Biology subjects

Ferrero, M.

Publications and source records attributed to Ferrero, M..

5 recordsLinked to original sources

bioRxiv2023

Daylong Acoustic Recordings of Grazing and Rumination Activities in Dairy Cows

Monitoring livestock feeding behavior may help assess animal welfare and nutritional status, and to optimize pasture management. The need for continuous and sustained monitoring requires the use of automatic techniques based on the acquisition and analysis of sensor data. This work describes an open dataset of acoustic recordings of the foraging behavior of dairy cows. The dataset includes 662 h of daily records obtained using unobtrusive and non-invasive instrumentation mounted on five lactating multiparous Holstein cows continuously monitored for six non-consecutive days in pasture and barn. Labeled recordings precisely delimiting grazing and rumination bouts are provided for a total of 400 h and for over 6,200 ingestive and rumination jaw movements. Companion information on the audio recording quality and expert-generated labels is also provided to facilitate data interpretation and analysis. This comprehensive dataset is a useful resource for studies aimed at exploring new tools and solutions for precision livestock farming.

animal behavior and cognition↗

bioRxiv2023

Neutrophil efferocytosis reprograms mitochondrial metabolism to switch alveolar macrophages to a pro-resolution phenotype at the cost of bacterial control

Resolution of lung injuries is vital to maintain gas exchange. Concurrently, there is an increased risk of secondary bacterial infections. Alveolar macrophages (AMs) are crucial to clear bacteria and control initiation and resolution of inflammation, but environmental cues that switch functional phenotypes of AMs remain elusive. Here, we discovered an incapacity of AMs to mount an effective immune response to bacteria during resolution of inflammation. AM efferocytosis of neutrophils (PMNs), a hallmark of resolution of inflammation, switched mitochondrial metabolism to shift AM functions. Mechanistically, PMN-derived myeloperoxidase (MPO) fueled canonical glutaminolysis via uncoupling protein 2 (UCP2) resulting in decreased mtROS-dependent killing of bacteria and secretion of pro-inflammatory cytokines. Instead, MPO-enhanced UCP2 expression inhibited mitochondrial hyperpolarization and boosted efferocytosis irrespective of the presence of bacterial pathogens. In contrast, efferocytosis of epithelial cells resulted in a distinct anti-inflammatory phenotype of AMs maintaining phenotypic plasticity towards bacteria. Overall, uptake of apoptotic PMNs switches AMs to prioritize resolution of inflammation over antibacterial responses and similarly affects murine macrophages at extra-pulmonary sites, and human AMs. One sentence summaryNeutrophil efferocytosis reprograms mitochondrial metabolism to switch alveolar macrophages to a pro-resolution phenotype at the cost of bacterial control.

immunology↗

bioRxiv2022

AA-amyloidosis in cats (Felis catus) housed in shelters

Systemic AA-amyloidosis is a protein-misfolding disease that is characterized by fibril deposition of serum amyloid-A protein (SAA) in several organs in humans and many animal species. Fibril deposits originate from abnormally high serum levels of SAA during chronic inflammation. In domestic short-hair cats, AA-amyloidosis has only been anecdotally reported and is considered a rare disease. Here we report that an astonishing 57-73% of early deceased short-hair cats kept in three independent shelters suffer from amyloid deposition in the liver, spleen, or kidney. Histopathology and mass spectrometry of post-mortem extracted deposits identified SAA as the major protein source. The duration of stay in the shelters was positively associated with a histological score of AA-amyloidosis (B=0.026, CI95%=0.007-0.046; p=0.010). Presence of SAA fragments in bile secretions raises the possibility of fecal-oral transmission of the disease.

pathology↗

bioRxiv2019

PREDATION CAPACITY OF SOIL-DWELLING PREDATORY MITES ON TWO GROUND BEETLE IMMATURE STAGES: A BIOLOGICAL CONTROL PERSPECTIVE FOR TWO MAJOR MAIZE PESTS.

Soil-dwelling predatory mites already proved their efficiency as biocontrol agents against many pests (Carrillo et al. 2015). Western Corn Rootworm (WCR), (Diabrotica virgifera virgifera) and Wireworm (WW) (Agriotes sordidus) are important pests of various crops (Furlan et al. 2002; Krysan et al., 1986; Ritter and Richter 2013; Wesseler and Fall 2010) whose eggs and first instar larvae also inhabit the first centimeters of soil (Furlan 2004; Vidal et al., 2005). In order to evaluate the potential of predatory mites as biological control agents against WCR and WW, we investigated the predation capacity of Stratiolaelaps scimitus, Gaeolaelaps aculeifer and Macrocheles robustulus on immature stages of these two prey species. First, we observed if one or more species could feed upon eggs and first instar larvae as Prischmann et al. (2011) suggested for WCR. We then explored their predation abilities through time using a survival analysis to identify the best biocontrol agent among the species tested. Surprisingly, none of the predator species tested identified WCR or WW eggs as preys. However, at least 50% of WCR and WW first instar larvae have been attacked by G. aculeifer and M. robustulus. Stratiolaelaps scimitus showing a slightly lower efficiency (30% of preys attacked). The survival analysis confirmed this trend with slower predation dynamics for S. scimitus. These results show a potential of soil-dwelling predatory mites as biocontrol agents against WCR and WW. Furthermore, targeting the neonate stage instead of the egg stage in pest management strategies seems necessary for maximizing efficiency.

ecology↗

bioRxiv2018

Mice harboring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity.

Spinocerebellar ataxia 28 is an autosomal dominant neurodegenerative disorder caused by missense mutations affecting the proteolytic domain of AFG3L2, a major component of the mitochondrial m-AAA protease. However, little is known of the underlying pathogenetic mechanisms or how to treat patients with SCA28. Currently available Afg3l2 mutant mice harbour deletions that lead to severe, early-onset neurological phenotypes that do not faithfully reproduce the late-onset and slowly progressing SCA28 phenotype. Here we describe production and detailed analysis of a new knock-in murine model harbouring an Afg3l2 allele carrying the p.Met665Arg patient-derived mutation. Heterozygous mutant mice developed normally but signs of ataxia were detectable by beam test at 18 months. Cerebellar pathology was negative; electrophysiological analysis showed increased spontaneous firing in Purkinje cells from heterozygous mutants with respect to wild-type controls, although not statistically significant. As homozygous mutants died perinatally with evidence of cardiac atrophy, for each genotype we generated mouse embryonic fibroblasts (MEFs) to investigate mitochondrial function. MEFs from mutant mice showed altered mitochondrial bioenergetics, with decreased basal oxygen consumption rate, ATP synthesis and mitochondrial membrane potential. Mitochondrial network formation and morphology was also altered, in line with greatly reduced expression of Opa1 fusogenic protein L-isoforms. The mitochondrial alterations observed in MEFs were also detected in cerebella of 18-month-old heterozygous mutants, suggesting they may be a hallmark of disease. Pharmacological inhibition of de novo mitochondrial protein translation with chloramphenicol caused reversal of mitochondrial morphology in homozygous mutant MEFs, supporting the relevance of mitochondrial proteotoxicity for SCA28 pathogenesis and therapy development.

genetics↗