Women's empowerment and child stunting in Peru: a nationally representative analysis.
Authors: Chumán-Sánchez M, Ortiz-Saavedra B, Uribe-Cavero LJ, Llamo-Vilcherrez AP, Moxey JW, Toro-Huamanchumo CJ
Journal: BMC pediatrics
mental health
psychology
open access
Abstract
Inflammatory bowel disease (IBD) is a chronic autoimmune disorder that affects the gastrointestinal tract and extra-intestinal organs, encompassing various clinical-histological variants including ulcerative colitis (UC), Crohn’s disease (CD), and indeterminate colitis [–]. The prevalence of IBD has risen globally, with nearly 30% of cases occurring in children and adolescents [], leading to significant financial burdens on healthcare systems [, ]. In China, the age-standardized incidence of IBD varies from 1.77 per 100,000 to 3.14 per 100,000 [, ], while the incidence of IBD in Chinese children has risen from 5 per 100,000 in 2001 to 6 per 1,000,000 in 2010 []. Children with IBD are primarily treated the induction and maintenance of remission []. Nevertheless, the pathogenesis underlying IBD remains poorly understood. Thus, further investigation into the development and treatment of IBD is warranted. The establishment of the gut microbiota in early life plays a pivotal role in shaping IBD risk [], yet this process is highly vulnerable to disruption by antibiotics, particularly in neonates frequently exposed to broad-spectrum agents [–]. A nested case-control study found that 58% of children with IBD received antibiotics in their first year of life, compared to only 39% of controls []. This association underscores the susceptibility of the developing gut microbiota during a critical window that antibiotics such as ceftriaxone may profoundly disturb, potentially leading to long-lasting immune dysregulation. Ceftriaxone was selected for this study due to its widespread pediatric use and well-documented disruptive effects on the early-life gut ecosystem. species can alleviate IBD through immunomodulation, oxidative stress reduction, and barrier fortification [, ]. Various strains exert protective effects via distinct mechanisms: CNCM I-403 activates innate immunity through TLR2/9 [] and TLR5/9; C50 suppresses pro-inflammatory cytokines by inhibiting AP-1 and NF-κB []; M-16 V attenuates MAPK-driven chemokine production []. Despite these documented immunomodulatory properties, the efficacy of probiotics in counteracting early-life antibiotic-induced dysbiosis is highly strain-specific. It remains unclear whether 207-1, a strain isolated from the healthy infant gut, can restore immune homeostasis following early antibiotic exposure and thereby confer long-term protection against colitis.