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• Racial inequities in maternal and infant health are vast and well-documented. • Sleep duration and quality is central to overall health and well-being, particularly in perinatal women. • Focus is needed on multi-level influences on maternal sleep health stemming from structural racism. • Moreover understanding the biological underpinnings of health disparities is critical. • This review synthesizes the literature on sleep, racial disparities, and psychoneuroimmunology. Racial inequities in health are vast and well-documented, particularly regarding maternal and infant health. Sleep health, including but not limited to duration and quality, is central to overall health and well-being. However, research has not adequately addressed how racism embedded in structures and systems, in addition to individual experiences, may affect maternal health by impacting sleep. In this critical review, we aim to 1) synthesize findings, emphasizing collaborative studies within our group, 2) highlight gaps in knowledge, and 3) propose a theoretical framework and methodological approach for moving the field forward. Specifically, we focus on findings and future directions linking perinatal sleep, cardiovascular and immune function, and racial disparities in maternal health. Because too few studies look beyond individual-level determinants of sleep deficiencies among Black Americans, we assert a critical need for research that bridges multiple levels of analysis (e.g., individual, community, society) and provides recommendations for specific health parameters that researchers in this area can target. Although the need to understand and address perinatal health disparities is clear, the goal of identifying multilevel mechanisms underlying how racism in one's environment and daily life may interact to affect health extends far beyond pregnancy research. [ABSTRACT FROM AUTHOR]

Objective: To investigate the associations between data-driven dietary patterns, immune function, and incident type 2 diabetes (T2D) and the mediating effects of immune function. Methods: This study included 375,665 participants without diabetes at baseline in the UK Biobank study. Dietary patterns were derived through principal component analysis of food frequency questionnaire data. Immune function was assessed using 14 individual inflammatory markers and an integrated low-grade inflammation score (INFLA-score). Cox proportional hazard models were used to estimate the associations of dietary patterns or immune function with incident T2D. Linear regressions were used to estimate the associations of dietary patterns with immune function. Mediating effects of immune function were quantified. Results: During a median 14.6-year follow-up, 13,932 participants developed T2D. Four dietary patterns were identified: prudent diet (high in whole grains, vegetables, fruits, fish), wheat/dairy/eggs restrictive diet (limiting these foods), meat-based diet (high in red/processed meat, salt), and full-cream dairy diet (preference for full cream milk or dairy products). The prudent diet was negatively (HRQ4 vs Q1, 0.69 [95% CI, 0.65–0.72]), while the wheat/dairy/eggs restrictive diet (HRQ4 vs Q1, 1.08 [95% CI, 1.03–1.13]), meat-based diet (HRQ4 vs Q1, 1.12 [95% CI, 1.06–1.17]), and full-cream dairy diet (HRQ4 vs Q1, 1.08 [95% CI, 1.03–1.12]) were positively associated with incident T2D (all p for trend ≤0.04). The prudent diet was negatively and the full-cream dairy diet was positively associated with most inflammatory markers. Most inflammatory markers, especially INFLA-score (HR, 1.18 [95% CI, 1.16–1.20]), were positively associated with incident T2D. INFLA-score mediated 13% of the association with incident T2D for the prudent diet and 34% for the full-cream dairy diet. Conclusions: This study identified four distinct dietary patterns and a range of inflammatory markers associated with incident T2D. A notable proportion of the associations between dietary patterns and T2D was mediated by immune function. [ABSTRACT FROM AUTHOR]

Bile acids (BA) are receiving a great deal of attention and interest as critical regulators of the immune system of immune organs. Nevertheless, there are few researches on the effect of BA on immunity of aquatic animals. Hence, the objective of this research was to evaluated the effects of BA supplementation on immune function and the mechanisms in immune organs [head-kidney (HK), spleen (SP) and skin (SK)] of grass carp (Ctenopharyngodon idella). A total of 540 fish (the average body weight was 179.85 ± 1.34 g) were randomly assigned to a normal diet group (NPNL: 29 % protein and 5 % lipid) and five low protein and high lipid diet groups (LPHL: 26 % protein and 6 % lipid) with graded levels of 0 (no supplement), 80, 160, 240 and 320 mg/kg BA for 50 days. Grass carp were subjected to a 14-day challenge with Aeromonas hydrophila after growth experiment. Results indicated that: (1) LPHL group (without BA supplementation) increased SK lesion morbidity compared to NPNL group, and LPHL+160 mg/kg BA supplementation improved the disease resistance; (2) LPHL group (without BA supplementation) decreased the levels of antimicrobial compounds and the gene expressions of antimicrobial peptides in immune organs compared to NPNL group, and LPHL+(160–240) mg/kg BA supplementation significantly increased (P < 0.05) lysozyme (LZ) and acid phosphatase (ACP) activities, complement (C3, C4) and immunoglobulin M (IgM) contents, as well as the gene expressions of hepcidin , antimicrobial peptide 2 A (Leap-2 A), Leap-2B , Mucin2 , βdefensin-1 in immune organs of fish; (3) LPHL group (without BA supplementation) aggravated inflammatory response by upregulated pro-inflammatory factors and downregulated anti-inflammatory factors gene expressions compared to NPNL group, and LPHL+240 mg/kg BA supplementation significantly increased transforming growth factor (TGF)-β1 , interleukin 11 (IL-11), −4/13 A , TOR , eIF4E-binding proteins (4E-BP)1 , S6K1 , but markedly reduced (P < 0.05) the gene expressions of tumor, necrosis factor α (TNF-α) , interferon γ2 (IFN-γ2) , IL-1β , IL-6 , IL-8 , IL-15 , IL-17D , IL-12p35 , nuclear factor kappa B p65 (NF-κB p65) , c-Rel, inhibitor of κBα (IκBα) , IκB kinase β (IKKβ) , IKKγ in immune organs of fish. In conclusion, LPHL diet (without BA supplementation) increased SK lesion morbidity and impaired the immunity of immune organs. In addition, LPHL+(160–240) mg/kg BA supplementation enhanced the disease resistance and immunity of grass carp by inhibiting NF-κB signaling molecule and activating TOR signaling molecule. • Bile acid enhanced immune parameter of fish. • Bile acid regulated inflammatory response in immune organ of fish. • Bile acid could activate TOR and NF-κB signaling pathways to regulate immune response. • 165–211.69 mg/kg bile acid may be added into the feed to improve immunity of fish. [ABSTRACT FROM AUTHOR]

Respiratory infections and diseases pose significant challenges to society and healthcare systems, underscoring the need for preventative and therapeutic strategies. Recent research in rodent models indicates that short-chain fatty acids (SCFAs), metabolites produced by gut bacteria, may offer medicinal benefits for respiratory conditions. In this opinion, we summarize the current literature that highlights the potential of SCFAs to enhance immune balance in humans. SCFAs have demonstrated the potential to decrease the risk of primary and secondary respiratory infections, modulate allergic airway exacerbations, and improve overall epithelial pathogen defenses. Therefore, we suggest that systemic SCFA levels could be targeted to support gut and respiratory health in specific groups, such as patients in hospital, women and their offspring, children, older adults, and athletes/military personnel., Competing Interests: Declaration of interests None declared by authors., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)