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Article Publish Status: FREE
Abstract Title:

Andrographolide Attenuates Gut-Brain-Axis Associated Pathology in Gulf War Illness by Modulating Bacteriome-Virome Associated Inflammation and Microglia-Neuron Proinflammatory Crosstalk.

Abstract Source:

Brain Sci. 2021 Jul 9 ;11(7). Epub 2021 Jul 9. PMID: 34356139

Abstract Author(s):

Punnag Saha, Peter T Skidmore, LaRinda A Holland, Ayan Mondal, Dipro Bose, Ratanesh K Seth, Kimberly Sullivan, Patricia A Janulewicz, Ronnie Horner, Nancy Klimas, Mitzi Nagarkatti, Prakash Nagarkatti, Efrem S Lim, Saurabh Chatterjee

Article Affiliation:

Punnag Saha

Abstract:

Gulf War Illness (GWI) is a chronic multi-symptomatic illness that is associated with fatigue, pain, cognitive deficits, and gastrointestinal disturbances and presents a significant challenge to treat in clinics. Our previous studies show a role of an altered Gut-Brain axis pathology in disease development and symptom persistence in GWI. The present study utilizes a mouse model of GWI to study the role of a labdane diterpenoid andrographolide (AG) to attenuate the Gut-Brain axis-linked pathology. Results showed that AG treatment in mice (100 mg/kg) via oral gavage restored bacteriome alterations, significantly increased probiotic bacteria,, and, the genera that are known to aid in preserving gut and immune health. AG also corrected an altered virome with significant decreases in virome familiesandknown to be associated with gastrointestinal pathology. AG treatment significantly restored tight junction proteins that correlated well with decreased intestinal proinflammatory mediators IL-1β and IL-6 release. AG treatment could restore Claudin-5 levels, crucial for maintaining the BBB integrity. Notably, AG could decrease microglial activation and increase neurotrophic factor BDNF, the key to neurogenesis. Mechanistically, microglial conditioned medium generated from IL-6 stimulationwith or without AG in a concentration similar to circulating levels found in the GWI mouse model and co-incubated with neuronal cells in vitro, decreased Tau phosphorylation and neuronal apoptosis. In conclusion, we show that AG treatment mitigated the Gut-Brain-Axis associated pathology in GWI andmay be considered as a potential therapeutic avenue for the much-needed bench to bedside strategies in GWI.

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