Diane M. Janowicz, MD
Assistant Professor of Clinical Medicine
Emerson Hall, Suite 435 545 N Barnhill Dr
Indianapolis, IN 46202-5124
Titles & Appointments
- Fellowship Program Director
DksA and (p)ppGpp have unique and overlapping contributions to Haemophilus ducreyi pathogenesis in humans.
Phosphoethanolamine Transferase LptA in Haemophilus ducreyi Modifies Lipid A and Contributes to Human Defensin Resistance In Vitro.
A (p)ppGpp-null mutant of Haemophilus ducreyi is partially attenuated in humans due to multiple conflicting phenotypes.
Outer membrane protein P4 is not required for virulence in the human challenge model of Haemophilus ducreyi infection.
Permeases of the sap transporter are required for cathelicidin resistance and virulence of Haemophilus ducreyi in humans.
Expression of the Flp proteins by Haemophilus ducreyi is necessary for virulence in human volunteers.
Sialylation of lipooligosaccharides is dispensable for the virulence of Haemophilus ducreyi in humans.
Role played by CD4+FOXP3+ regulatory T Cells in suppression of host responses to Haemophilus ducreyi during experimental infection of human volunteers.
Activation of the CpxRA system by deletion of cpxA impairs the ability of Haemophilus ducreyi to infect humans.
Experimental infection of human volunteers with Haemophilus ducreyi: fifteen years of clinical data and experience.
Dysregulated immune profiles for skin and dendritic cells are associated with increased host susceptibility to Haemophilus ducreyi infection in human volunteers.
Experimental infection with Haemophilus ducreyi in persons who are infected with HIV does not cause local or augment systemic viral replication.
[Effect of thymus cells, resistant to the action of hydrocortisone, on the proliferation of hematopoietic stem cells].
American Board of Internal Medicine - Infectious Disease