Citations 3

Isolation of Mycoplasma hominis from a brain abscess

Journal of Clinical Microbiology | January 6, 2020 | Volume: 35 | Issue: 4 | Pages: 992-994

10.1128/jcm.35.4.992-994.1997 | PMID 9157171

Mycoplasma hominis is a commensal in the genital tract of women and has been associated with urogenital and extragenital infections. However, central nervous system infections with this organism in adults are very rare. Here we describe the recovery of M. hominis from a brain abscess associated with a postpartum infection. Seroconversion to the isolated strain was detected by both a metabolic inhibition test and an immunoblotting assay. This case demonstrates the pathogenic potential of M. hominis and the need for rapid recognition of the organism so that appropriate chemotherapeutic intervention can occur.
Nystatin Induces Secretion of Interleukin (IL)-1β, IL-8, and Tumor Necrosis Factor Alpha by a Toll-Like Receptor-Dependent Mechanism

Antimicrobial Agents and Chemotherapy | July 27, 2005 | Volume: 49 | Issue: 8 | Pages: 3546-3549

10.1128/aac.49.8.3546-3549.2005 | PMID 16048981

ABSTRACT Nystatin is an antifungal compound with potent proinflammatory properties. Herein, we demonstrate that nystatin induces interleukin (IL)-1β, IL-8, and tumor necrosis factor alpha secretion through its activation of toll-like receptor 1 (TLR1) and TLR2. Hence, a TLR-dependent mechanism could serve as the molecular basis for the proinflammatory properties of nystatin.
Secretion of Proinflammatory Cytokines and Chemokines during Amphotericin B Exposure Is Mediated by Coactivation of Toll-Like Receptors 1 and 2

Antimicrobial Agents and Chemotherapy | March 25, 2005 | Volume: 49 | Issue: 4 | Pages: 1617-1621

10.1128/aac.49.4.1617-1621.2005 | PMID 15793154

ABSTRACT Amphotericin B (AmB) is a ligand of toll-like receptor 2 (TLR2). Here, we demonstrate the participation of TLR1 in AmB-induced cell activation that led to the secretion of tumor necrosis factor alpha, interleukin 6 (IL-6), and IL-8. Hence, TLR2-TLR1 coactivation serves as the underlying mechanism for the proinflammatory toxicities associated with AmB.