A mouse study found that Lyme disease itself may be suppressing antibody responses to the pathogen. The bug is able to short circuit the germinal centers in the lymph nodes that produce long term responses to infections. Months later the mice were still unable to mount an effective immune response to Lyme bacteria. In the fact the immune depression caused by the bacteria appears to affect other immune functioning. Mice infected with Lyme disease failed to mount a strong immune response to influenza vaccination given shortly after the infection.
This means the waning antibody response seen after antibiotic treatment may not be a sign that the infection has been vanquished but could simply be a sign that the body simply is unable to produce antibodies to the bacteria.
Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.
This means the waning antibody response seen after antibiotic treatment may not be a sign that the infection has been vanquished but could simply be a sign that the body simply is unable to produce antibodies to the bacteria.
For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections.
The researchers found that following Borrelia burgdorferi infection, this process even prevented induction of strong immune responses to an influenza infection.
Read more at http://scienceblog.com/79136/lyme-d...events-future-protection/#RxSGS7qlZZPSpiEr.99
Similar to many other infections, infection with B. burgdorferi results in strong antibody response induction....clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies.
We show here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates.
These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain of B.burgdorferi.
Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response.
Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.