Author ORCID Identifier
Biosketch
Dr. Shah E Jahan Gulzar completed her Ph.D. in the School of Chemical & Biotechnologyfrom SASTRA Deemed to be University, Thanjavur, India. Her doctoral research focused on understanding host–pathogen interactions during Mycobacterium tuberculosis infection, with particular emphasis on intercellular communication, bystander macrophage responses, and infection-induced epigenetic reprogramming. Her work revealed how IL-1β–mediated signalling drives chromatin remodelling and trained immunity in uninfected bystander macrophages, providing new insights into non-cell-autonomous immune regulation.
During her Ph.D., she gained extensive expertise in cell biology, host–pathogen biology, advanced fluorescence microscopy, quantitative imaging, molecular biology, epigenetics, and transcriptomics. She has contributed to peer-reviewed publications in international journals, including studies on lysosomal biology, mechanosensitive ion channels, and antiviral strategies targeting viral entry pathways.
Dr. Gulzar is broadly interested in innate immune memory, organelle dynamics, and intercellular signalling in infectious diseases and cancer. She aims to further explore how immune cell plasticity and tissue microenvironments shape disease outcomes. Her long-term goal is to contribute to translational research that bridges fundamental cell biology with therapeutic strategies for infectious and inflammatory diseases.
Date of Award
11-2-2026
Document Type
Thesis
School
School of Chemical & Biotechnology
Programme
Ph.D.-Doctoral of Philosophy
First Advisor
Dr. Varadharajan Sundaramurthy
Second Advisor
Dr. Bhaskar Chandra Mohan Ramisetty
Keywords
Mycobacterium tuberculosis, Macrophages, Bystander cells, IL-1β signaling, Epigenetic reprogramming, H3K27Ac Trained immunity
Abstract
Mycobacterium tuberculosis (Mtb) remodels host cell functions to support its intracellular persistence. While the effects of Mtb infection on infected macrophages are well characterized, responses of uninfected bystander cells in the same microenvironment remain poorly understood. Here, we show that Mtb infection triggers widespread epigenetic reprogramming not only in infected macrophages but also in neighbouring bystander cells. These bystander macrophages acquire active chromatin marks, exhibit distinct transcriptional changes, and display enhanced immune responsiveness, thereby increasing resistance to both homologous and heterologous infections. We identify interleukin-1 beta secreted by infected cells as a key mediator of this process. Functionally, trained bystander macrophages restrict Mtb growth upon subsequent infection. These findings reveal that intercellular signalling during Mtb infection promotes trained immunity within the macrophage population, positioning bystander cells as active participants in shaping the innate immune response. Targeting these intercellular pathways may offer new strategies to modulate host defence beyond the directly infected cells.
Recommended Citation
Jahan Gulzar, Shah E. Mr, "Mycobacteria Infection Induced Cascade of Epigenetic Alterations Promote Training in Bystander Macrophages" (2026). Theses and Dissertations. 202.
https://knowledgeconnect.sastra.edu/theses/202