VCOM Louisiana Research Day Program Book 2024

Biomedical Research: Section 1

Krishna Patel, BS; Sarah Voth, PhD; Adam Morrow, PhD; Rebekah Morrow, PhD ULM; VCOM 12 EXPRESSION OF AMYLOID PRECURSOR PROTEIN IN PULMONARY ENDOTHELIAL INFECTION

Background: Pseudomonas aeruginosa has long been known as a primary cause of nosocomial pneumonia. Our study aims to further understand the cellular pathophysiology of pulmonary infection, in efforts to help prevent elevated mortality rates from secondary organ damage/failure in patients suffering from nosocomial pneumonia, also known as hospital-acquired pneumonia. We are currently looking at how lung endothelium responds to Pseudomonas infection in terms of cell damage and response mechanisms involved. Toll-like receptors (TLR) are pattern recognition receptors that act as part of the innate immune response in endothelial cells. Objective: We hypothesize that TLR-2 heterodimer signaling contributes to the amyloid beta innate immune response in lung endothelium. Methods: We treated rat pulmonary microvascular endothelial cells with either a strain of Pseudomonas (∆PcrV) or TLR agonists to initiate immune responses and collected whole cell lysates. We conducted a western blot to measure protein expression of amyloid precursor protein (APP) and performed densitometry to quantify changes in protein expression.

Results: Treatment with TLR agonists increases expression of TAK1 and APP, but does not increase expression of NF-kB. Conclusions: TAK1 is downstream from TLR1/2 receptors and TLR2/6 receptors. ExoY is suggested to shut down TAK1. This may be why ExoY inhibits TLR signaling.

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