Natural Antibody Affects Survival of the Spirochete<i>Borrelia burgdorferi</i>within Feeding Ticks

Belperron, Alexia A.

doi:10.1128/iai.69.10.6456-6462.2001

Cited by 40 publications

(54 citation statements)

References 39 publications

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“…We found that B1a cells increase during infection with B. burgdorferi and may be the source of natural IgM that targets this organism while it is within the vector (71). In contrast, B1a cells are expendable in the host response to B. hermsii and were not significantly responsive to B. crocidurae in this study (20).…”

Section: Discussioncontrasting

confidence: 44%

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

Malkiel

Kuhlow

Mena

et al. 2009

The Journal of Immunology

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T cell-independent Abs are protective against Lyme disease and relapsing fever, illnesses caused by Borrelia spirochetes with distinct blood-borne phases of infection. To understand this protective response, we characterized splenic and peritoneal B cell compartments during infection using flow cytometry and immunohistochemistry. In the spleen, early after infection, Borrelia crocidurae, a relapsing fever species, induced a striking loss of marginal zone (MZ) B cells from the MZ, while Borrelia burgdorferi, the agent of Lyme disease, induced the expansion of this subset. At the same time, no significant changes were observed in follicular B cells in response to either species of Borrelia. In the peritoneal cavity, a further loss was demonstrated early in response to B. crocidurae in the B1b, B1c, and B2 cell subsets, but B1a cells were not significantly altered. The loss of B1c and B2 cells was sustained through subsequent peaks of spirochetemia, suggesting these subsets may be important in resolving relapsing episodes. In contrast, an early and significant increase in peritoneal B1a, B1b, and B1c cells, but not B2 cells, occurred in response to B. burgdorferi. Later in the course of infection, both species of Borrelia induced the selective expansion of peritoneal B1b cells, suggesting that B1b cells may participate in long-lasting immunity to Lyme and relapsing fever spirochetes. Our data demonstrate that different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a complex interplay of MZ and multiple peritoneal B cell subsets in the early response to infection.

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Section: Discussioncontrasting

confidence: 44%

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

Malkiel

Kuhlow

Mena

et al. 2009

The Journal of Immunology

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“…The signals for this profound change in surface protein expression are not known, but a recent study has shown that natural antibody in nonimmune mice is a significant factor (9). Ninety percent of spirochetes in the salivary glands of ticks feeding upon B-cell-deficient mice were shown to express OspA, in contrast to only 5% of spirochetes from ticks feeding upon naïve, immunocompetent mice.…”

Section: Discussionmentioning

confidence: 99%

“…Other workers (9) have shown that natural antibodies in naïve mice interact with spirochetes in feeding ticks and influence OspA expression within the tick. Therefore, the effect of normal mouse serum on ospA mRNA transcription in infected C3H-scid mice was investigated.…”

Section: Downloaded Frommentioning

confidence: 99%

“…OspA has been the subject of intensive investigation since its initial discovery (3,10,22,26,37,52). Among the factors that have been shown to modulate OspA expression are temperature (34,48), pH (51,52), cocultivation with tick cells (34), exposure to tick hemolymph (20), the presence of anti-OspA antibody within feeding ticks (17), the presence of natural antibody (9), and serum starvation (1).…”

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confidence: 99%

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Immunoglobulin-Regulated Expression ofBorrelia burgdorferiOuter Surface Protein A In Vivo

et al. 2005

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Borrelia burgdorferi, the agent of Lyme disease, down-regulates outer surface protein A (OspA), which is abundantly expressed in ticks, during infection of the mammalian host. In this study we examined the signals that may be responsible for maintaining the OspA-negative state of spirochetes during infection. Transcription of ospA mRNA was found in tissues of C3H-severe combined immunodeficient (C3H-scid) mice, but not immunocompetent C3H mice, inoculated with cultured B. burgdorferi, tick-borne spirochetes, and host-adapted spirochetes. Transcription was more frequent at 4 weeks than at 1 week. Transcription was present at the host-tick interface as early as 24 h after tick attachment but declined at 48 and 72 h. Thus, ospA mRNA transcription in distant tissues and at later times in C3H-scid mice is probably due to up-regulation during infection. Adoptive lymphocyte transfer from naïve C3H mice to infected C3H-scid mice resulted in OspA seroconversion, confirming OspA expression in the host. Passive transfer of normal mouse serum, immunoglobulin M (IgM) from normal mouse serum, or IgG from normal mouse serum into infected C3H-scid mice resulted in down-regulation of ospA, but transfer of normal mouse serum depleted of immunoglobulin did not influence ospA mRNA transcription. Collectively, our results indicate that ospA mRNA transcription in the host is regulated by nonspecific immunoglobulin, which may be a natural antibody.

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“…The ability of infected mouse serum to kill live B. burgdorferi in the presence of complement was determined by borreliacidal assay, as previously described (9). Briefly, B. burgdorferi was incubated with the serum samples in the presence of exogenous complement.…”

mentioning

confidence: 99%

β2 Integrins Control the Severity of Murine Lyme Carditis

2005

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Infection of C57BL/6 (B6) mice with the Lyme disease spirochete Borrelia burgdorferi can result in development of arthritis and carditis. B. burgdorferi induces expression of ␤2/CD18 integrins, adhesion molecules that mediate the firm adhesion of leukocytes to the endothelium necessary for cellular extravasation during inflammation. The important role of ␤2/CD18 integrins during extravasation suggests that these molecules play a role in the development of Lyme arthritis and carditis. The dependency of these inflammatory processes on the ␤2 integrins was investigated in CD18 hypomorph mice, which express low levels of CD18. The results indicate that CD18 deficiency did not abrogate development of Lyme arthritis or carditis. Moreover, it resulted in increased severity of Lyme carditis. B. burgdorferi-infected CD18 hypomorph mice showed an increased macrophage infiltration of the heart, while they produced lower levels of borreliacidal anti-B. burgdorferi antibodies compared to wild-type mice. In accordance with these results, we demonstrate that dendritic cells from CD18 hypomorph mice secrete higher levels of monocyte/macrophage chemoattractant protein 1 (MCP-1/CCL2) in response to B. burgdorferi. Similarly, we show by real-time PCR that B. burgdorferi-infected hearts from CD18 hypomorph mice express increased levels of MCP-1 RNA compared to wild-type mice. Overall, our results indicate that ␤2 integrin deficiency does not abrogate B. burgdorferi-induced inflammation; rather, it results in increased recruitment of macrophages into the B. burgdorferi-infected heart, likely due to the increased expression of MCP-1 in this tissue. Thus, ␤2 integrins may play a regulatory role in B. burgdorferiinduced inflammation beyond mediating adhesion of leukocytes to the endothelium.

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Natural Antibody Affects Survival of the SpirocheteBorrelia burgdorferiwithin Feeding Ticks

Cited by 40 publications

References 39 publications

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

The Loss and Gain of Marginal Zone and Peritoneal B Cells Is Different in Response to Relapsing Fever and Lyme Disease Borrelia

Immunoglobulin-Regulated Expression ofBorrelia burgdorferiOuter Surface Protein A In Vivo

β2 Integrins Control the Severity of Murine Lyme Carditis

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