Biology subjects

Tomasello, A.

Publications and source records attributed to Tomasello, A..

3 recordsLinked to original sources

bioRxiv2026

Adipose tissue as a site of immune activation and dysfunction in individuals with obesity and asthma

Obesity increases local inflammatory responses in adipose tissue. Individuals with obesity have increased asthma incidence and severity and reduced responses to asthma therapeutics through unknown mechanisms. To identify mechanisms by which increased fat mass augments asthma pathogenesis, single cell RNA sequencing of the immune-rich stromovascular fraction of subcutaneous adipose tissue was conducted from well-characterized adults with obesity-associated asthma matched to adults without asthma. Individuals with asthma had increased abundance of perivascular macrophages and lymphoid-associated macrophages (LAMs) and reduced abundance of classical monocytes and CD4+ and CD8+ naive T cells. Pseudo-bulk differential expression (DE) identified upregulation of cellular metabolism, specifically oxidative phosphorylation, and decreased immune homeostatic pathways in asthma across immune cell subsets. Cell type specific DE analysis of effector cell subtypes identified significant induction of metallothionein gene expression in asthma, a signature of immune cell dysfunction characterized by both an activation and exhaustion phenotype. Gene co-expression analysis identified gene modules associated with asthma diagnosis, lung function, and biomarkers of type 2 inflammation were enriched in effector cells. These data identify adipose tissue dysfunction occurs in obesity-associated asthma and support adipose tissue as therapeutic target to address the enhanced asthma risk among those with obesity. Grant SupportNIH U01AI155299, P30DK020593, R01AI182159, K23HL159351, UL1RR024975-03, P30CA68485, P30EY08126, G20RR030956, 5UL1TR002243, KL2TR002245, P30AI110527, DK020593, American Heart Association 17SFRN33520017.

immunology↗

bioRxiv2025

Ovarian Hormones and Obesity Drive Th17-mediated Airway Inflammation through Estrogen Receptor Signaling

Obesity is a risk factor for increased prevalence and severity of asthma, particularly in females. As adults, females have increased prevalence of asthma compared to males. Yet, the mechanisms remain unclear on how sex hormones and obesity increase airway inflammation. We hypothesize that estrogen signaling through estrogen receptor-alpha (ER-) in T cells increased airway inflammation in the context of obesity. To test our hypothesis, we utilized a high fat (HFD) on female and male mice that underwent ovariectomy or gonadectomy or in Esr1fl/fl X Cd4Cre+ male and female mice. As controls, mice in similar groups were fed normal chow. After 8-12 weeks on diets, house dust mite (HDM) sensitization and challenge occurred in all mice. Lungs and BAL fluid were harvested 24 hours after the last challenge. Ovarian hormones and ER- signaling in T cells increased eosinophils, neutrophils, and Th17-mediated airway inflammation in the lungs of obese female mice. Additionally, using PBMCs from a well-characterized obese asthma cohort, we determined that obese women with asthma had increased Th17 cells compared to obese men with asthma. Our results show that ER- signaling in T cells increases Th17-mediated airway inflammation in obese mice and that Th17 cells circulate at higher frequencies in women with asthma compared to men with asthma. Further research into the interplay between hormonal signaling and immune responses in asthma is essential for developing personalized treatments. One Sentence SummaryEstrogen receptor-alpha signaling, in the context of obesity, increases allergen-induced Th17-mediated airway inflammation in female mice.

immunology↗

bioRxiv2023

The invasive brown seaweed Rugulopteryx okamurae (Dictyotales, Ochrophyta) continues to expand: first record in Italy.

The brown seaweed Rugulopteryx okamurae (Dictyotales, Ochrophyta), native to the Pacific Ocean and widely distributed in Asia, has been recently recognized as an emblematic case of biological invasion by marine macroalgae in European waters. Since 2015 and from the Strait of Gibraltar, R. okamurae has rapidly spread towards Atlantic and Mediterranean coastal areas exhibiting an invasive behaviour with significant ecological and economic impacts. Here, we report by morphology and genetics the first observation of this species in Italy along the north-western coast of Sicily (Gulf of Palermo), as drifted material and an established population on Posidonia oceanica, representing its new eastern distribution limit in the Mediterranean Sea, previously established in Marseilles (France). Furthermore, we have performed with the current introduced distribution of the species a favorability distribution model for the Mediterranean, which shows most of the western Mediterranean, including the Balearic archipelago, Corsica and Sardinia, central Mediterranean, including Sicily, and the northern coast of Africa together with eastern Mediterranean basin, as highly favorable for R. okamurae. Arrival of the species into this new area is suggested by means of sea currents and maritime traffic, including fishing activities, hypothesis supported by some of the ranked variables that entered the favorability model, i.e, current velocity, and proximity of fishing ports. These results are a warning that the species can cover large sea distances favored by sea currents, thus also threatening the ecosystems and marine resources of the central and eastern Mediterranean, highly favorable regions for the species. We suggest coordinated actions at the European level regarding prevention, among which those that have the complicity of the fishing sector should be considered, both because it is a highly affected sector and because it potentially has a very important role in the dispersion of the species.

plant biology↗