Diabetes Exacerbates Infection via Hyperinflammation by Signaling through TLR4 and RAGE.

For more than a century, diabetic patients have been considered immunosuppressed due to defects in phagocytosis and microbial killing. We confirmed that diabetic mice were hypersusceptible to bacteremia caused by Gram-negative bacteria (GNB), dying at inocula nonlethal to nondiabetic mice. Contrary to the pervasive paradigm that diabetes impedes phagocytic function, the bacterial burden was no greater in diabetic mice despite excess mortality.

Cryopreservation of virulent Acinetobacter baumannii to reduce variability of in vivo studies.

Background: Microbiological assays require accurate and reproducible preparation of bacterial inocula. Inocula prepared on different days by different individuals can vary significantly from experiment to experiment. This variance is particularly problematic for Gram-negative bacterial infections, for which threshold effects can result in marked variations in host outcome with minor differences in inocula.

Host fate is rapidly determined by innate effector-microbial interactions during Acinetobacter baumannii bacteremia.

Background: Acinetobacter baumannii is one of the most antibiotic-resistant pathogens. Defining mechanisms driving pathogenesis is critical to enable new therapeutic approaches.

Methods: We studied virulence differences across a diverse panel of A.