Biology subjects

Joyce, N.

Publications and source records attributed to Joyce, N..

4 recordsLinked to original sources

bioRxiv2026

Plantago lanceolata and Lolium perenne metabolite profiles, their impact on soil microbial community structures and soil biological nitrification inhibition

Background and aimsExcess nitrate (NO3-), from fertilizer overuse and intensive agriculture, can pollute water and contribute to greenhouse gas production (nitrous oxide - N2O). Plant metabolites from pastural herbs such as Plantago lanceolata (plantain) can inhibit microbial nitrification of ammonium to NO3- (biological nitrification inhibition - BNI) and change soil nitrogen cycle dynamics (lower potential nitrification rate - PNR). The main aim was to investigate differential plant metabolite expression associated with BNI and lowered PNR in different soil types. MethodsSix plantain cultivars were tested for BNI potential and screened for metabolites that correlated with inhibition of the ammonia oxidising bacterium (AOB) Nitrosospira multiformis. PNR and microbiome change was then investigated in four different New Zealand soils under the plantain cultivar Agritonic and ryegrass cultivar One50. ResultsPNR under plantain was 11 to 41% lower than fallow soil while PNR under ryegrass was 0 to 39% lower. In addition to verbascoside and aucubin, plantain metabolites associated with lower PNR included plantamajoside, riboflavin 3- and 5-sulfate, plantagoguanidinic acid. Chlorogenic acid was associated with lowered PNR under ryegrass. PNR reductions, microbiome structure and the ratio of ammonia oxidising archaea (AOA) relative to AOB was modulated by soil type. ConclusionPlantain and ryegrass lowered the PNR in four different soils and was correlated with metabolites beyond just aucubin and verbascoside. Based on candidate BNI-associated metabolites identified, it was hypothesised that lowered PNR is likely indirect through mechanisms such as chelation and appears to be dependent on both plant physiology and soil physicochemistry.

systems biology↗

bioRxiv2026

Linking plantain derived metabolites in sheep urine with nitrification inhibition in soil

Metabolites from Plantago lanceolata (plantain) biomass have been linked with biological nitrification inhibition (BNI) in soil. After grazing, leaf metabolite chemistry is altered via digestion, and a suite of secondary metabolites are then delivered onto soil via dung and urine. The purpose of this study was to establish if urine from sheep grazed on plantain had BNI activity when added to pasture soil, and to identify the metabolite profile(s) that most likely contribute to the BNI effects observed. Groups of sheep (n=5 sheep per group) were grazed on one of nine different plantain cultivars in autumn and spring with analysis of leaf material, urine, soil incubation and BNI bioassay data used to identify potential metabolite candidates implicated with BNI. The urinary nitrogen and metabolite composition of sheep fed plantain varied significantly between cultivars and season. After 28 days of incubation, all soil microcosms treated with plantain-derived urine had up to 35% less nitrate than comparative ryegrass urine controls in both seasons, except one in autumn. The key phytochemistry associated with lower soil nitrate concentrations was phenylethanoid and iridoid glycosides resulting in a higher output of glucuronidated, methylated and sulfated secondary metabolites in the urine. Among 19 secondary metabolites identified in the urine, hydroxytyrosol-related metabolites as well as catechol glucuronide, 2-methoxyphenyl sulfate and guaiacol-{beta}-D-glucuronide appear to be the most likely target compounds with respect to the BNI effects observed. Variation in metabolites from different plantain cultivars affected the ratio of metabolite derivatives in urine, which ultimately affected soil nitrification rates. Cultivar phytochemistry is therefore an important consideration with respect to BNI under urine patches. HighlightsO_LISheep grazing different plantain cultivars had different urine compositions C_LIO_LIUrines elicited biological nitrification inhibition (BNI) in soil and in vitro C_LIO_LIDifferent BNI response was related to differential expression of urine metabolites C_LIO_LIKey urine metabolites associated with BNI are derived from glycosidic compounds C_LI

systems biology↗

bioRxiv2025

Postoperative Stress Accelerates Atherosclerosis through Inflammatory Remodeling of the HDL Proteome and Impaired Reverse Cholesterol Transport

BACKGROUNDOver 10 million patients undergoing non-cardiac surgery annually experience major cardiovascular complications within 30 days, many due to destabilized atherosclerotic plaques. Reverse cholesterol transport (RCT), a key pathway for cholesterol removal by HDL and apoA-I, is critical in preventing plaque progression. While surgery-induced inflammation is known to impair HDL function, its effects on RCT and plaque stability remain unclear. METHODSTo isolate the impact of surgical inflammation, independent of blood loss, we developed an abdominal laparotomy model in apoE-/- mice on a Western diet, minimizing blood loss and avoiding perioperative blood sampling. We assessed plasma cholesterol efflux capacity, performed proteomic analysis of HDL, and analyzed atherosclerotic plaques for lipid content, perilipin-2 (PLIN2), cleaved-caspase-3 (c-Casp-3), and necrotic core expansion. A novel dual-label, dual-cell-type in vivo RCT model was developed to compare RCT from macrophage-derived (BMDMs) and vascular smooth muscle cells (VSMCs)-derived foam cells. Recombinant apoA-I (rApoA-I) was tested for therapeutic rescue of impaired RCT. RESULTSSurgery significantly reduced RCT for at least 48 hours, paralleled by a drop in cholesterol efflux capacity and inflammatory remodeling of HDL, marked by elevated serum amyloid A (SAA1/2) and reduced apoA-I. Plaques showed a 1.6-fold increase in intracellular lipids and PLIN2 expression at 24 hours post-surgery, with elevated c-Casp-3 indicating lipid-driven apoptosis. Foam cell analysis revealed increased PLIN2 in both CD45+ (leukocyte) and CD45- (non-leukocyte) subtypes, with leukocyte foam cells expressing higher PLIN2. c-Casp-3+ apoptotic cells were predominantly PLIN2high and of both leukocytic and non-leukocytic origin. By day 15, the necrotic core area increased by 1.5-fold with sustained loss of plaque cellularity. Using our dual-cell-type RCT model, we found that surgery significantly impaired BMDM RCT in vivo, while VSMC RCT remained largely unaffected, highlighting foam cell subtype-specific vulnerability to surgical inflammation. These findings were mirrored in general surgery patients, whose postoperative plasma exhibited markedly reduced cholesterol efflux capacity. In mice, rApoA-I treatment partially restored RCT and reduced plaque lipid accumulation. CONCLUSIONSSurgical inflammation acutely impairs HDL function and RCT, triggering lipid accumulation, foam cell apoptosis, and accelerated plaque destabilization independent of blood loss. Immediate restoration of apoA-I at the time of surgery, aiming to counteract the acute phase response, may offer a targeted strategy to reduce postoperative cardiovascular risk.

biochemistry↗

bioRxiv2025

A Rosella-PLIN2 Knock-in Mouse Reveals Lipophagy and Immunometabolic Interplay in Atherosclerosis

Cytosolic lipid droplets (LDs) regulate lipid homeostasis, with abnormal LD dynamics linked to metabolic diseases like atherosclerosis. In macrophage foam cells, LDs undergo autophagic degradation via lipophagy, but the extent of this process in vascular smooth muscle cell (VSMC) foam cells remains unclear. To track lipophagy in real time, we developed a Rosella-PLIN2 biosensor by tagging perilipin 2 (PLIN2) with the fluorescent pH-biosensor Rosella. We show that proatherogenic lipoproteins and autophagy activators stimulate lipophagy in human macrophages. Targeting LDs with an LC3 fusion protein or LD-autophagy tethering compounds (LD-ATTECs) selectively enhanced lipophagy, promoting foam cell LD clearance. In an atherosclerosis model, Rosella-PLIN2 accurately tracked lipophagy in arterial foam cells, revealing distinct PLIN2 expression patterns in macrophage and non-leukocyte foam cells. We identified a lipophagy deficiency in VSMC foam cells and demonstrate that enhancing lipophagy promotes LD catabolism in primary VSMC foam cells. TREM2+ macrophages exhibited high lipid content and low lipophagy flux, whereas TREM2- macrophages had low lipid content and high lipophagy flux. Our findings highlight a cell-specific interplay between lipophagy and immunometabolism in arterial foam cells, unveiling novel therapeutic avenues for atherosclerosis. Additionally, the Rosella-PLIN2 model provides a powerful tool for studying LD metabolism, offering new insights into lipid homeostasis and disease mechanisms.

cell biology↗