Suppression of Host Humoral Immunity by Borrelia burgdorferi Varies Over the Course of Infection

Date

2024-03-21

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0000-0002-8760-8128 (Williams, Megan)
0000-0002-2934-382X (Berg, Rance)
0000-0001-5784-4659 (Zhang, Yan)
0000-0003-2293-8078 (Allen, Michael S.)

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Abstract

Lyme disease is the most common vector-borne illness in the U.S. with approximately 476,000 cases each year. Borrelia burgdorferi, the spirochetal agent of Lyme disease, utilizes a variety of strategies to evade and suppress the host immune response, which enables it to chronically persist in the host. These strategies include complement inhibition, antigenic variation, and suppression of adaptive immunity. The resulting immune response is characterized by unusually strong IgM production and a lack of long-term protective immunity. Previous studies in mice have shown that infection with B. burgdorferi also broadly suppresses host antibody responses against unrelated antigens. Here we aimed to assess how the host’s ability to produce antibodies against an unrelated antigen may change over the course of infection with B. burgdorferi and whether, if at all, the immune system returns to baseline following antibiotic treatment. Mice infected with B. burgdorferi and concomitantly immunized with recombinant SARS-CoV-2 spike protein had an abrogated antibody response to the immunization. To further define how long this humoral immune suppression lasts, mice were immunized at 2-, 4-, and 6-weeks post-infection. Suppression of host antibody production against the SARS-CoV-2 spike protein peaked at 2 weeks post-infection but continued for all timepoints measured. Antibody responses against the SARS-CoV-2 spike protein were also assessed following antibiotic treatment to determine whether this immune suppression persists or resolves following clearance of B. burgdorferi. Host antibody production against the SARS-CoV-2 spike protein returned to baseline following antibiotic treatment; however, anti-SARS-CoV-2 IgM remained high, comparable to levels found in B. burgdorferi-infected but untreated mice. Thus, our data demonstrate restored IgG responses following antibiotic treatment but persistently elevated IgM levels, indicating lingering effects of B. burgdorferi infection on the immune system following treatment.

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