Humans as well as other vertebrates are often exposed to lipopolysaccharide (LPS), for instance via enterobacteria. LPS responses are mediated via Toll-like receptor 4 (TLR4), a member of the TLR protein family that play a fundamental role in pathogen recognition and activation of the innate immune system. TLR4 signaling activates various transcription factors like nuclear factor kappa-light-chain-enhancer (NF-κB), activator protein 1 (AP1), signal transducers and activators of transcription family of transcription factors (STAT1) and interferon regulatory factors (IRF's). This leads to the induction of several inflammatory pathways thereby promoting inflammation. Given the key role of the TLR4 signaling pathway in the induction of inflammation, it has been proposed that inhibition of this pathway has potential as a treatment for inflammatory disorders. This LPS molecule is derived from the cell membrane of the gram-negative bacterium Bartonella quintana. In contrast to LPS derived from Escherichia coli, B. quintana LPS is a potent antagonist of TLR4, as it inhibited both mRNA transcription and the release of tumor necrosis factor alpha, interleukin 1 (IL1), and IL-6. Because TLR4 proinflammatory signals are involved in a variety of pathological inflammatory reactions, the use of the TLR4 antagonistic properties of B. quintana LPS may be of potential therapeutic value.