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1.
Figure 3

Figure 3. IL-1β responses to Candida albicans are mediated by NLRP3, ASC and Caspase-1. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) IL-1β responses of macrophages from Asc-/-, Nlrp3-/- and wild-type mice primed for 4 h with 500 ng/ml LPS then stimulated with C. albicans at ~ 106/ml; (b) Western blot of supernatants from wild-type or Asc-/- macrophages probed with anti-IL-1β antibody; (c) IL-1β responses of macrophages from Casp1-/- and wild-type mice stimulated overnight with C. albicans at ~ 106/ml; (d) IL-1β responses of macrophages from P2X7R-/- and wild-type mice stimulated overnight with C. albicans at ~ 106/ml. (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
2.
Figure 7

Figure 7. Serum IL-1β responses to in vivo infection with C. albicans is dependent on TLR2, Dectin-1 and the NLRP3 inflammasome. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) IL-1β responses in serum collected from wild-type, Nlrp3-/- or Asc-/- mice orally infected with C. albicans; (b) IL-1β responses in serum collected from orally infected wild-type, Tlr2-/- or double Tlr2/dect1-/- mice; (c) IL-1β responses in serum collected from orally infected wild-type or Dect1-/- mice (*** P < 0.001; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
3.
Figure 2

Figure 2. IL-1β responses to Candida albicans are dependent on TLR2 and dectin-1. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) Up-regulation of IL-1β mRNA by qPCR of macrophages from Tlr2-/-, Dect1-/- and wild-type mice stimulated for 8 h with C. albicans of different morphological stages at ~ 106/ml; (b) IL-1β protein levels in supernatants of macrophages from Tlr2-/-, Dect1-/- and wild-type mice stimulated overnight with C. albicans of different morphological stages at ~ 106/ml; (c) IL-1β responses of wild-type macrophages stimulated O/N with LPS at 500 ng/ml, β-glucan at 10 μg/ml or zymosan at 1 μg/ml alone, or primed for 6 h then removed and stimulated for an additional 8 h by C. albicans at ~ 106/ml. (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
4.
Figure 6

Figure 6. Innate PRRs enhance survival after oral infection with Candida albicans. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) Quantitative fungal burden of tongues, and (b) kidneys of Dect1-/- and wild-type (WT) mice after oral infection with C. albicans; (c) Kaplan-Meier survival plots of WT and Dect1-/- mice after infection (P = 0.0009); (d) Mean clinical severity score of Dect1-/- and WT after 3 or 7d of infection; (e) Quantitative fungal burden of tongues and (f) kidneys of Tlr2-/- and wild-type (WT) mice after oral infection with C. albicans; (g) Kaplan-Meier survival plots of WT and Tlr2-/- mice after infection (P = 0.0002); (h) Mean clinical severity score of Tlr2-/- and WT after 3, 7, 14 or 21d of infection. (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
5.
Figure 1

Figure 1. In vitro IL-1β responses to Candida albicans are morphological stage dependent and blocked by caspase-1 inhibitor. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) IL-1β responses of normal PBMC primed for 3 h with LPS then stimulated with fixed preparations of C. albicans of different morphological stages at ~ 106/ml; (b) Inhibition of IL-1β responses after the addition of caspase-1 specific inhibitor, Z-YVAD-FMK; (c) Western blot of supernatants from PBMC stimulation probed with anti-IL-1β antibody; (d) IL-1β responses of bone-marrow derived macrophages from wild-type mice primed for 3 h with LPS then stimulated with C. albicans at ~ 106/ml; (e) Western blot of supernatants from BMDM stimulation probed with anti-IL-1β antibody, (f) and anti-caspase-1 antibody. (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
6.
Figure 5

Figure 5. NLRP3 inflammasome plays a critical role in host defense to mucosal infection with Candida albicans. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) Quantitative fungal burden of tongues, and (b) kidneys of Asc-/- and WT mice after oral infection with C. albicans; (c) Kaplan-Meier survival plots of WT and Asc-/- mice after infection (P = 0.0002); (d) Mean clinical severity score of Asc-/- and WT after 3, 7, 14 or 21d of infection; (e) Quantitative fungal burden of tongues, and (f) kidneys of Nlrp3-/- and WT mice after oral infection with C. albicans; (g) Mean clinical severity score of Nlrp3-/- and WT after 3 and 7d of infection. (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.
7.
Figure 4

Figure 4. Protective role of IL-1β in a murine modal of oral infection with Candida albicans. From: An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans.

(a) Fold induction of IL-1β mRNA measured by quantitative real-time PCR by oral buccal epithelium after infection with C. albicans; (b) IL-1β (pg/ml) protein production in homogenized whole tongues of mice after infection with C. albicans; (c) Quantitative fungal burden of tongues, and (d) kidneys of Il-1r1-/- and wild-type (WT) mice after oral infection with C. albicans; (e) Fungal burden of tongues, and (f) kidneys of Casp1-/- and WT mice after oral infection with C. albicans; (g) Kaplan-Meier survival plots of WT, Il-1r1-/- and Casp1-/- mice after infection (P <0.0001); (h) Mean clinical severity score of Il-1r1-/-, Casp1-/- and wild-type after 3, 7, 14 or 21d of infection; (*** P < 0.001; ** P < 0.01; * P < 0.05)

Amy G. Hise, et al. Cell Host Microbe. ;5(5):487-497.

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