Posts by:
Gabriella True

Anti-lysoganglioside and other anti-neuronal autoantibodies in post-treatment Lyme Disease and Erythema Migrans after repeat infection

Anti-lysoganglioside and other anti-neuronal autoantibodies in post-treatment Lyme Disease and Erythema Migrans after repeat infection

Brian A.Fallon, BarbaraStrobino, SeanReim, JulieStoner, Madeleine W.Cunningham Brain, Behavior, & Immunity – Health, Volume 2, February 2020, 100015. https://doi.org/10.1016/j.bbih.2019.100015

This study examines molecular mimicry targeting neural tissue after Borrelia burgdorferi (Bb) infection. Patients with Lyme disease have a greater frequency of specific anti-neuronal autoantibodies and functional neuronal activation compared to community controls without a history of Lyme disease.

“Highlights

  • The EM ​+ ​prior LD group had significantly elevated anti-neuronal antibodies.
  • The EM ​+ ​prior LD group had significantly elevated CaM Kinase activation.
  • Anti-Lysoganglioside Antibodies are significantly elevated in the PTLS group.
  • Prior infection may lead to immune priming and increased autoantibodies.”
Brain-Immune Alterations and Mitochondrial Dysfunctions in a Mouse Model of Paediatric Autoimmune Disorder Associated with Streptococcus: Exacerbation by Chronic Psychosocial Stress

Ajmone-Cat MA, Spinello C, Valenti D, Franchi F, Macrì S, Vacca RA, Laviola G. Journal of Clinical Medicine. 2019; 8(10):1514. DOI: 10.3390/jcm8101514

  • Adverse psychosocial experiences have been shown to modulate individual responses to immune challenges and affect mitochondrial functions.
  • Results show chronic psychosocial stress altered the expression of neuroinflammatory markers in the hippocampal and hypothalamic regions, exacerbated the neuroinflammatory alterations induced by experimental GAS exposures in the same areas.
  • Psychosocial stress exacerbated individual response to GAS administrations whereby mice exposed to both treatments exhibited altered cytokine and immune-related enzyme expression in the hippocampus and hypothalamus.
  • Showed impaired mitochondrial respiratory chain complexes IV and V, and reduced adenosine triphosphate (ATP) production by mitochondria and ATP content.
  • These brain abnormalities, observed in GAS-Stress mice, were associated with blunted titers of plasma corticosterone.
  • Present data support the hypothesis that challenging environmental conditions, in terms of chronic psychosocial stress, may exacerbate the long-term consequences of exposure to GAS processes through the promotion of central immunomodulatory and oxidative stress.
The immune system and psychiatric disease: a basic science perspective
Bennett FC, Molofsky AV. The immune system and psychiatric disease: a basic science perspective. Clin Exp Immunol. 2019 Sep;197(3):294-307. doi: 10.1111/cei.13334. Epub 2019 Jun 9. PMID: 31125426; PMCID: PMC6693968.
“Mental illness exerts a major burden on human health, yet evidence-based treatments are rudimentary due to a limited understanding of the underlying pathologies. Clinical studies point to roles for the immune system in psychiatric diseases, while basic science has revealed that the brain has an active and multi-cellular resident immune system that interacts with peripheral immunity and impacts behavior. In this perspective, we highlight evidence of immune involvement in human psychiatric disease and review data from animal models that link immune signaling to neuronal function and behavior. We propose a conceptual framework for linking advances in basic neuroimmunology to their potential relevance for psychiatric diseases, based on the subtypes of immune responses defined in peripheral tissues. Our goal is to identify novel areas of focus for future basic and translational studies that may reveal the potential of the immune system for diagnosing and treating mental illnesses.”