small intestine cdna library  (TaKaRa)

Journal: Frontiers in Neuroscience

Article Title: Sulfate reducing bacteria induce α-synuclein in intestinal and neuronal cells and tissues and inhibit tyrosine hydroxylase in neuronal cells

doi: 10.3389/fnins.2025.1672793

Figure Lengend Snippet: DSV induces increase in number of cells with α-synuclein aggregates and synuclein expression in intestinal enteroendocrine STC-1 cells (A) . Cells were infected for 24 h. with various DSV MOIs. Cells were then fixed and processed for immunofluorescence using an antibody that specifically recognizes aggregated α-synuclein. (B) Percentage of cells positive for α-syn aggregates were counted and values were compared to control (uninfected) cells. Data represent mean ± SEM. (C) Cells were infected with DSV and harvested for western blotting to probe for α-syn expression. Actin was used as loading control. (D) Western blot images were quantified using Fiji Image J. Data represent mean ± SEM as a fold change difference compared to control. Control values were set as 1. The blot shown is a representative image of multiple independent experiments that were conducted atleast three times. The blot was cut to allow probing for two proteins on the same gel, actin for the upper bands while the lower bands were used for probing synuclein.** p < 0.01, * p < 0.05.

Article Snippet: Mouse small intestinal enteroendocrine cells (STC-1) and Human neuronal (SH-Sy5y) cells were purchased from ATCC (Manassas, VA).

Techniques: Expressing, Infection, Immunofluorescence, Control, Western Blot

Journal: Frontiers in Neuroscience

Article Title: Sulfate reducing bacteria induce α-synuclein in intestinal and neuronal cells and tissues and inhibit tyrosine hydroxylase in neuronal cells

doi: 10.3389/fnins.2025.1672793

Figure Lengend Snippet: Schematic representation of how DSV may be contributing to the pathogenesis of PD. In the setting of dysbiosis, DSV overgrowth may occur in the intestine. Higher number of DSV could then induce increase in α-synuclein aggregates in the intestinal cells such as enteroendocrine cells (EEC) that are known to produce α-syn. In addition, DSV causes secretion of α-syn aggregates from EEC. DSV is also known to disrupt intestinal tight junction barrier leading to leaky gut which, in turn, leads to the translocation of bacteria in the bloodstream. Extracellular α-synuclein aggregates along with DSV could be carried by vagus nerve and/or blood circulation to the brain. In the brain, the transported α-synuclein may further spread to neurons and seed endogenous α-syn aggregation in these cells. Gut-derived α-syn could also activate microglia to produce and secrete TNF-a which in turn could induce α-syn aggregation in the neurons. Furthermore, DSV translocated through leaky gut could directly access neurons to cause α-syn aggregation in these cells. DSV may also activate microglia to secrete TNF-a which in turn could induce α-syn aggregation in neuronal cells. In the neurons, DSV further directly inhibits tyrosine hydroxylase (TH) either by an unknown mechanism and/or mediates its inhibitory effects on TH via its induction of α-syn. Figure was generated using Biorender.com .

Article Snippet: Mouse small intestinal enteroendocrine cells (STC-1) and Human neuronal (SH-Sy5y) cells were purchased from ATCC (Manassas, VA).

Techniques: Translocation Assay, Bacteria, Derivative Assay, Generated