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The gut serves as a vital immunological organ orchestrating immune responses and influencing distant mucosal sites, notably the respiratory mucosa. It is increasingly recognized as a central driver of critical illnesses, with intestinal hyperpermeability facilitating bacterial translocation, systemic inflammation, and organ damage. The “gut-lung” axis emerges as a pivotal pathway, where gut-derived injurious factors trigger acute lung injury (ALI) through the systemic circulation. Direct and indirect effects of gut microbiota significantly impact immune responses. Dysbiosis, particularly intestinal dysbiosis, termed as an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes, influences adaptive immune responses, including differentiating T regulatory cells (Tregs) and T helper 17 (Th17) cells, which are critical in various lung inflammatory conditions. Additionally, gut and bone marrow immune cells impact pulmonary immune activity, underscoring the complex gut-lung interplay. Moreover, lung microbiota alterations are implicated in diverse gut pathologies, affecting local and systemic immune landscapes. Notably, lung dysbiosis can reciprocally influence gut microbiota composition, indicating bidirectional gut-lung communication. In this review, we investigate the pathophysiology of ALI/acute respiratory distress syndrome (ARDS), elucidating the role of immune cells in the gut-lung axis based on recent experimental and clinical research. This exploration aims to enhance understanding of ALI/ARDS pathogenesis and to underscore the significance of gut-lung interactions in respiratory diseases.
The gut serves as a vital immunological organ orchestrating immune responses and influencing distant mucosal sites, notably the respiratory mucosa. It is increasingly recognized as a central driver of critical illnesses, with intestinal hyperpermeability facilitating bacterial translocation, systemic inflammation, and organ damage. The “gut-lung” axis emerges as a pivotal pathway, where gut-derived injurious factors trigger acute lung injury (ALI) through the systemic circulation. Direct and indirect effects of gut microbiota significantly impact immune responses. Dysbiosis, particularly intestinal dysbiosis, termed as an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes, influences adaptive immune responses, including differentiating T regulatory cells (Tregs) and T helper 17 (Th17) cells, which are critical in various lung inflammatory conditions. Additionally, gut and bone marrow immune cells impact pulmonary immune activity, underscoring the complex gut-lung interplay. Moreover, lung microbiota alterations are implicated in diverse gut pathologies, affecting local and systemic immune landscapes. Notably, lung dysbiosis can reciprocally influence gut microbiota composition, indicating bidirectional gut-lung communication. In this review, we investigate the pathophysiology of ALI/acute respiratory distress syndrome (ARDS), elucidating the role of immune cells in the gut-lung axis based on recent experimental and clinical research. This exploration aims to enhance understanding of ALI/ARDS pathogenesis and to underscore the significance of gut-lung interactions in respiratory diseases.
<b>Objective:</b> To study the structure of concomitant pathologies in low birth weight premature newborns with respiratory distress syndrome (RDS). To identify mortality risk factors in these newborns.<br /> <b>Materials and methods:</b> Data from 374 premature newborns weighing less than 1500 g and gestational age less than 32 weeks with RDS treated in the intensive care unit were analyzed.<br /> <b>Results:</b> Several comorbidities were more common among children with RDS compared to children without RDS. Thus, disseminated intravascular coagulation syndrome (DIC) occurred 2 times, atelectasis 1.3 times, necrotizing enterocolitis (NEC) 2.4 times, and anemia 1.8 times more often among children with RDS compared to those without RDS.<br /> In multivariate logistic regression, such factors as 1-3 points on the Apgar scale at 1 minute (OR - 2.478, 95% CI - 1.289-4.764, p = 0.007), 1-3 points on the Apgar scale at 5 minutes ( OR - 3.754, 95% CI - 1.788-7.878, p<0.0001), DIC (OR -4.428, 95% CI -2.206-8.887, p<0.0001), NEC (OR - 4.508, 95% CI - 2.270-8.954, p<0.0001) showed a positive association with death in children with RDS.<br /> When assessing the effect of the combination of DIC and NEC on death, it was found that the combination of these two pathologies in children with RDS increases the risk of death by more than 2 times. Thus, the area under the curve (AUC) for DIC was 0.283, for NEC the AUC was 0.335, and for the combination ICE+NEC it was 0.782).<br /> <b>Conclusions:</b> The structure of comorbidities in low birth weight infants with RDS differs from that of infants without RDS. Premature infants with RDS were more likely to develop anemia, DIC, atelectasis, and NEC. The presence of comorbidities increases the risk of death in low birth weight infants with RDS. Low Apgar score, DIC syndrome, and NEC can increase the risk of death in low birth weight premature infants with RDS. It is anticipated that the collected data will enhance personalized care for low birth weight, premature infants with multiple health conditions, ultimately reducing mortality rates in this vulnerable patient group.
Background: Nutrition significantly impacts the outcomes of critically ill children in intensive care units (ICUs). Due to the evolving metabolic, neuroendocrine, and immunological disorders associated with severe illness or trauma, there are dynamically changing phases of energy needs requiring tailored macronutrient intake. Objectives: This study aims to assess the changing dietary needs from the acute phase through recovery, provide recommendations for implementing evidence-based strategies to ensure adequate energy and nutrient provision in pediatric ICUs, and optimize patient outcomes. Methods: A comprehensive search of the MEDLINE-PubMed database was conducted, focusing on randomized controlled trials, meta-analyses, and systematic reviews related to the nutrition of critically ill children. The study highlights recent guidelines using the GRADE approach, supplemented by relevant adult studies, current clinical practices, challenges, gaps in knowledge, and future directions for research aimed at improving nutritional interventions. Results: Early personalized, incremental enteral feeding helps mitigate the negative energy balance during the acute phase, aids organ function restoration in the stabilization phase, and supports growth during the recovery phase and beyond. Conversely, early full nutritional support, high protein doses, or isolated micronutrient administration have not demonstrated benefits due to anabolic resistance in these patients. Moreover, early parenteral nutrition during the acute phase may suppress autophagy and lead to worse outcomes. Accurate assessment of nutritional status and monitoring of daily energy and protein needs are crucial. Conclusions: Strong evidence supports the establishment of a dedicated nutritional team and the implementation of individualized nutritional protocols in the ICU to reduce morbidity and mortality in critically ill children.
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