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The Impact of Neuroimmune Alterations in Autism Spectrum Disorder.

Gottfried C, Bambini-Junior V, Francis F, Riesgo R, Savino W - Front Psychiatry (2015)

Bottom Line: In the past decade, studies of ASD have substantially increased, in both humans and animal models.Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD.Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

View Article: PubMed Central - PubMed

Affiliation: Translational Research Group in Autism Spectrum Disorder (GETTEA), Federal University of Rio Grande do Sul , Porto Alegre , Brazil ; Research Group in Neuroglial Plasticity, Department of Biochemistry, Federal University of Rio Grande do Sul , Porto Alegre , Brazil.

ABSTRACT
Autism spectrum disorder (ASD) involves a complex interplay of both genetic and environmental risk factors, with immune alterations and synaptic connection deficiency in early life. In the past decade, studies of ASD have substantially increased, in both humans and animal models. Immunological imbalance (including autoimmunity) has been proposed as a major etiological component in ASD, taking into account increased levels of pro-inflammatory cytokines observed in postmortem brain from patients, as well as autoantibody production. Also, epidemiological studies have established a correlation of ASD with family history of autoimmune diseases; associations with major histocompatibility complex haplotypes and abnormal levels of immunological markers in the blood. Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD. Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

No MeSH data available.


Related in: MedlinePlus

Evidence for neuroimmune interactions in autism spectrum disorder (ASD). Blood and postmortem brain alterations in individuals with ASD. (1) Antibody production in blood against brain antigens. (2) Brain cell infiltration of Th1 lymphocytes, monocytes and mast cells. (3) Increase in blood brain barrier (BBB) permeability. (4) Increase in IgG and IgM levels. (5) Less antioxidant defenses. (6) Changes in cytokine levels. (7) Decrease in cell adhesion molecules, such as Selectins and PCAM-1. 8. Increase in oxidative stress. All these alterations can promote neuroinflammation, followed by neuron–glial response and brain connectivity dysfunction that ultimately can influence behavioral features in ASD. GSH, glutathione; GPx, glutathione peroxidase; NO, nitric oxide; Th, T-helper; OS, oxidative stress; CCL2, C–C motif chemokine 2.
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Figure 1: Evidence for neuroimmune interactions in autism spectrum disorder (ASD). Blood and postmortem brain alterations in individuals with ASD. (1) Antibody production in blood against brain antigens. (2) Brain cell infiltration of Th1 lymphocytes, monocytes and mast cells. (3) Increase in blood brain barrier (BBB) permeability. (4) Increase in IgG and IgM levels. (5) Less antioxidant defenses. (6) Changes in cytokine levels. (7) Decrease in cell adhesion molecules, such as Selectins and PCAM-1. 8. Increase in oxidative stress. All these alterations can promote neuroinflammation, followed by neuron–glial response and brain connectivity dysfunction that ultimately can influence behavioral features in ASD. GSH, glutathione; GPx, glutathione peroxidase; NO, nitric oxide; Th, T-helper; OS, oxidative stress; CCL2, C–C motif chemokine 2.

Mentions: Figure 1 illustrates alterations found in both blood and postmortem brains of patients with ASD, including blood/brain cell activation, autoantibody production, and alterations in levels of different molecules that can modify cell signaling, brain response, and BBB permeability. The associated neuroinflammatory process does support the hypothesis of neuroimmune interactions in the pathogenesis of ASD.


The Impact of Neuroimmune Alterations in Autism Spectrum Disorder.

Gottfried C, Bambini-Junior V, Francis F, Riesgo R, Savino W - Front Psychiatry (2015)

Evidence for neuroimmune interactions in autism spectrum disorder (ASD). Blood and postmortem brain alterations in individuals with ASD. (1) Antibody production in blood against brain antigens. (2) Brain cell infiltration of Th1 lymphocytes, monocytes and mast cells. (3) Increase in blood brain barrier (BBB) permeability. (4) Increase in IgG and IgM levels. (5) Less antioxidant defenses. (6) Changes in cytokine levels. (7) Decrease in cell adhesion molecules, such as Selectins and PCAM-1. 8. Increase in oxidative stress. All these alterations can promote neuroinflammation, followed by neuron–glial response and brain connectivity dysfunction that ultimately can influence behavioral features in ASD. GSH, glutathione; GPx, glutathione peroxidase; NO, nitric oxide; Th, T-helper; OS, oxidative stress; CCL2, C–C motif chemokine 2.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4563148&req=5

Figure 1: Evidence for neuroimmune interactions in autism spectrum disorder (ASD). Blood and postmortem brain alterations in individuals with ASD. (1) Antibody production in blood against brain antigens. (2) Brain cell infiltration of Th1 lymphocytes, monocytes and mast cells. (3) Increase in blood brain barrier (BBB) permeability. (4) Increase in IgG and IgM levels. (5) Less antioxidant defenses. (6) Changes in cytokine levels. (7) Decrease in cell adhesion molecules, such as Selectins and PCAM-1. 8. Increase in oxidative stress. All these alterations can promote neuroinflammation, followed by neuron–glial response and brain connectivity dysfunction that ultimately can influence behavioral features in ASD. GSH, glutathione; GPx, glutathione peroxidase; NO, nitric oxide; Th, T-helper; OS, oxidative stress; CCL2, C–C motif chemokine 2.
Mentions: Figure 1 illustrates alterations found in both blood and postmortem brains of patients with ASD, including blood/brain cell activation, autoantibody production, and alterations in levels of different molecules that can modify cell signaling, brain response, and BBB permeability. The associated neuroinflammatory process does support the hypothesis of neuroimmune interactions in the pathogenesis of ASD.

Bottom Line: In the past decade, studies of ASD have substantially increased, in both humans and animal models.Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD.Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

View Article: PubMed Central - PubMed

Affiliation: Translational Research Group in Autism Spectrum Disorder (GETTEA), Federal University of Rio Grande do Sul , Porto Alegre , Brazil ; Research Group in Neuroglial Plasticity, Department of Biochemistry, Federal University of Rio Grande do Sul , Porto Alegre , Brazil.

ABSTRACT
Autism spectrum disorder (ASD) involves a complex interplay of both genetic and environmental risk factors, with immune alterations and synaptic connection deficiency in early life. In the past decade, studies of ASD have substantially increased, in both humans and animal models. Immunological imbalance (including autoimmunity) has been proposed as a major etiological component in ASD, taking into account increased levels of pro-inflammatory cytokines observed in postmortem brain from patients, as well as autoantibody production. Also, epidemiological studies have established a correlation of ASD with family history of autoimmune diseases; associations with major histocompatibility complex haplotypes and abnormal levels of immunological markers in the blood. Moreover, the use of animal models to study ASD is providing increasing information on the relationship between the immune system and the pathophysiology of ASD. Herein, we will discuss the accumulating literature for ASD, giving special attention to the relevant aspects of factors that may be related to the neuroimmune interface in the development of ASD, including changes in neuroplasticity.

No MeSH data available.


Related in: MedlinePlus