Case reportJarisch-Herxheimer reaction complicating the treatment of chronic Q fever endocarditis: elevated TNFα and IL-6 serum levels
References (7)
- et al.
Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection
Cell
(1993) Clinical pathology of the Jarisch-Herxheimer
J Infect Dis
(1976)- et al.
Lipoproteins of Borrelia burgdorferi and Treponema pallidum activate cachectin/tumor necrosis factor synthesis
Cited by (21)
Mechanisms of Ototoxicity and Otoprotection
2021, Otolaryngologic Clinics of North AmericaCitation Excerpt :Pilot studies of neonates treated with aminoglycosides likely confirm these preclinical findings.58,59 Aminoglycoside-induced lysis of bacteria elevates the inflammatory response (ie, the Jarisch-Herxheimer reaction).60,61 The mechanisms underlying the potentiation of hearing loss by inflammation remain to be established.62,63
Coxiella
2014, Molecular Medical MicrobiologyThe Jarisch-Herxheimer reaction: Revisited
2013, Travel Medicine and Infectious DiseasePro-inflammatory cytokines IL6, TNF-α, IL1β, procalcitonin, lipopolysaccharide binding protein and C-reactive protein in infective endocarditis
2007, Journal of InfectionCitation Excerpt :IL 6 is likely to be elevated in IE because bacteria display surface molecules which stimulate the release of IL 6 from monocytes and endothelial cells. IL 6 is a pleiotropic cytokine, however one important function of IL 6 is to promote the transition from neutrophil to monocyte recruitment by inducing chemokines which favour monocytes.23 Although monocytes may be protective in IE, once bound to the endothelium, monocytes also promote fibrin clotting by promoting the activation of tissue factor.
Mechanisms and Impact of Aminoglycoside-Induced Vestibular Deficits
2023, American Journal of AudiologyMechanisms of aminoglycoside-and cisplatin-induced ototoxicity
2021, American Journal of Audiology