Christoph Konradt

Christoph Konradt Profile Picture

Assistant Professor 
PhD from College of Veterinary Medicine
 

Contact Info:

ckonradt@purdue.edu
c.konradt@gmail.com
765-496-3455
215-917-7317
VPTH 103a
Konradt Lab

Training Group(s):
Microbiology, Immunology and Infectious Diseases

Active Mentor - currently hosting PULSe students for laboratory rotations and recruiting PULSe students into the laboratory; serves on preliminary exam committees

Current Research Interests:

Research Focus 1: The role of EC in the immune response There are more than 10 trillion EC in the human body, that cover 4000 m2, and these are an important replicative niche for a subset of micro-organisms such as Dengue virus, West Nile Virus, CMV, S. aureus and T. gondii. For many micro-organisms the ability to infect EC is a key part of their pathogenesis. Indeed, EC express TLR and influence coagulation and neutrophil recruitment and their activation can lead to vascular damage, while expression of adhesion molecules promotes extravasation of inflammatory cells. Numerous in vitro studies have demonstrated that EC can be activated by cytokines to limit viral, bacterial and parasite replication. Furthermore, evidence that EC interact with the adaptive response is implicit in the ability of EC to present MHC class I & II restricted antigens. However, whether EC antigen presentation via MHC-I or MHC-II has a tolerogenic or inflammatory role during infection remains unclear. Therefore, there is a major knowledge gap in our understanding in the involvement of EC in orchestrating a T cell response or how the immune system reacts to infected EC in vivo. Research Focus 2: Immune responses at the Maternal-Fetal Interface The maternal-fetal interface is the interface between the uterine mucosa and the extraembryonic tissues of the developing conceptus. The placenta functions as the primary nutrient and gas exchange organ of the fetus by diverting maternal blood flow from the uterus. Once inside the placenta, maternal blood exchanges nutrients, gases, and metabolic waste products with fetal blood coursing through a physically separate vasculature that connects to the fetus via the umbilical cord. A successful pregnancy involves complex interactions between fetal trophoblasts, endothelial cells and maternal decidual immune cells, creating an immunologically unique site that allows the tolerance to the allogenic fetus but still maintains host defense against possible pathogens. Infections are a well-described cause for fetal losses and stillbirths, as well as for perinatal morbidity. Indeed, infections are accounted for up to 15% of early miscarriages and up to 66% of late miscarriages. Moreover, infections can further lead to preterm birth or infants with birth defects leading to lifelong disabilities. This is accompanied with significant health care costs and a burden for the mothers mental health and psychological wellbeing. Immune responses at the maternal-fetal interface during infection are poorly understood and there is a real need for a better understanding of the immunological mechanisms at this site.

Selected Publications:

Konradt C, Hunter CA. Pathogen interactions with endothelial cells and the induction of innate and adaptive immunity. Eur. J. Immunol. 2018 Sep 21;48(10):1607–20.

O’Brien CA, Overall C, Konradt C, O’Hara Hall AC, Hayes NW, Wagage S, et al. CD11c-Expressing Cells Affect Regulatory T Cell Behavior in the Meninges during Central Nervous System Infection. The Journal of Immunology. 2017 May 15;198(10):4054–61.

Glatman Zaretsky A*, Konradt C* et al. T Regulatory Cells Support Plasma Cell Populations in the Bone Marrow. Cell Reports 18, 1906–1916 (2017). * These authors contributed equally.

Weinkopff T, Konradt C, Christian DA, Discher DE, Hunter CA and Scott P. Leishmania major Infection-Induced VEGF-A/VEGFR-2 Signaling Promotes Lymphangiogenesis That Controls Disease. The Journal of Immunology 197, 1823–1831 (2016).

Konradt C, et al. Endothelial cells are a replicative niche for entry Toxoplasma gondii to the central nervous system. Nature Microbiology. 2016; 1:16001.

Harris TH, Banigan EJ, Christian DA, Konradt C, Tait Wojno ED, Norose K, Wilson EH, John B, Weninger W, Luster AD, Liu AJ, Hunter CA. Generalized Lévy walks and the role of chemokines in migration of effector CD8+ T cells. Nature. 2012 Jun 28;486(7404) :545-8.

Konradt C, et al. The Shigella flexneri type three secretion system effector IpgD inhibits T cell migration by manipulating host phosphoinositide metabolism. Cell Host Microbe. 2011 Apr 21;9(4):263-72.

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