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Mondino, A.

Publications and source records attributed to Mondino, A..

15 recordsLinked to original sources

Rapid and dynamic reprogramming within the tumor microenvironment drives EDA-CAR-T dysfunction and compromised therapeutic efficacy in solid tumors

BackgroundChimeric antigen receptor (CAR)-T cell therapies efficacy in solid tumors remains limited, largely due to the profoundly immunosuppressive tumor microenvironment (TME) which drives CAR-T cells to dysfunction and poor persistence. A comprehensive understanding of the dynamic interplay between CAR-T cells and the TME is therefore critical for the rational design of more effective CAR-T strategies for solid cancers. MethodsHere, we performed single-cell RNA sequencing of tumor samples from immunocompetent mice treated with stroma-targeting EDA-CAR-T cells, profiling CAR-T cell states and TME programs at the peak of antitumor response and during subsequent tumor progression. ResultsOur analysis revealed a marked temporal remodeling of EDA-CAR-T cells within the TME, where early antitumor efficacy is associated with concurrent expansion of cytotoxic effector CD8 CAR-T cells and activation of memory CD4 CAR-T subsets. Moreover, EDA-CAR-T cells effectively engaged the myeloid compartment, resulting in strengthened communication networks involving T cell activation. However, by tumor progression, EDA-CAR-T cells suffered a widespread transcriptional reprogramming towards dysfunction, characterized by loss of effector programs alongside induction of exhaustion and immunoregulatory pathways within the TME, including PD-L1/PD-L2 and TGF{beta} signaling, which impairs sustained immune responses. Notably, early CAR-T cell activation led to increased susceptibility to TME-mediated immunosuppression, revealing EDA-CAR-T-specific soluble galectin-mediated cell-to-cell interaction networks. ConclusionsTogether, this works offers a high-resolution view of CAR-T cell dynamics within the solid TME, uncovering cellular and molecular mechanisms of rapid functional decline and identifying regulatory pathways within the TME that can be exploited to improve CAR-T cell therapy efficacy in solid tumors. KEY MESSAGES OF THE ARTICLEO_ST_ABSWhat is already known on this topicC_ST_ABSThe determinants of CAR-T cell therapeutic efficacy in solid tumors remain poorly defined, largely due to the complexity of the immunosuppressive tumor microenvironment. In this effort, it is necessary to perform comprehensive and detailed mechanistic studies that capture CAR-T cell dynamics within the solid tumor microenvironment to understand treatment failure. What this study addsWe performed single-cell profiling of stroma-targeting EDA-CAR-T cells, revealing their dynamic reprogramming toward dysfunction within the solid tumor microenvironment. We dissected CAR-T cell states and their cell-to-cell interactions with the tumor microenvironment across response and tumor progression and identified mechanisms linking CAR-T cell functionality and therapeutic failure. How this study might affect research, practice or policyThis study provides comprehensive mechanistic insights from an immunocompetent model that can be leveraged to identify shared determinants of CAR-T cell functionality in solid tumors and potentially guide the rational development of improved CAR-T cell therapies.

genomics↗

Study of changes in brain dynamics during sleep cycles in dogs under effect of trazodone

Sleep is a fundamental biological process essential for cognitive function, memory consolidation, and overall health in both humans and animals. Dogs, in particular, share many physiological and neurological similarities with humans, making them a valuable model for sleep research. Similar to humans, dogs can experience sleep disorders that disrupt sleep cycles and impair cognitive function. While serotonin antagonist and reuptake inhibitors (SARIs), like trazodone, have been shown to alleviate these conditions in dogs, their underlying neural mechanisms remain poorly understood. This study investigates the effects of trazodone on brain dynamics in healthy dogs using electroencephalographic (EEG) analysis. We compared treated subjects with a control group by characterizing EEG activity across wakefulness, drowsiness, Non-REM (NREM), and REM sleep states. Hypnogram analysis was used to assess sleep architecture, including alterations in cycle patterns and time spent in each stage. Additionally, we examined linear and non-linear EEG dynamics using Power Spectral Density (PSD), Permutation Entropy (PE), and Lempel-Ziv complexity (LZC), as well as connectivity changes through Phase Lag Index (PLI) and coherence analysis. Our findings indicate that trazodone significantly alters sleep structure by modifying sleep cycles, reducing power in lower frequency bands across most sleep stages, and increasing power in frequencies above 13 Hz during Drowsiness and NREM. Furthermore, treated dogs exhibited increased signal entropy and complexity in lower frequency bands across all sleep stages, along with a reduction in brain connectivity in most stages and frequency bands. These results provide new insights into the short-term effects of trazodone on brain activity during sleep, with potential implications for its clinical use as a sleep aid in dogs.

animal behavior and cognition↗

Regulation of REM Sleep Onset and Homeostasis by Preoptic Glutamatergic Neurons

The preoptic area of the hypothalamus is key for the control of sleep onset and sleep homeostasis. Although traditionally considered exclusively somnogenic, recent studies identified a group of preoptic glutamatergic neurons that promote wakefulness. Specifically, our previous investigations demonstrated that chemogenetic stimulation of glutamatergic neurons within the medial-lateral preoptic area (MLPO_VGLUT2) promotes wakefulness, fragments non-rapid eye movement sleep (NREMs), and suppresses REM sleep (REMs). This evidence is further supported by recent work showing that preoptic glutamatergic neurons are activated during microarousals that fragment sleep in response to stress, and optogenetic stimulation of these neurons promotes microarousals and wakefulness. Thus, while the wake-promoting function of MLPO_VGLUT2 is clear, their role in sleep homeostasis has not been assessed. We tested the hypothesis that MLPO_VGLUT2 are wake-active, and their activation will increase wakefulness and disrupt sleep homeostasis via projections to arousal-promoting systems. Using fiber photometry, we found that MLPO_VGLUT2 were highly active during REMs, wakefulness and brief arousals, and remained minimally active during NREMs. Chemogenetic stimulation of MLPO_VGLUT2 inhibited REMs onset and suppressed the REMs homeostatic response after total sleep deprivation. Chemogenetic inhibition of MLPO_VGLUT2 increased REMs time (during the light phase only) but did not influence REMs and NREMs homeostasis. Anterograde projection mapping revealed that MLPO_VGLUT2 innervate central regions that promote wakefulness and inhibit REMs. We conclude that MLPO_VGLUT2 powerfully suppress REMs and that exogenous --and possibly pathologic-- activation of these neurons disrupts REMs recovery, presumably by directly or indirectly activating REMs-inhibitory mechanisms. SIGNIFICANCE STATEMENTThe preoptic area of the hypothalamus has been extensively studied and its role in sleep regulation is well-established. Importantly, recent work identified a group of preoptic glutamatergic neurons (MLPO_VGLUT2) that are wake-active and promote wakefulness. However, whether these neurons influence sleep homeostasis remains unknown. We demonstrate that MLPO_VGLUT2 are maximally active during REM sleep (REMs), wakefulness and brief arousals from sleep, and innervate wake-promoting and REMs-inhibitory regions. MLPO_VGLUT2 stimulation inhibits REMs and REMs rebound after sleep deprivation, whereas their inactivation increases REMs but does not alter REMs homeostatic response. We thus identified a preoptic mechanism that powerfully suppresses REMs, which we propose may engage during normal sleep-to-wake transitions to block REMs intrusions into subsequent wakefulness.

neuroscience↗

A Randomized, Controlled Clinical Trial Demonstrates Improved Cognitive Function in Senior Dogs Supplemented with a Senolytic and NAD+ Precursor Combination.

Age-related decline in mobility and cognition are associated with cellular senescence and NAD+ depletion in dogs and people. A combination of a novel NAD+ precursor and senolytic, LY-D6/2 was examined in this randomized controlled trial. Seventy dogs were enrolled and allocated into placebo, low or full dose groups. Primary outcomes were change in cognitive impairment measured with the owner-reported Canine Cognitive Dysfunction Rating (CCDR) scale and change in activity measured with physical activity monitors. Fifty-nine dogs completed evaluations at the three-month primary endpoint, and 51 reached the six-month secondary endpoint. There was a significant difference in CCDR score across treatment groups from baseline to the primary endpoint (p=0.02) with the largest decrease in the full dose group. There were no significant differences between groups in changes in measured activity. However, the proportion of dogs that improved in frailty and owner-reported activity levels and happiness was higher in the full dose group than other groups. Adverse events occurred equally across groups. All groups showed improvement in cognition, frailty, and activity suggesting placebo effect and benefits of trial participation. We conclude that LY-D6/2 significantly improves owner-assessed cognitive function and may have broader effects on frailty, activity and happiness as reported by owners.

animal behavior and cognition↗

Characterizing the power spectrum dynamics of the NREM to REM sleep transition

The transition from NREM to REM sleep is considered a transitional or intermediate stage (IS), characterized by high amplitude spindles in the frontal cortex and theta activity in the occipital cortex. Early reports in rats showed an IS lasting from 1 to 5 s, but recent studies suggested a longer duration of this stage. To further characterize the IS, we analyzed its spectral characteristics on electrocorticogram (ECoG) recordings of the olfactory bulb (OB), motor (M1), somato-sensory (S1) and secondary visual cortex (V2) in twelve Wistar male adult rats. By comparing the IS to consolidated NREM/REM epochs, our results reveal that the IS has specific power spectral patterns that statistically differ from both NREM and REM sleep states. Specifically, the main findings were that sigma (11-16 Hz) and beta (17-30 Hz) power in OB, M1, and S1 increased during the IS compared to NREM and REM sleep and began 55 s before REM sleep onset. Additionally, low gamma (31-48 Hz) in the OB started transitioning from NREM levels to REM ones 65 s before its onset. Finally, the high-frequency oscillations (102-198 Hz) in OB, M1, and S1 showed a power increase that began 40 s before REM sleep and reached REM sleep values 10 s after its onset. Thus, we argue that the NREM to REM transition contains its own spectral profile and is more extended than previously described.

neuroscience↗

The transcriptional regulator Sin3A balances IL-17A and Foxp3 expression in primary CD4 T cells

The Sin3 transcriptional regulator homolog A (Sin3A) is the core member of a multi-protein chromatin-modifying complex known to control gene transcription via epigenetic mechanisms. Its inactivation in developing thymocytes halts T cell maturation. We and others had previously shown that Sin3A controls STAT3 transcriptional activity. Given the role of STAT3 in the differentiation of T helper 17 cells critical in inflammatory disorders and against opportunistic infections, we asked whether Sin3A could also contribute to their differentiation. To this aim, we exploited CD4-Cre and CD4-CreERT2deleter strains for conditional and inducible Sin3A deletion in CD4 cell subsets. We report that Sin3A inactivation in vivo arrested thymocyte development at the double positive stage, hindering the characterization of mature T cells. At difference, tamoxifen-inducible Sin3A deletion proved permissive for in vitro proliferation of T cells in Th17 skewing conditions and the acquisition of memory markers. Transcriptional profiling indicated that while Sin3A inactivation imprinted T cells with a mTORC1 signaling gene signature, Sin3A deficient cells lacked the expression of IL-17A, the signature Th17 cytokine. This reflected a defective induction of Il17a, and also of the Il23R and Il22 genes, which occurred in spite of proper upregulation of the lineage defining transcription factor ROR{gamma}t. We found that Sin3A inactivation was paralleled by increased STAT3 phosphorylation and nuclear representation, and by higher fractions of IL-2 and FoxP3 expressing cells. Such events proved causally linked as inhibiting Foxp3 partially rescued IL-17A expression, and neutralizing IL-2 simultaneously lowered the representation of FoxP3+cells, while rescuing IL- 17A+ ones. Thus, together our data underline a previously unappreciated role for Sin3A in Th17 differentiation and the shaping of their immunoregulatory potential. StatementThis study identifies a new role for the transcriptional regulator Sin3A in the shaping of Th17 cell differentiation. Data indicate that by controlling IL-2 expression, and mTORC1 signaling, it balances IL-17A and Foxp3 levels, shaping Th17 inflammatory potentials.

immunology↗

Electroencephalographic Signatures of Canine Cognitive Dysfunction

Canine cognitive dysfunction (CCD) is a highly prevalent neurodegenerative disease considered the canine analog of Alzheimers disease (AD). Unfortunately, CCD cannot be cured. However, early therapeutic interventions can slow the progression of cognitive decline and improve quality of life of the patients; therefore, early diagnosis is ideal. In humans, electroencephalogram (EEG) findings specific to AD have been described, and some of them have successfully detect early stages of the disease. In this study we characterized the EEG correlates of CCD, and we compared them with the EEGs of healthy aging dogs and dogs at risk of developing CCD. EEG recordings were performed in 25 senior dogs during wakefulness. Dogs were categorized in normal, at risk of CCD or with CCD according to their score in the Rofina questionnaire. We demonstrated that, quantitative EEG can detect differences between normal dogs and dogs with CCD. Dogs with CCD experience a reduction in beta and gamma interhemispheric coherence, and higher Joint Lempel Ziv complexity. Dogs at risk of developing CCD, had higher alpha power and interhemispheric coherence, making these features potential markers of early stages of the disease. These results demonstrate that EEG could be an additional biomarker that can contribute to the diagnosis of CCD, and reinforce the CCD as a translational model of AD.

animal behavior and cognition↗

Low Frequency Oscillations drive EEG's complexity changes during wakefulness and sleep

Recently, the sleep-wake states have been analysed using novel complexity measures, complementing the classical analysis of EEGs by frequency bands. This new approach consistently shows a decrease in EEGs complexity during slow-wave sleep, yet it is unclear how cortical oscillations shape these complexity variations. In this work, we analyse how the frequency content of brain signals affects the complexity estimates in freely moving rats. We find that the low-frequency spectrum - including the Delta, Theta, and Sigma frequency bands - drives the complexity changes during the sleep-wake states. This happens because low-frequency oscillations emerge from neuronal population patterns, as we show by recovering the complexity variations during the sleep-wake cycle from micro, meso, and macroscopic recordings. Moreover, we find that the lower frequencies reveal synchronisation patterns across the neocortex, such as a sensory-motor decoupling that happens during REM sleep. Overall, our works shows that EEGs low frequencies are critical in shaping the sleep-wake states complexity across cortical scales.

neuroscience↗

Urethane Anesthesia Exhibits Neurophysiological Correlates of Unconsciousness and is Distinct from Sleep

Urethane is a general anesthetic widely used in animal research. It is unique among anesthetics because urethane anesthesia alternates between macroscopically distinct electrographic states: a slow-wave state that resembles NREM sleep (NREMure), and an activated state with features of both REM sleep and wakefulness (REMure). However, the relationship between urethane anesthesia and physiological sleep is still unclear. In this study, electroencephalography (EEG) and electromyography were recorded in chronically prepared rats during natural sleep-wake states and during urethane anesthesia. We subsequently analyzed the EEG signatures associated with the loss of consciousness and found that, in comparison to natural sleep-wake states, the power, coherence, directed connectivity and complexity of brain oscillations are distinct during urethane. We also demonstrate that both urethane states have clear EEG signatures of general anesthesia. Thus, despite superficial similarities that have led others to conclude that urethane is a model of sleep, the electrocortical traits of depressed and activated states during urethane anesthesia differ from physiological sleep states.

neuroscience↗

Glutamatergic neurons in the preoptic hypothalamus promote wakefulness, destabilize NREM sleep, suppress REM sleep, and regulate cortical dynamics

Clinical and experimental data from the last nine decades indicate that the preoptic area of the hypothalamus is a critical node in a brain network that controls sleep onset and homeostasis. By contrast, we recently reported that a group of glutamatergic neurons in the lateral and medial preoptic area increases wakefulness, challenging the long-standing notion in sleep neurobiology that the preoptic area is exclusively somnogenic. However, the precise role of these subcortical neurons in the control of behavioral state transitions and cortical dynamics remains unknown. Therefore, in this study we used conditional expression of excitatory hM3Dq receptors in these preoptic glutamatergic (Vglut2+) neurons and show that their activation initiates wakefulness, decreases non-rapid eye movement (NREM) sleep, and causes a persistent suppression of rapid eye movement (REM) sleep. Activation of preoptic glutamatergic neurons also causes a high degree of NREM sleep fragmentation, promotes state instability with frequent arousals from sleep, and shifts cortical dynamics (including oscillations, connectivity, and complexity) to a more wake-like state. We conclude that a subset of preoptic glutamatergic neurons may initiate -but not maintain- arousals from sleep, and their inactivation may be required for NREM stability and REM sleep generation. Further, these data provide novel empirical evidence supporting the conclusion that the preoptic area causally contributes to the regulation of both sleep and wakefulness.

neuroscience↗

Power and coherence in the EEG of the rat: impact of behavioral states, cortical area, lateralization and light/dark phases

The sleep-wake cycle is constituted by three behavioral states: wakefulness (W), non-REM (NREM) and REM sleep. These states are associated with drastic changes in cognitive capacities, mostly determined by the function of the thalamo-cortical system. Thalamo-cortical activity can be examined by means of the intra-cranial electroencephalogram (iEEG). With the purpose to study in depth the basal activity of the iEEG in adult rats, we analyzed the spectral power and coherence of the iEEG during W and sleep in the paleocortex (olfactory bulb), as well as in motor, somatosensory and visual neocortical areas. We also analyzed the laterality (right Vs. left hemispheres) of the signals, as well as the iEEG in function of the light and dark phases. We found that the iEEG power and coherence of the whole spectrum were largely affected by behavioral states and were highly dependent on the cortical areas recorded. We also determined that there are night/day differences in power and coherence during sleep, but not in W. Finally, while we did not find right/left differences in power either in W or sleep, we observed that during REM sleep intra-hemispheric coherence differs between both hemispheres. We conclude that the iEEG dynamics is highly dependent on the cortical area and behavioral states. We also determine that there are light/dark phases disparities in the iEEG that emerge during sleep, and that intra-hemispheric connectivity differs between both hemispheres only during REM sleep.

neuroscience↗

Gamma band alterations and REM-like traits underpin the acute effect of the atypical psychedelic ibogaine

Ibogaine is a psychedelic alkaloid that has attracted scientific interest because of its important antiaddictive properties evidenced in observational studies in humans, and in models for substance-use-disorders in rodents. Its subjective effect has been described as intense vivid dream-like experiences occurring while awake; hence, ibogaine is often referred to as an oneirogenic psychedelic. While this unique dream-like profile has been hypothesized to aid the antiaddictive effects in the past, the electrophysiological signatures of the ibogaine psychedelic state remain unknown. In our previous work, we showed in rats that ibogaine administration promotes a waking state with abnormal motor behavior, accompanied by a decrease in NREM and REM sleep. Here, we performed an in-depth analysis of the intracranial electroencephalogram during "ibogaine wakefulness". Ibogaine induced gamma oscillations with larger power than control levels but less coherent and less complex; i.e., this state shows clear REM sleep traits within the gamma frequency band. Thus, our results provide novel biological evidence for the association between the psychedelic state and REM sleep, and an empirical basis for the oneirogenic conjecture of ibogaine.

neuroscience↗

Communication through coherence by means of cross-frequency coupling

The theory of communication through coherence (CTC) posits the synchronization of brain oscillations as a key mechanism for information sharing and perceptual binding. In a parallel literature, hippocampal theta activity (4 - 10 Hz) has been shown to modulate the appearance of neocortical fast gamma oscillations (100 - 150 Hz), a phenomenon known as cross-frequency coupling (CFC). Even though CFC has also been previously associated with information routing, it remains to be determined whether it directly relates to CTC. In particular, for the theta-fast gamma example at hand, a critical question is to know if the phase of the theta cycle influences gamma synchronization across the neocortex. To answer this question, we designed a new screening method for detecting the modulation of the cross-regional high-frequency synchronization by the phase of slower oscillations. Upon applying the method, we found that the long-distance synchronization of neocortical fast gamma during REM sleep depends on the instantaneous phase of the theta rhythm. These results show that CFC is likely to aid long-range information transfer by facilitating the cross-regional synchronization of faster rhythms, thus consistent with classical CTC views.

neuroscience↗

Electrocortical temporal complexity during wakefulness and sleep: an updated account

The states of sleep and wakefulness are critical physiological processes associated with different brain patterns of activity. The intracranial electroencephalogram allows us to measure these changes, thus, it is a critical tool for its study. Recently, we showed that the electrocortical temporal complexity decreased from wakefulness to sleep. Nevertheless, the origin of this complex activity remains a controversial topic due to the existence of possible artifacts contaminating the brain signals. In this work, we showed that complexity decreases during sleep, independently of the electrode configuration employed. This fact strongly suggests that the basis for the behavioral-state differences in complexity does not have an extracranial origin; i.e., generated from the brain.

neuroscience↗

Decreased electrocortical temporal complexity distinguishes sleep from wakefulness

In most mammals, the sleep-wake cycle is constituted by three behavioral states: wakefulness (W), non-NREM (NREM) sleep, and REM sleep. These states are associated with drastic changes in cognitive capacities, mostly determined by the function of the thalamo-cortical system. The intra-cranial electroencephalogram or electocorticogram (ECoG), is an important tool for measuring the changes in the thalamo-cortical activity during W and sleep. In the present study we analyzed broad-band ECoG recordings of the rat by means of a time-series complexity measure that is easy to implement and robust to noise: the Permutation Entropy (PeEn). We found that PeEn is maximal during W and decreases during sleep. These results bring to light the different thalamo-cortical dynamics emerging during sleep-wake states, which are associated with the well-known spectral changes that occur when passing from W to sleep. Moreover, the PeEn analysis allows to determine behavioral states independently of the electrodes cortical location, which points to an underlying global pattern in the signal that differs among the cycle states that is missed by classical methods. Consequently, our data suggest that PeEn analysis of a single EEG channel could allow for cheap, easy, and efficient sleep monitoring.

neuroscience↗