Supplementary Materials

Supplementary Material for:

CXCR1-mediated neutrophil degranulation and fungal killing promote Candida clearance and host survival

Muthulekha Swamydas, Ji-Liang Gao, Timothy J. Break, Melissa D. Johnson, Martin Jaeger, Carlos A. Rodriguez, Jean K. Lim, Nathaniel M. Green, Amanda L. Collar, Brett G. Fischer, Chyi-Chia Richard Lee, John R. Perfect, Barbara D. Alexander, Bart-Jan Kullberg, Mihai G. Netea, Philip M. Murphy, Michail S. Lionakis*

*Corresponding author. E-mail: lionakism{at}niaid.nih.gov

Published 20 January 2016, Sci. Transl. Med. 8, 322ra10 (2016)
DOI: 10.1126/scitranslmed.aac7718

This PDF file includes:

  • Methods
  • Fig. S1. Cxcr1 deficiency does not result in developmental renal defects.
  • Fig. S2. Cxcl5 promotes dose-dependent Cxcr1-mediated calcium flux in mouse neutrophils.
  • Fig. S3. Cxcl1 and Cxcl2 do not promote significant Cxcr1-dependent calcium flux in mouse neutrophils.
  • Fig. S4. Systemic candidiasis results in increased renal tissue injury in Cxcr1−/− mice.
  • Fig. S5. Cxcr1 deficiency does not impair fungal clearance in the liver, spleen, or brain after Candida infection.
  • Fig. S6. Cxcr1 deficiency does not result in histological abnormalities in the liver, brain, or spleen after Candida infection.
  • Fig. S7. Gating strategy for FACS sorting of hematopoietic cells from kidney.
  • Fig. S8. Kidney neutrophils express Cxcr1 and Cxcl5 at steady state and after systemic candidiasis.
  • Fig. S9. Cxcr1 deficiency does not affect the production of neutrophils in the bone marrow after Candida infection.
  • Fig. S10. Cxcr1 deficiency does not affect the accumulation of neutrophils in the blood after Candida infection.
  • Fig. S11. Cxcr1 deficiency does not impair the induction of Cxcl5 in the Candida-infected kidney.
  • Fig. S12. Cxcr1 deficiency does not impair the accumulation of mononuclear phagocytes in the kidney after Candida infection.
  • Fig. S13. Cxcr1 does not impair the induction of proinflammatory cytokines and chemokines in the kidney after Candida infection.
  • Fig. S14. Cxcr2 is expressed on blood and kidney neutrophils of Cxcr1+/+ and Cxcr1−/− mice at steady state and during systemic candidiasis.
  • Fig. S15. A selective Cxcr2 antagonist does not decrease neutrophil accumulation in the Candida-infected kidney of Cxcr1−/− mice.
  • Fig. S16. Cxcr1 deficiency results in a cell-intrinsic defect in killing of Candida yeast forms.
  • Fig. S17. Cxcr1 deficiency does not impair the formation of neutrophil extracellular traps ex vivo.
  • Fig. S18. Cxcr1 deficiency does not impair the accumulation of NK cells or the induction of Il23a and Gmcsf in the kidney after Candida infection.
  • Fig. S19. Cxcr1 deficiency does not impair the production of reactive oxygen species by bone marrow neutrophils at steady state.
  • Table S1. Demographic and clinical characteristics of the candidemic and control subjects enrolled in the present study.
  • Table S2. Association of the mutant CXCR1-T276 allele with susceptibility to systemic candidiasis in subjects of mixed European descent (n = 304).
  • Table S3. Association of the mutant CXCR1-T276 allele with development of persistent fungemia in candidemic patients of mixed European descent (n = 153).
  • References (3235)

[Download PDF]

Other Supplementary Material for this manuscript includes the following:

  • Data File 1. Excel file with all data values in tabular format.