Open AccessEffect of Systemic Lipopolysaccharide‐Induced Inflammation on Cytokine Levels in the Murine Cochlea: A Pilot Study
Author(s) -
QuintanillaDieck Lourdes,
Larrain Barbara,
Trune Dennis,
Steyger Peter S.
Publication year - 2013
Publication title -
otolaryngology–head and neck surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.232
H-Index - 121
eISSN - 1097-6817
pISSN - 0194-5998
DOI - 10.1177/0194599813491712
Subject(s) - cytokine , lipopolysaccharide , medicine , inflammation , systemic inflammation , tumor necrosis factor alpha , immunology , proinflammatory cytokine , interleukin , aminoglycoside , systemic administration , pharmacology , biology , in vivo , antibiotics , microbiology and biotechnology
The objective was to detect changes in cytokine expression within cochleae in a murine model of systemic inflammation, with or without aminoglycoside exposure. Four groups of mice received 1 of the following: saline only, systemic bacterial lipopolysaccharides (LPS) for 6 hours to induce endotoxemia and inflammatory responses, systemic gentamicin for 3 hours, or both treatments. After exsanguination, pooled cochleae (4/group) were processed for enzyme‐linked immunosorbent assay (ELISA) for 16 cytokines. Gentamicin alone did not change cochlear cytokine levels, while LPS (±gentamicin) substantially elevated cochlear expression of several cytokines, particularly interleukin‐1α, interleukin‐6, monocyte chemotactic protein‐1, macrophage inflammatory protein‐1α, and RANTES. Since cytokines increase blood‐brain barrier permeability, we hypothesize that cytokine‐enhanced permeability of the blood‐labyrinth barrier (BLB) could potentiate aminoglycoside‐induced ototoxicity. This pilot study demonstrated the feasibility of detecting cytokine expression in murine cochleae using ELISA and facilitates future studies investigating BLB permeability in animal models of systemic inflammation.