Supplementary Materials

The PDF file includes:

  • Methods
  • Fig. S1. Experimental model of NEC in mice resembles the human intestinal disease observed in premature infants.
  • Fig. S2. Histological examination reveals comparable features of brain development between infants with and without NEC.
  • Fig. S3. Effect of the hypoxia component of the experimental NEC protocol (5% O2, 10 min twice a day for 4 days) on cerebral myelination and brain volume.
  • Fig. S4. Effect of the enteric bacteria component of experimental NEC protocol on microglial activation, accumulation of ROS, and cerebral myelination.
  • Fig. S5. Generation of microglia-specific TLR4 knockout mice.
  • Fig. S6. NEC is characterized by increased circulating levels of HMGB1 in human serum.
  • Fig. S7. Effect of the hypoxia component of the NEC protocol on ROS accumulation and microglial activation.
  • Fig. S8. Dendrimer distribution within the brain after oral administration to mice with and without experimental NEC.
  • Fig. S9. Oral administration of D-NAC–coupled dendrimers after 48 hours of experimental NEC does not prevent the development of the intestinal disease.
  • Table S1. Bacterial (genus) composition found in the stool of an infant with NEC used to induce NEC in mice.
  • Table S2. Bacterial (genus) composition found in the stool of a healthy infant used as control in mice.
  • Table S3. List of primers used for qRT-PCR.
  • Table S4. Human brain pathology specimens.
  • Table S5. Postconceptual age at the time of HMGB1 blood sample collection.
  • Legend for data file S1

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Other Supplementary Material for this manuscript includes the following: