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Activation of the classical complement pathway occurs to varying degrees within strains of the  Borrelia burgdorferi sensu lato  complex, which contain a group of pathogenic spirochetes that cause tick-borne Lyme borreliosis, including the agent of Lyme disease in the United States,  B. burgdorferi . Despite this information, details related to the control of  B. burgdorferi  by the classical pathway are not clear. To address this question, we infected C1qα −/−  mice, which cannot assemble the C1 complex and thus fail to activate the classical pathway, with  B. burgdorferi sensu stricto  strain B31. Using bioluminescent  in vivo  imaging, we found that C1qα −/−  mice harbored more  B. burgdorferi  following 10 days of infection relative to their isogenic C57BL/6 parent. Quantitative PCR (qPCR) demonstrated that C1qα −/−  mice harbored significantly more  B. burgdorferi  than parent mice did within lymph nodes, skin, heart, and joints. The increased  B. burgdorferi  load in C1qα −/−  mice was observed at 21 and 28 days of infection, consistent with the classical pathway promoting complement-dependent, antibody-mediated killing following the development of a  B. burgdorferi -specific humoral immune response. In addition, circulating borrelial-specific IgM was higher in C1qα −/−  mice relative to their parent mouse strain and did not decrease at 21 and 28 days post-infection, indicating that IgG class switching was delayed in C1qα −/−  mice. At day 28, both  Borrelia -specific IgG1 and IgG3 levels were higher in infected C1qα −/−  mice, but that these antibodies were not sufficient to control borrelial infection in the absence of the classical pathway. Furthermore, the lack of C1q also altered the balance of the Th1/Th2 response, as both circulating Th1 (MIP-1α, IL-2, IL-12, and TNFα), Th2 (IL-4, IL-10, and MCP-1), and Th17 (IL-17) cytokines were elevated in infected C1qα −/−  mice. These data imply that C1q and the classical pathway play important roles in controlling borrelial infection  via  antibody and complement-dependent killing, as well as altering both antibody maturation processes and the T cell response following exposure to infectious  B. burgdorferi .

The Classical Complement Pathway Is Required to Control Borrelia burgdorferi Levels During Experimental Infection