An analysis of Candida glabrata-epithelial cell interaction
Sandip Patra and Rupinder Kaur
Laboratory of Fungal Pathogenesis, Centre for DNA Fingerprinting and Diagnostics, Uppal, Hyderabad-500039 India
Candida glabrata is a haploid non-dimorphic budding yeast which resides as a commensal in the oral cavity, and gastrointestinal and genitourinary tracts in healthy individuals. It also causes deep-seated mucosal and systemic fungal infections in immunocompromised patients. Phylogenetically, this non-albicans Candida species is more closely related to the non-pathogenic yeast Saccharomyces cerevisiae, and these two yeasts share a common ancestor. Although anti-fungal resistance and intracellular survival mechanisms of C. glabrata are currently being studied extensively, the interaction of C. glabrata with host epithelial and endothelial cells remains largely unexplored. An interaction with tissue-resident immune cells as well as epithelial and endothelial cells is pivotal to the colonization and invasion of host niches. In the current study, I have established two in vitro model systems, using renal epithelial cell line A-498 and gastric epithelial cell line AGS, and showed that C. glabrata displays robust adherence to both cell lines, and a family of eleven cell surface- associated aspartyl proteases modulates this process of epithelial cell adhesion through one of the major adhesins Epa1. Super resolution microscopy reveals the intracellular replication of C. glabrata wild-type strain; while the yapsin deficient mutant could not be able to survive upon C. glabrata-epithelial cell co-culture. Additionally, I have investigated the role of CgYps1 and CgYps7 aspartyl proteases in tissue adherence and modulation of host intracellular signaling pathways, as this proteases are uniquely required to survive under cell wall stress condition in vitro. These results along with the proteomics analysis upon CgYps1/CgYps7-epithelial cell lysate co-incubation will be presented.

**An analysis of _Candida glabrata_-epithelial cell interaction**
Sandip Patra and Rupinder Kaur
Laboratory of Fungal Pathogenesis, Centre for DNA Fingerprinting and Diagnostics, Uppal, Hyderabad-500039 India
_Candida glabrata_ is a haploid non-dimorphic budding yeast which resides as a commensal in the oral cavity, and gastrointestinal and genitourinary tracts in healthy individuals. It also causes deep-seated mucosal and systemic fungal infections in immunocompromised patients. Phylogenetically, this non-_albicans_ _Candida_ species _is more closely related to the non-pathogenic yeast _Saccharomyces cerevisiae_, and these two yeasts share a common ancestor. Although anti-fungal resistance and intracellular survival mechanisms of _C. glabrata_ are currently being studied extensively, the interaction of _C. glabrata_ with host epithelial and endothelial cells remains largely unexplored. An interaction with tissue-resident immune cells as well as epithelial and endothelial cells is pivotal to the colonization and invasion of host niches. In the current study, I have established two in vitro model systems, using renal epithelial cell line A-498 and gastric epithelial cell line AGS, and showed that _C. glabrata_ displays robust adherence to both cell lines, and a family of eleven cell surface- associated aspartyl proteases modulates this process of epithelial cell adhesion through one of the major adhesins Epa1. Super resolution microscopy reveals the intracellular replication of _C. glabrata wild-type_ strain; while the yapsin deficient mutant could not be able to survive upon _C. glabrata_-epithelial _cell co-culture_._ Additionally, I have investigated the role of CgYps1 and CgYps7 aspartyl proteases in tissue adherence and modulation of host intracellular signaling pathways, as this proteases are uniquely required to survive under cell wall stress condition _in vitro_. These results along with the proteomics analysis upon CgYps1/CgYps7-epithelial cell lysate co-incubation will be presented.__

An analysis of Candida glabrata-epithelial cell interaction

Exploring the intricacies of host-pathogen communication is vital in order to understand why
some microbes persist within a host, while others are effectively cleared. As such,
host-pathogen communication is an urgent area of research underpinning human health
and disease, especially given the emerging concerns of antibiotic resistance.
Understanding host-pathogen pathways requires intricate knowledge in the fields of both
microbiology and immunology.

Living in a world of specialists, where scientists sometimes invest their whole career
studying one organism, a specific pathway or a protein, multidisciplinary discussions of
host-pathogen interactions are highly needed. This international conference will provide
such a forum for scientific exchange at the highest level, between scientists from different
research areas related to host-pathogen interactions, with the aim to trigger fruitful
collaborations addressing the urgent questions in the field.

This meeting has an additional special focus of bringing researchers from Ireland, Denmark
and Israel together to learn about cutting edge biology and form new collaborations.
Thus, the conference will be a showcase for the exciting and original research emanating
from these three small but innovative countries.

Host-Pathogen Communication (HPC) 2021

Awards & close

Initiation and Regulation of Innate Immunity

Plasmacytoid dendritic cells sense SARS-CoV-2 through TLR2-IL6 and TLR7-INFα pathways that protect epithelial cells from infection

Mouse models carrying patient-derived mutations in IRF3 and TBK1 enable mechanistic characterization of herpes simplex encephalitis

A diamidobenzimidazole STING agonist protects against SARS-CoV-2 infection

Coordinating immune-defence functions of MLKL: endosomal targeting of MLKL by site specific ubiquitination facilitates lysosomal destruction of intracellular pathogenes