Biology subjects

Olivas, J.

Publications and source records attributed to Olivas, J..

3 recordsLinked to original sources

bioRxiv2026

Small intestine microbiota development prevents early-life adiposity via IL-22-mediated intestinal PPARα suppression

Perturbation to the early-life microbiota has long-term detrimental effects on health and development, leading to increased risk for metabolic dysfunction and childhood obesity. Despite the central role of the small intestine (SI) in energy balance, the impact of SI microbiota establishment on the regulation of host metabolism and early-life adiposity remains unclear. Here, we report that disruption of a critical SI microbiota-intestinal epithelial cell circuit, specifically during a critical early-life period, drives long-lasting obesity. We demonstrate that the SI microbiota expands in abundance and diversity significantly between 2 and 3 weeks of life, and that segmented filamentous bacteria (SFB) and Lactobacillus intestinalis establish residence. Disruption of the early-life SI microbiota with antibiotics leads to enhanced lipid uptake and adiposity, driven by increased peroxisome proliferator-activated receptor alpha (PPAR) expression and activity in SI epithelial cells (IECs). We demonstrate that SFB and L. intestinalis are key regulators of PPAR in SI IECs by increasing intestinal IL-22 levels specifically during weaning, which is necessary for inhibition of antibiotic-induced adiposity in a PPAR-dependent manner. Together, this work provides mechanistic insights into beneficial microbiota-induced epithelial-immune crosstalk in the SI that is specific to early life, a critical protective mechanism against excessive adiposity in infancy, and offers insight into how antibiotics during infancy may increase the risk of childhood obesity. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=123 SRC="FIGDIR/small/731695v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@1b32f07org.highwire.dtl.DTLVardef@d4a5a6org.highwire.dtl.DTLVardef@c76d1borg.highwire.dtl.DTLVardef@cc479d_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2026

Aspartate aminotransferase is required for Salmonella expansion in the inflamed gut via TCA anaplerosis

Aspartate represents an important proteogenic amino acid in all living organisms. Many microorganisms can produce aspartate through various biosynthetic processes, utilizing it for energy production and as a precursor for synthesizing other biomolecules, such as amino acids and nucleotides. The enteric pathogen Salmonella Typhimurium (S. Tm) has developed mechanisms to access aspartate as a nutrient source during expansion in the inflamed gut. However, how S. Tm deals with aspartate starvation during infection remains unknown. To address this knowledge gap, we interrogated Salmonellas reliance on the bi-directional aspartate aminotransferase encoded by aspC for growth in vitro and during host colonization using murine models of Salmonella infection. AspC can interconvert aspartate and the TCA intermediate oxaloacetate and is hypothesized to support S. Tm cellular demands for aspartate during starvation or support refueling of the TCA cycle via oxaloacetate synthesis. Herein, we find that loss of aspC results in a gut-specific S. Tm colonization defect that increases with the course of infection. Importantly, aspC is dispensable for S. Tm systemic colonization in CBA/J mice. Additionally, we report that loss of aspC results in a significant growth defect during respiration of inflammation-derived electron acceptors in vitro. Interruption of oxidative TCA cycle progression via TCA enzyme deletion or supplementation with TCA intermediates (e.g., oxaloacetate) abrogates the defect observed in {Delta}aspC S. Tm in vitro. Thus, suggesting the requirement for AspC to catabolize aspartate and support the TCA cycle during respiration. Altogether, we report that AspC plays a critical role in S. Tm pathogenesis in a gut-specific manner during inflammation through supporting energy generation.

microbiology↗

bioRxiv2025

High-Resolution Proteomics Unveils Salivary Gland Disruption and Saliva-Hemolymph Protein Exchange in Plasmodium-Infected Mosquitoes

Plasmodium sporozoites, the stage that initiates a malaria infection, must invade the mosquito salivary glands (SGs) before transmitting to a vertebrate host. However, the effects of sporozoite invasion on salivary gland physiology and saliva composition remain largely unexplored. We examined the impact of Plasmodium infection on Anopheles gambiae salivary glands using high-resolution proteomics, gene expression, and morphological analysis. The data revealed differential expression of various proteins, including the enrichment of humoral proteins in infected salivary glands originating from the hemolymph. These proteins diffused into the SGs due to structural damage caused by the sporozoites during invasion. Conversely, saliva proteins diffused out into the circulation of infected mosquitoes. Moreover, infection altered saliva protein composition, as shown by proteomes from saliva collected from mosquitoes infected by P. berghei or P. falciparum, revealing a significant reduction of immune proteins compared to uninfected mosquitoes. This reduction is likely due to the association of these proteins with the surface of sporozoites within the mosquito salivary secretory cavities. The saliva protein profiles from mosquitoes infected with both Plasmodium species were remarkably similar, suggesting a conserved interaction between sporozoites and salivary glands. Our results provide a foundation for understanding the molecular interactions between Plasmodium sporozoites and mosquito salivary glands.

microbiology↗