This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common vector borne disease in the United States. Since 2002, more than 20,000 cases have been reported annually. Numerous organ systems may be affected during the early - disseminated phase (weeks to months after initial tick bite), resulting in neurological complications, joint pain and heart abnormalities. Among patients with confirmed tick-borne infection, coinfection rates as high as 39% have been reported. The most commonly recognized coinfection in most of the United States is Lyme borreliosis and babesiosis, caused by the red blood cell parasite, Babesia microti, accounting for ~80% of coinfections. Moreover, studies of clinical outcomes indicate that patients with acute Babesia coinfection have more severe symptoms and longer duration of illness than patients with Lyme borreliosis alone. Coinfections can modify the immune response and alter the severity of arthritis in animal models. However, little is known about the mechanisms underlying immune regulation and increased arthritis in Lyme borreliosis and babesial coinfections. We have recently shown in a series of experiments that coinfection of B. microti and B. burgdorferi resulted in more severe Lyme arthritis and is correlated with significant reduction of expression of certain key anti-inflammatory cytokines such as Interleukin 10 (IL-10) and IL-13 in a mouse model of Lyme disease. Our efforts have been directed to understand how B. microti regulates the immune response resulting in a more favorable environment for increased arthritis causes by the Lyme disease agent.
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