Microbiota-derived short chain fatty acids in pediatric health and diseases: from gut development to neuroprotectionThe infant gut microbiota undergoes significant changes during early life, which are essential for immune system maturation, nutrient absorption, and metabolic programming. Among the various microbial metabolites, short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, produced through the fermentation of dietary fibers by gut bacteria, have emerged as critical modulators of host-microbiota interactions. SCFAs serve as energy sources for colonic cells and play pivotal roles in regulating immune responses, maintaining gut barrier integrity, and influencing systemic metabolic pathways. Recent research highlights the potential neuroprotective effects of SCFAs in pediatric populations. Disruptions in gut microbiota composition and SCFA production are increasingly associated with a range of pediatric health issues, including obesity, allergic disorders, inflammatory bowel disease (IBD), and neurodevelopmental disorders. This review synthesizes current knowledge on the role of microbiota-derived SCFAs in pediatric health, emphasizing their contributions from gut development to neuroprotection. It also underscores the need for further research to unravel the precise mechanisms by which SCFAs influence pediatric health and to develop targeted interventions that leverage SCFAs for therapeutic benefits.
The role of ω-3 polyunsaturated fatty acids in child development. Adequate intake of ω-3 PUFAs is essential for the development and functioning of the central nervous system, immune system and vision in children. The body content of ω-3 PUFAs is closely related to the nutrition. In the Russian Federation, consumption of fish and other products containing ω-3 PUFAs is traditionally low. The majority of the Russian population has a deficiency in ω-3 PUFA consumption. With an unbalanced diet, supplementation of ω-3 PUFAs is necessary.
EFFICACY AND TOLERABILITY OF JANUS KINASE INHIBITOR TOFACITINIB IN JUVENILE LINEAR SCLERODERMA. CASE SERIES OF 5 PATIENTS.AIM: to analyze the efficacy of the Janus kinase inhibitor tofacitinib (TF) in children with linear form of juvenile localized scleroderma (JLSL). MATERIALS AND METHODS: 5 patients with JLSL were treated with TF, we evaluated the efficacy of therapy retrospectively. RESULTS: The mean disease duration prior to TF therapy was high at 71 months. All patients did not respond well to glucocorticosteroid (Glu) and methotrexate (MTX) therapy, two did not respond to combination therapy of Glu, MTX, mycophenolate mofetil (MFM), which prompted the initiation of TF therapy. All patients received TF in combination with MFM or MTX or GCS. The mean duration of TF therapy was 12.8±1.78 months. From 3 to 6 months of TF therapy, we observed positive changes in scleroderma skin and joint involvement. The positive results continued to increase up to the 12th month of treatment, as evidenced by the reduction of the mLoSSI and LoSDI indices. We decided to continue treatment for up to 18 months. The patients tolerated TF well, there were no serious infections, abnormalities in liver function. CONCLUSION: Our case series showed a significant improvement in skin and joint damage after 12 months of TF therapy in resistant JLSL patients. Further experience with TF is needed to determine its place in the treatment of juvenile scleroderma.
Preliminary IL-1 Family Cytokine Signature for Crohn’s Disease Onset in Pediatric Juvenile Idiopathic ArthritisA Polyanskaya, Anna G. Soboleva, Alexandre Mezentsev et al.|International Journal of Molecular Sciences|2026 Crohn’s disease (CD) in children with juvenile idiopathic arthritis (JIA) is frequently diagnosed late due to overlapping symptoms and non-specific biomarkers. We hypothesized that longitudinal cytokine profiling could identify a pre-symptomatic signature predictive of CD conversion in pediatric JIA patients. Ninety pediatric participants (JIA, CD, psoriatic arthritis, healthy controls) underwent serum cytokine profiling (IL-1α, IL-1β, IL-36α, IL-37, IL-6, IL-18, IL-27, IL-31) at baseline and 12 months. Statistical analysis used Mann–Whitney U tests for two-group comparisons, the Kruskal–Wallis test with Dunn’s post hoc for multi-group comparisons, Fisher’s Exact Test for categorical outcomes, and exploratory principal component analysis (PCA). Baseline screening identified a subgroup of JIA patients (N = 4) with significantly elevated IL-1α, IL-1β, and IL-36α. At 12 months, all four patients in this subgroup received a secondary CD diagnosis (4/4 converters vs. 0/21 non-converters; Fisher’s Exact Test: p < 0.0001). The longitudinal analysis at conversion revealed a broader pro-inflammatory shift, with marked increases in IL-18 and IL-31, alongside elevated IL-37, suggesting a compensatory regulatory response. PCA confirmed that converters clustered distinctly from both stable JIA and established CD. A baseline IL-1 family signature may represent a preliminary predictive signature for CD onset in pediatric JIA. Although constrained by the small converter subgroup (N = 4), these data support cytokine profiling for earlier diagnosis in high-risk populations.
Association of MMP9 and NOS3 Polymorphisms with Distinct Clinical Forms of Juvenile Scleroderma and Characteristics of Humoral ImmunityOsminina Mk, V.A. Podzolkova, Maria Litvinova et al.|International Journal of Molecular Sciences|2026 Juvenile scleroderma (JS), comprising localized (JLSd) and systemic (JSSc) forms, is a rare autoimmune disorder. This study investigated associations of polymorphisms in extracellular matrix (MMP1, MMP9) and vascular homeostasis (NOS3) genes with JS risk and immunological phenotypes. A case–control study involved 215JS patients (194 JLSd, 21 JSSc) and 72 controls. SNPs (MMP1 rs1799750, MMP9 rs3918242, NOS3 rs1799983) were genotyped using real-time PCR followed by minisequencing and mass spectrometric analysis of reaction products. Associations with disease risk, subtypes, and immunological markers were analyzed statistically. The MMP9 (rs3918242) CT genotype was significantly associated with JLSd (OR = 2.23, 95% CI: 1.14–4.37, p = 0.022), showing a trend in linear facial forms. The NOS3 (rs1799983) GG genotype demonstrated a trend toward association with JSSc (OR = 2.61, 95% CI: 0.92–7.37, p = 0.065). No significant associations were found for rs1799750 MMP1 and risk of disease development. The MMP9 risk genotype did not correlate with scleroderma-specific autoantibodies, while the NOS3 GG genotype was associated with lower serum levels of anti-collagen IV antibodies (p = 0.039). Genetic associations differ for JS subtypes: MMP9 with JLSd and NOS3 with JSSc. Children with CT polymorphism MMP9 (rs3918242) and with NOS3 (rs1799983) GG genotype were found to be genetically predisposed for the development of JS.