Research Group
Pozzi Group
Developmental Neuroimmunology
Our goal is to understand how critical early biological processes in neuronal development, such as neuronal excitability and GABAergic signaling are shaped by environmental stressors and soluble immune-derived molecules, and to define how these interactions contribute to both normal brain maturation and the emergence of neurodevelopmental pathologies.
The challenge
The early stages of neurodevelopment involve critical and highly vulnerable biological processes that are essential for the proper maturation of the central nervous system and the establishment of adult behavior. Among these processes, the emergence of synchronized network activity in the early postnatal period is especially crucial, relying on the coordinated development of GABAergic and glutamatergic synaptic signaling. Soluble immune-derived factors, such as cytokines and chemokines, produced endogenously or upon pathological conditions, can subtly but persistently influence developmental trajectories, potentially reshaping brain function across the lifespan. Dissecting how these immune signals integrate with and modulate the maturation of early neuronal activity represents a key frontier in neurobiology, with the potential to transform our understanding of neurodevelopmental disorders.
Main Research Areas
Perinatal Environmental Stressors and Their Impact on Early Neuronal Excitability
Epidemiological evidence indicates that prenatal and perinatal environmental stressors—such as physical stress or inflammatory conditions—increase the risk of various neurodevelopmental disorders, supporting the notion that many diseases may have a fetal origin. Our research investigates how inflammation-related molecules, triggered by different types of perinatal stressors, interfere with critical aspects of neuronal functioning emerging during early postnatal stages, including intrinsic excitability and synaptic activity. By combining functional and morphological approaches, we aim to elucidate the molecular and cellular mechanisms through which early-life immune activation disrupts neuronal function, alters brain development, and increases susceptibility to long-term neuropsychiatric outcomes.
Mechanisms of GABAergic System Development and the Role of Immune Factors
The fetal-maternal interface is a critical site of communication through which maternal immune signals can influence embryonic development. Our research explores the physiological and pathological role of maternal immune factors in regulating perinatal biological processes essential for proper neurodevelopment. A particular focus is placed on the maturation of the GABAergic system, whose developmental switch from excitatory to inhibitory signaling is a key milestone in the establishment of functional neural circuits and balanced brain activity.
Selected publications
Embryo-restricted responses to maternal IL-17A promote neurodevelopmental disorders in mouse offspring.
Loss of interleukin 1 signaling causes impairment of microglia- mediated synapse elimination and autistic-like behaviour in mice.
Immune synaptopathies: how maternal immune activation impacts synaptic function during development.
Maternal immune activation leads to defective brain-blood vessels and intracerebral hemorrhages in male offspring.
Brain mapping across 16 autism mouse models reveals a spectrum of functional connectivity subtypes.
Prenatal interleukin 6 elevation increases glutamatergic synapse density and disrupts hippocampal connectivity in offspring.
The enhancement of activity rescues the establishment of Mecp2 null neuronal phenotypes.
Environmental regulation of the chloride transporter KCC2: switching inflammation off to switch the GABA on?
Maternal Immune Activation Delays Excitatory-to-Inhibitory Gamma-Aminobutyric Acid Switch in Offspring.
The Communication Between the Immune and Nervous Systems: The Role of IL-1β in Synaptopathies.
Group members
