Early and Late Cutaneous Manifestations in <i>Ixodes</i>‐borne Borreliosis (Erythema Migrans Borreliosis, Lyme Borreliosis)<sup>a</sup>

Asbrink, E; Hovmark, A

doi:10.1111/j.1749-6632.1988.tb31833.x

Cited by 211 publications

(142 citation statements)

References 28 publications

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“…Borrelia burgdorferi, the causative agent of Lyme disease, causes a vast array of clinical symptoms in the human host including but not limited to erythema migrans skin lesions, meningitis, myocarditis, and arthritis (5,12,50). In order to establish infection, the spirochete migrates from the initial site of inoculation, spreads into the surrounding skin, and subsequently enters the bloodstream, where it can colonize more distal organs.…”

mentioning

confidence: 99%

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

Heilpern

Wertheim

et al. 2009

Infect Immun

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Borrelia burgdorferi, the causative agent of Lyme arthritis, does not produce any exported proteases capable of degrading extracellular matrix despite the fact that it is able to disseminate from a skin insertion site to infect multiple organs. Prior studies have shown that B. burgdorferi induces the host protease, matrix metalloproteinase 9 (MMP-9), and suggested that the induction of MMP-9 may allow the organism to disseminate and produce local tissue destruction. We examined the role of MMP-9 in dissemination of B. burgdorferi and pathogenesis of Lyme arthritis. In a MMP-9؊/؊ mouse model, MMP-9 was not required for the dissemination of the spirochete to distant sites. However, MMP-9 ؊/؊ exhibited significantly decreased arthritis compared to wild-type mice. The decrease in arthritis was not due to an inability to control infection since the spirochete numbers in the joints were identical. Levels of inflammatory chemokines and cytokines were also similar in MMP-9 ؊/؊ and wild-type mice. We examined whether decreased inflammation in MMP-9 ؊/؊ mice may be the result of decreased production of neoattractants by MMP-9-dependent cleavage of collagen. MMP-9 cleavage of type I collagen results in increased monocyte chemoattraction. MMP-9 plays an important role in regulating inflammation in Lyme arthritis, potentially through the cleavage of type I collagen.

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confidence: 99%

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

Heilpern

Wertheim

et al. 2009

Infect Immun

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“…Infection with Borrelia burgdorferi, the causative agent of Lyme disease, results in a broad array of clinical manifestations, including, but not limited to, erythema migrans skin lesions, myocarditis, meningitis, neuritis, and arthritis (4,25,36). Pathology in these organs is thought to be due to local stimulation of the host immune system resulting in the infiltration of inflammatory cells.…”

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confidence: 99%

MyD88 Deficiency Results in Tissue-Specific Changes in Cytokine Induction and Inflammation in Interleukin-18-Independent Mice Infected withBorrelia burgdorferi

et al. 2006

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Toll-like receptors (TLRs) play an important role in the control of infection with Borrelia burgdorferi.Deficiencies in TLR-2 or the shared TLR adapter molecule MyD88 have been shown to result in greatly increased bacterial burdens in mice. However, although in vitro studies have shown that the activation of TLR pathways by B. burgdorferi results in the release of inflammatory cytokines, studies in deficient mice have shown either no change or increased rather than decreased inflammation in infected animals. In this study, we looked at mechanisms to explain the increase in inflammation in the absence of MyD88. We found that MyD88-deficient mice infected with B. burgdorferi did not show increased inflammation at sites typically associated with Lyme disease (joints and heart). However, there was markedly increased inflammation in the muscles, kidneys, pancreas, and lungs of deficient animals. Muscle inflammation was typically seen perivascularly and perineuronally similar to that seen in infected humans. Chemotactic chemokines and cytokines were greatly increased in the muscle and kidneys of MyD88-deficient animals but not in the joints or heart tissue, suggesting that MyD88-independent pathways for recognizing B. burgdorferi and inducing these chemokines are present in the muscle and kidneys. Interleukin-18 signaling through MyD88 does not appear to play a role in either control of infection or inflammation.

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“…Lyme disease is the most common arthropod-borne disorder in the United States, with a variable spectrum of clinical manifestations ranging from localized infection to systemic disease (1,11,54,55). Borrelia burgdorferi, the spirochetal agent of Lyme disease, is normally maintained in an enzootic cycle between wild mammals and Ixodes ticks (30).…”

mentioning

confidence: 99%

Altered Stationary-Phase Response in a Borrelia burgdorferi rpoS Mutant

Elias¹,

Bono²,

Carroll

et al. 2000

J Bacteriol

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The homolog of the chromosomally encoded stationary-phase sigma factor RpoS in Borrelia burgdorferi was inactivated using gyrB r as a selectable marker. Two-dimensional nonequilibrium pH gradient electrophoresis of stationary-phase cell lysates identified at least 11 differences between the protein profiles of the rpoS mutant and wild-type organisms. Wild-type B. burgdorferi had a growth phase-dependent resistance to 1 N NaCl, similar to the stationary-phase response reported for other bacteria. The B. burgdorferi rpoS mutant strain was less resistant to osmotic stress in stationary phase than the isogenic rpoS wild-type organism. The results indicate that the B. burgdorferi rpoS homolog influences protein composition and participates in stationaryphase-dependent osmotic resistance. This rpoS mutant will be useful for studying regulation of gene expression in response to changing environmental conditions.

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Early and Late Cutaneous Manifestations in Ixodes‐borne Borreliosis (Erythema Migrans Borreliosis, Lyme Borreliosis)^a

Cited by 211 publications

References 28 publications

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

MyD88 Deficiency Results in Tissue-Specific Changes in Cytokine Induction and Inflammation in Interleukin-18-Independent Mice Infected withBorrelia burgdorferi

Altered Stationary-Phase Response in a Borrelia burgdorferi rpoS Mutant

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Early and Late Cutaneous Manifestations in Ixodes‐borne Borreliosis (Erythema Migrans Borreliosis, Lyme Borreliosis)a

Cited by 211 publications

References 28 publications

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

Matrix Metalloproteinase 9 Plays a Key Role in Lyme Arthritis but Not in Dissemination ofBorrelia burgdorferi

MyD88 Deficiency Results in Tissue-Specific Changes in Cytokine Induction and Inflammation in Interleukin-18-Independent Mice Infected withBorrelia burgdorferi

Altered Stationary-Phase Response in a Borrelia burgdorferi rpoS Mutant

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Early and Late Cutaneous Manifestations in Ixodes‐borne Borreliosis (Erythema Migrans Borreliosis, Lyme Borreliosis)^a