Data for: Radiation of the Urinary Bladder Attenuates the Development of Lipopolysaccharide-Induced Cystitis

Published: 14 March 2020| Version 1 | DOI: 10.17632/mjrfwfh7z5.1
Contributors:
Lucie Podmolikova,
Annika Janina Dahlqvist,
Marie Francoise Mukanyangezi,
Asa Torinsson Naluai,
Lars Ny,
Daniel Giglio

Description

In the present study we assessed how ionization radiation affects TLR4-stimulated immune activation in lipopolysaccharide (LPS)-induced cystitis. LPS or saline was administered intravesically to female rats followed by urinary bladder irradiation (20 Gy) 24 hours later or sham treatment. Presence in the urinary bladder of inflammatory cells (mast cells, CD3+, ionized calcium-binding adapter molecule 1 (Iba-1)+, CD68+, CD40+, CD80+, CD11c+ and CD206+ cells) and expression of oxidative stress (8-OHdG), hypoxia (HIF1α) and anti-oxidative responses (NRF2, HO-1, SOD1, SOD2, catalase) were assessed 14 days later with western blot, qPCR and/or immunohistochemistry. LPS stimulation resulted in a decrease of Iba-1+ cells in the urothelium, an increase in mast cells in the submucosa and a decrease in the bladder protein expression of HO-1, while no changes in the bladder expression of 8-OHdG, NRF2, SOD1, SOD2, catalase and HIF1α were observed. Bladder irradiation inhibited the LPS-driven increase in mast cells and the decrease in Iba1+ cells. Combining LPS and radiation increased the expression of 8-OHdG and number of CD3-positive cells in the urothelium and led to a decrease in NRF2α gene expression in the urinary bladder. In conclusion, irradiation may attenuate LPS-induced immune responses in the urinary bladder but potentiates LPS-induced oxidative stress, which as a consequence may have an impact on the urinary bladder immune sensing of pathogens and danger signals.

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Categories

Radiation, Inflammation, Lipopolysaccharides, Toll-Like Receptor, Innate Immune Response

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