expression of Gal-9 associated with H. pylori infection is not observed in adults. Therefore, the increased expression of Gal-9 associated with H. pylori infection is specific to pediatric patients.

Conclusion: The increased expression of Gal-1 and Gal-9 may suppress Th1 and Th17 immune responses against H. pylori infection during childhood, promote H. pylori colonization, and reduce inflammation in the gastric mucosa of pediatric patients.

Background: The increasing prevalence of antimicrobial-resistant Escherichia coli (E. coli) in the community is a global public health challenge. This study investigated the prevalence of third-generation cephalosporin-resistant (3GCR) E. coli fecal carriage in children, identified associated risk factors, and determined antimicrobial resistance patterns of E. coli across three regions of Taiwan.

Methods: Stool samples from children aged 0-18 years were collected in southern, northern, and eastern Taiwan from community or outpatient clinics between July 2022 and May 2023. E. coli colonies were selected and examined for antimicrobial susceptibility and multilocus sequence typing. Participant demographic data and potential risk factors for carrying resistant E. coli were surveyed using a questionnaire.

Results: Of the 246 children surveyed, 59.3% carried multidrug-resistant (MDR) E. coli, and 37.4% carried 3GCR E. coli. The prevalence of 3GCR E. coli carriage was highest in southern Taiwan (42.7%), followed by northern Taiwan (35.5%) and eastern Taiwan (28.4%). The study identified several risk factors which may be associated with the fecal carriage of 3GCR E. coli, such as having lower paternal education levels, being overweight or obese, having a nonvegetarian diet, and consuming eggs, with variations observed across regions.

Conclusion: This study documented elevated fecal carriage rates of 3GCR and MDR E. coli across regions of Taiwan. The study also identified numerous demographic and environmental factors that require implementing comprehensive strategies to address this public health challenge.

Background: Hypoxic-ischemic (HI) insult in infants induces brain injury and results in motor coordination impairments associated with cerebral palsy; however, preventive measures for HI brain injury in preterm infants remain unclear. We investigated the impact of progesterone (P4) in a rat HI insult model that mimics HI brain injury in preterm infants.

Methods: Neonatal male rats with their right common carotid artery coagulated were exposed to a 1-h hypoxia (6% oxygen) on postnatal day (PND) 3. P4 (0.2 mg) was subcutaneously administered daily from PND4-12. Motor coordination function and muscular strength were evaluated on PND50 using rotarod and grip strength tests, respectively. Brain histology was evaluated via immunohistochemistry using anti-NeuN, anti-Olig2, and anti-IbaI antibodies on PND15 and PND50.

Results: In male rats, P4 significantly improved the latency-to-fall off on the rotarod test in the insult rats to the levels of the sham-operation rats. Neither the insult nor P4 administration impacted the grip strength results. No significant differences were observed in the number of neurons, oligodendrocyte progenitor cells (OPCs), and microglia in the motor and somatosensory area of the cortex between the insult and insult followed by P4-administered rats on PND50. The number of OPCs in the corpus callosum was significantly increased in the ipsilateral side compared with the contralateral side of the insult in the P4-administered rats, indicating that P4 facilitates recruitment of OPCs to the corpus callosum. HI insult accelerated neuronal differentiation in rats on PND15, which was abrogated in the P4-administerd group, suggesting that P4 suppresses transient neuronal differentiation caused by the insult.

Conclusion: P4 administration restored motor coordination impairments caused by postnatal HI insult in male rats. The insult timing corresponds to that of human preterm infants, indicating P4's potential for protecting HI brain injury in preterm male infants.