Transcriptoma de codornas japonesas é modulado por temperatura embrionária e desafio imune

Abstract

Embryogenesis is a critical programming period, as environmental factors can modulate the physiology of organisms. In birds, incubation temperature has been widely studied as an inducer of genetic responses that influence embryonic development and response to post- hatch challenges. In this context, the present study aimed to investigate the effects of embryonic thermal manipulation on the immune response of Japanese quails (Coturnix coturnix japonica) challenged with lipopolysaccharide (LPS) after hatching, using transcriptome analysis (RNA- seq). For this purpose, an experiment was carried out in a 2x2 factorial design, with two incubation temperatures: control temperature (CTL - 37.5°C) and high temperature (AT - 39°C) and two inoculation statuses: quails inoculated with LPS (LPS) and quails not inoculated with 49 LPS (SLPS). Eggs remained at the respective treatment temperatures throughout the incubation period, and 25 days after hatching, chicks were challenged with LPS or saline (placebo). After inoculation, jejunal tissue was collected for gene expression analysis via RNA-seq. Incubation temperature significantly reduced (p<0.05) hatching rates but did not affect (p>0.05) the morphological performance of surviving embryos. LPS induced significant changes (p<0.05) in the spleen, indicating immune system activation. Transcriptomic analysis revealed differentially expressed genes (adjusted p<0.05) associated with metabolic processes, immune response, and oxidative stress, with distinct patterns between the contrasts evaluated (CTL+LPS 57 vs. CTL+SLPS and AT+LPS vs. AT+SLPS). Under control conditions, LPS induced the differential expression of genes, notably IL1R2, IL18BP, and S100A12, related to inflammatory modulation, mucosal barrier integrity, and energy metabolism. In birds incubated at high temperature, LPS triggered broad changes, activating pathways associated with inflammation, lipid homeostasis, protein control, energy metabolism (glycolysis, pentose and Krebs cycles), and vesicular trafficking, while suppressing genes crucial for adaptive immunity, angiogenesis, cellular differentiation, and epigenetic regulation. A conserved set of inflammatory genes (MMP7, PI3, SLC6A14) was upregulated (adjusted p<0.05) under both thermal conditions, suggesting activation of central defense mechanisms. We conclude that high temperature during incubation compromises hatching, but not the phenotype of the offspring; However, it profoundly modulates the molecular response to LPS, altering inflammatory, metabolic, and regenerative pathways, which may impact intestinal adaptation to future stresses.