Using autologous umbilical cord blood and placental cells for hypoxic-ischemic encephalopathy: an exploratory safety and feasibility study.

Introduction. Hypoxic-ischemic encephalopathy (HIE) caused by lack of oxygen and perfusion to the brain can lead to acute neurological damage in newborns. Therapeutic hypothermia (TH) is the most effective and safest treatment.

HLA diversity in the Argentinian Umbilical Cord Blood Bank: frequencies according to donor's reported ancestry and geographical distribution.

Umbilical cord blood (UCB) is a suitable source for hematopoietic stem cell transplantation. The study of HLA genes by next generation sequencing is commonly used in transplants. Donor/patient HLA matching is often higher within groups of common ancestry, however "Hispanic" is a broad category that fails to represent Argentina's complex genetic admixture.

Differential vulnerability of adult neurogenesis by adult and prenatal inflammation: role of TGF-β1.

Peripheral inflammation, both during the prenatal period and in adulthood, impairs adult neurogenesis. We hypothesized that, similar to other programming effects of prenatal treatments, only prenatal inflammation causes long-term consequences in adult neurogenesis and its neurogenic niche. To test this, pregnant Wistar rats were subcutaneously injected with lipopolysaccharide (LPS; 0.

Neuroprotective effects of human umbilical cord mesenchymal stromal cells in an immunocompetent animal model of Parkinson's disease.

Microglial activation in the substantia nigra (SN) is a ubiquitous feature in PD which could mediate toxic effects. Human mesenchymal stromal cells (hMSCs) possess immunomodulatory properties. We evaluated whether the transplantation of hMSCs obtained from umbilical cord had a neuroprotective effect in a not-immunosuppressed rat Parkinson's disease (PD) model.

The degenerating substantia nigra as a susceptible region for gene transfer-mediated inflammation.

Parkinson's disease (PD) is characterized by the progressive degeneration of neurons in the substantia nigra pars compacta (SN). The naïve SN is highly susceptible to inflammation. In addition, microglial activation in the degenerating SN displays distinct characteristics that increase the reactivity of the region towards inflammatory stimuli.

Modulation of macrophage inflammatory profile in pregnant nonobese diabetic (NOD) mice.

During normal early pregnancy circulating monocytes are recruited to the maternal-placental interface where they differentiate to macrophages expressing different functional phenotypes for the maintenance of tissue homeostasis. Pregnancy in the nonobese diabetic (NOD) mouse model presents some pathological features in the pre-diabetic stage. The aim of this work was to analyze the functional profile of peritoneal macrophages faced with inflammatory and phagocytic stimuli in early pregnant pre-diabetic NOD mice and their modulation by vasoactive intestinal peptide (VIP).

The more you have, the less you get: the functional role of inflammation on neuronal differentiation of endogenous and transplanted neural stem cells in the adult brain.

The differentiation of neural stem cells toward a neuronal phenotype is determined by the extracellular and intracellular factors that form the neurogenic niche. In this review, we discuss the available data on the functional role of inflammation and in particular, pro- and anti-inflammatory cytokines, on neuronal differentiation from endogenous and transplanted neural stem/progenitor cells. In addition, we discuss the role of microglial cell activation on these processes and the fact that microglial cell activation is not univocally associated with a pro-inflammatory milieu.

Potential immunomodulatory role of VIP in the implantation sites of prediabetic nonobese diabetic mice.

Among several factors known to modulate embryo implantation and survival, uterine quiescence and neovascularization, maternal immunotolerance through the Th1/Th2 cytokine balance towards a Th2 profile, local regulatory T-cell (Treg) activation, and high levels of progesterone were assigned a prominent role. Vasoactive intestinal peptide (VIP) is a neuroimmunopeptide that has anti-inflammatory effects, promotes Th2 cytokines and CD4(+)CD25(+)FOXP3(+) Treg activation, and stimulates exocrine secretion, smooth muscle relaxation, and vasodilatation favoring uterus quiescence. The goal of the present work was to explore the participation of VIP in the implantation sites of normal and pregnant prediabetic nonobese diabetic (NOD) females, a mouse strain that spontaneously develops an autoimmune exocrinopathy similar to Sjögren's syndrome.

Vasoactive intestinal peptide inhibits TNF-alpha-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands.

Introduction: The role of apoptotic secretory epithelium as a pro-inflammatory triggering factor of exocrine dysfunction is currently explored in Sjogren's syndrome patients and in the nonobese diabetic (NOD) mouse model. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects in various models of chronic inflammation. Our goal was to analyse the effect of TNF-alpha on apoptotic mediators in isolated acinar cells from NOD submandibular gland and their modulation by VIP.

VIP modulates the pro-inflammatory maternal response, inducing tolerance to trophoblast cells.

Background And Purpose: Successful embryo implantation is followed by a local pro-inflammatory and Th1 response, subsequently controlled by a Th2 response. Vasoactive intestinal peptide (VIP) has anti-inflammatory effects and promotes tolerogenic/Th2 responses while favouring embryonic development. We investigated the potential regulatory role of VIP on human trophoblast cells, maternal pro-inflammatory responses and trophoblast-maternal leukocyte interactions.

Neuroimmune-endocrine interactions during early pregnancy in an autoimmune context: focus on macrophage activation.

Neuroimmune-endocrine interactions seem to be central to the dialogue between the mother and the growing embryo during normal pregnancy. A proinflammatory Th1 microenvironment appears to be associated with embryo implantation but an excess of these cytokines may be deleterious. When normal gestation is subjected to stressful stimuli as those provided by a chronic inflammatory milieu, the activation profile of T cells and macrophages may be temporarily changed.

NOD mice exocrinopathy: towards a neuroimmune link.

Sjogren's syndrome (SS) is a chronic autoimmune disorder of exocrine glands characterized as an autoimmune exocrinopathy and more specifically as an autoimmune epithelitis. An impaired balance of neuroimmune interactions mediated by vasoactive intestinal peptide (VIP) in the target organ at early stages of disease is explored by means of the nonobese diabetic (NOD) mouse model of SS. We have previously described a reduced salivary secretion and signaling upon VIP stimulation.

VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages.

The spontaneous non obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both autoimmune response and secretory dysfunction. Vasoactive intestinal peptide (VIP) is a neuro and immunopeptide with prosecretory effect in salivary glands and anti-inflammatory actions in various models of autoimmune disease. Our purpose was to analyze the response of peritoneal macrophages to an inflammatory stimulus during the decline of salivary secretion in NOD mice and the potential anti-inflammatory effect of VIP.

Reduced nitric oxide synthase and cyclo-oxygenase activity in the uterus of non-obese diabetic mice.

A functional interaction between progesterone, Th2 cytokines and a suitable balance between nitric oxide and prostaglandins in the uterus is considered to have a major role in the success of embryo implantation and pregnancy. Non-obese diabetic (NOD) mice offer a suitable model to study the modulatory role of Th1 cytokines on uterus signalling and function, since at the prediabetic stage they develop a spontaneous Th1 autoimmune response against exocrine glands similar to Sjögren's syndrome. Vasoactive intestinal peptide (VIP) is a vasoactive neuro- and immunopeptide that promotes Th2 profiles and contributes to the smooth muscle relaxation and vasodilation.

Inhibition of calcium-calmodulin kinase restores nitric oxide production and signaling in submandibular glands of a mouse model of salivary dysfunction.

Nitric oxide is an intracellular and diffusible messenger of neurotransmitters involved in salivary secretion, as well as an inflammatory mediator in salivary gland diseases. It is synthesized by three different isoforms of nitric oxide synthase (NOS), each subject to a fine transcriptional, post-transcriptional and/or post-translational regulation. Our purpose was to study the possible mechanisms leading to NOS downregulation in submandibular glands of normal mice and in the nonobese diabetic (NOD) mouse model of salivary dysfunction with lower NOS activity.

Lack of nitric oxide-mediated regulation of amylase secretion stimulated by VIP in parotid glands of NOD mice.

The non-obese diabetic (NOD) mouse is chosen among other experimental models to study autoimmune sialadenitis resembling Sjögren's syndrome (SS), because of its unique characteristic of developing salivary dysfunction. Based on the deep loss of nitric oxide synthase (NOS) activity in parotid glands of NOD mice observed from early stages of disease and the inhibitory effect of nitric oxide (NO) donors on amylase secretion in normal salivary glands, our goal was to investigate whether parotid glands from NOD mice lacking NOS activity presented this regulatory mechanism of amylase secretion. We found that parotid glands from NOD mice lack nitric oxide-mediated regulation of amylase secretion in response to VIP stimulation.