Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

Villamón, Eva; Gozalbo, Daniel; Roig, Patricia; O’Connor, José Enrique; Fradelizi, D; Gil, M. Luisa

doi:10.1016/j.micinf.2003.09.020

Cited by 193 publications

(191 citation statements)

References 31 publications

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“…And this effect is associated with decreased production of TNF-a and chemokines. 179 Accordingly, in an intraperitoneal model of candidiasis, fungal clearance is delayed in mice lacking TLR2. 180 However, a few other studies showed controversial results.…”

Section: The Roles Of Prrs: Findings Using Prr-deficient Micementioning

confidence: 99%

“…However, MR-/-mice has higher average fungal burdens in some of the organs but exhibited more competence in inflammatory cell recruitment and antibody production. 179 Galectin-3-deficient mice (gal3-/-) were more susceptible to C. albicans infection than wild-type (WT) mice. More specifically, gal3-/-mice died significantly faster and exhibited a trend toward increased fungal burden and increased abscess formation in infected brains compared to WT mice.…”

Section: The Roles Of Prrs: Findings Using Prr-deficient Micementioning

confidence: 99%

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The role of pattern recognition receptors in the innate recognition ofCandida albicans

Zheng

Wang

et al. 2015

Virulence

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Section: The Roles Of Prrs: Findings Using Prr-deficient Micementioning

confidence: 99%

Section: The Roles Of Prrs: Findings Using Prr-deficient Micementioning

confidence: 99%

The role of pattern recognition receptors in the innate recognition ofCandida albicans

Zheng

Wang

et al. 2015

Virulence

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“…For example, TLR2 or MyD88 -/-mice were highly susceptible to Staphylococcus aureus infection [8], while the survival rate of TLR2 -/-mice infected with Listeria monocytogenes was about 40% lower compared to wild-type (WT) mice [9]. TLR2 was also important for host defenses against Candida albicans infections since TLR2 -/-mice displayed a higher rate of lethality [10]. In a chronic model of Mycobacterium bovis BCG infection, however, TLR2, TLR4 and TLR6 appeared not to be essential for successful control of the infection by the host [11], while TLR4 was required to control chronic Mycobacterium tuberculosis infection [12].…”

Section: Introductionmentioning

confidence: 99%

Differential involvement of TLR2 and TLR4 in host survival during pulmonary infection with Chlamydia pneumoniae

Rodríguez

Wantia

Fend³

et al. 2006

Eur J Immunol

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The relevance of TLR2 and TLR4 for recognizing Chlamydia pneumoniae in vivo during pulmonary infection and to survive the infection was explored. We found that early immune responses triggered by C. pneumoniae partially depended on TLR2, but not on TLR4. The chemokines MIP-2 and MIP-1a were not induced, while IL-12p40 levels were higher in TLR2 -/-mice compared to wild-type mice. Secretion of TNF, keratinocytederived chemokine and monocyte chemoattractant protein-1 was attenuated in TLR2 -/-mice, while IFN-c was increased as in wild-type mice. The pulmonary cyto-and chemokine response of TLR2 -/-ÂTLR4 d/d was similar to TLR2 -/-mice. TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice also attracted fewer polymorphonuclear neutrophils into the lung, while TLR4 d/d mice recruited them. Attenuated recruitment of polymorphonuclear neutrophils correlated with reduced weight loss in TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice and a lower chlamydial burden 3 days post infection. At 9 days post infection, TLR2 -/-and TLR2 -/-ÂTLR4 d/d mice produced cyto-and chemokines as efficiently as wild-type mice, indicating that the involvement of TLR in inflammation varies over time. All TLR2 -/-ÂTLR4 d/d mice succumbed to the infection, while about 50% of TLR2 -/-mice died. Taken together, the function of TLR2 and TLR4 is required to survive pulmonary infection with C. pneumoniae.

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“…9,10 Components of the neutrophil microbicidal system, including NADPH oxidase and myeloperoxidase protect against infection, 11,12 while members of the Toll-like receptor (TLR) family appear to have disparate effects on infection outcome. [13][14][15][16] A T helper (Th)1-type response has been shown to be protective against reinfection with C. albicans, while a Th2 response is more frequently observed in susceptible strains. 17 Additionally, C. albicans has been shown to activate the complement system through the alternative pathway, 18 with the chemotactic and inflammatory activities of complement apparently the crucial components for mounting an effective host defence.…”

Section: Introductionmentioning

confidence: 99%

Genetic control of suceptibility to Candida albicans in susceptible A/J and resistant C57BL/6J mice

et al. 2005

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The importance of host factors in determining susceptibility to systemic Candida albicans infections is evident in both humans and mice. We have used a mouse model to study the genetic basis of susceptibility, using the inbred strains A/J and C57BL/6J, which are susceptible and resistant, respectively, based on different parameters of the response to infection. To identify genes responsible for this differential host response, brain and kidney fungal load were measured in 128 [A/J Â C57BL/6J] F 2 mice 48 h after infection with 5 Â 10 4 C. albicans blastospores. Segregation analysis in this informative population identified complement component 5 (C5/Hc) as the major gene responsible for this differential susceptibility (LOD of 22.7 for kidney, 19.0 for brain), with a naturally occurring mutation that causes C5 deficiency leading to enhanced susceptibility. C5 was also found to control heart fungal load, survival time, and serum TNF-a levels during infection. Investigation of the response to C. albicans challenge in a series of AcB/BcA recombinant congenic strains validated the importance of C5 in determining the host response. However, the strains BcA67 and BcA72 showed discordant phenotypes with respect to their C5 status, suggesting additional complexity in the genetic control of the inter-strain difference in susceptibility observed in A/J and C57BL/6J following systemic infection with C. albicans. Genes and Immunity (2005) 6, 672-682.

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Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

Cited by 193 publications

References 31 publications

The role of pattern recognition receptors in the innate recognition ofCandida albicans

The role of pattern recognition receptors in the innate recognition ofCandida albicans

Differential involvement of TLR2 and TLR4 in host survival during pulmonary infection with Chlamydia pneumoniae

Genetic control of suceptibility to Candida albicans in susceptible A/J and resistant C57BL/6J mice

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