Culture-Confirmed Infection and Reinfection with Borrelia burgdorferi

Nowakowski, John; Schwartz, Ira; Nadelman, Robert B.; Liveris, Dionysios; Agüero-Rosenfeld, Maria E.; Wormser, Gary P.

doi:10.7326/0003-4819-127-2-199707150-00006

Cited by 26 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We propose that the induction of apparently aberrant innate signals in lymph nodes represents an evasion strategy of B. burgdorferi designed to disrupt the development of protective immune responses. This may explain the rapid loss of germinal centers in lymph nodes of B. burgdorferi-infected mice (7) and/or the lack of adequate long-term immune protection observed following infection (9,33).…”

Section: Discussionmentioning

confidence: 99%

“…In the case of Lyme disease, we previously reported that they lack strong and sustained germinal centers. Others demonstrated the lack of strong functional immunity following infection with B. burgdorferi, which permits reinfections even with the same strain of B. burgdorferi (9,33). By revealing the two-step process that leads to the disruption of the lymph node architecture and the subsequent IFN-driven accumulation of B cells, we identify distinct mechanisms that B. burgdorferi employs to interact with and potentially to manipulate the host response to its advantage.…”

Section: Discussionmentioning

confidence: 99%

“…Mice also do not generate appreciable numbers of long-lived bone marrow plasma cells during the first 2 months of infection (3). Understanding the signals that disrupt the structure of the lymph nodes after B. burgdorferi infection may help to identify barriers to the development of infection-induced protective B cell responses and to the induction of functional immune memory, which appears lacking even after repeat infections (9,10).…”

mentioning

confidence: 99%

See 2 more Smart Citations

MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

et al. 2014

View full text Add to dashboard Cite

Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88-and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

et al. 2014

View full text Add to dashboard Cite

show abstract

“…At least three different species (Borrelia afzelii, B. garinii and B. burgdorferi sensu stricto) have been recognised as definitive aetiological agents in Europe and B. bissettii has also been isolated from several European patients [3], while in the USA B. burgdorferi sensu stricto has been described as the only human pathogen [1,4].…”

Section: Introductionmentioning

confidence: 99%

Susceptibility of Borrelia afzelii strains to antimicrobial agents

Ružić‐Sabljić¹,

Podreka²,

Maraspin

et al. 2005

International Journal of Antimicrobial Agents

View full text Add to dashboard Cite

“…In contrast, persons acquiring Lyme disease in Europe may be infected with one of several different species [2]. A surprising number of patients sustain a second (and sometimes even another subsequent) episode of early Lyme disease after the first episode has resolved [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18]. Although reinfection is well-recognized, there is little detailed information on the clinical and laboratory manifestations.…”

mentioning

confidence: 97%

Reinfection in Patients with Lyme Disease

Nadelman

Wormser

2007

Clinical Infectious Diseases

View full text Add to dashboard Cite

Lyme disease is the most common tick-borne infection in the United States and Europe. A surprising number of patients experience a subsequent episode of Lyme disease after the first episode has resolved. Reinfection has been well-documented only after successfully treated early infection (nearly always erythema migrans) and can often be recognized clinically by the development of a repeat episode of erythema migrans occurring at a different location on the skin during months when the principal tick vectors are abundant in the environment. Limited data suggest that the clinical and laboratory manifestations of reinfection in patients with Lyme disease with erythema migrans are not very different from those of initial infection. Patients with recurrent infections afford an opportunity to study the role of the immune response in this illness. Because patients with early Lyme disease continue to remain at high risk for reinfection, this population should be targeted for education about prevention of Lyme disease.

show abstract

Culture-Confirmed Infection and Reinfection with Borrelia burgdorferi

Cited by 26 publications

References 0 publications

MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

Susceptibility of Borrelia afzelii strains to antimicrobial agents

Reinfection in Patients with Lyme Disease

Contact Info

Product

Resources

About