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Dr Md Moniruzzaman

Postdoctoral Research Fellow

Faculty of Medicine
m.moniruzzaman@uq.edu.au

Overview

Dr Moniruzzaman is working as a Senior Postdoctoral Research Fellow at the UQ Faculty of Medicine and PA Hospital of Metro South Health. His research focuses on the molecular pathobiology of inflammatory diseases, in particular, how mucosal epithelial cells and gut microbiota regulate immune function in the gastrointestinal (GI) tract and contribute to different diseases, including inflammatory bowel diseases (IBD) and functional GI symptoms called disorders of gut-brain interactions (DGBI). Dr Moniruzzaman received his PhD from The University of Queensland in 2020, where he studied how the interleukin(IL)-20 family of cytokines (IL-20, IL-22, and IL-24) regulate mucosal epithelial and immune function in inflammatory and infectious diseases, including ulcerative colitis (UC) and respiratory syncytial virus. After graduation, he received postdoctoral training in the IBD Lab at Mater Research Institute – UQ and Nanomedicine Lab at UQ School of Pharmacy, where he investigated the role of cannabinoid receptors in UC and colitis-associated colorectal cancer, development of cannabinoid formulations to treat UC, and involvement of autophagy gene Atg7 in 6-Thioguanin mediated protection from UC. He was awarded a highly competitive UQ Postdoctoral Research Fellowship (2021-2022) and UQ School of Pharmacy Strategic Grant (2022) to study cannabinoids and Atg7 in UC, and Translational Research Institute LINC Grant (2023) to study cannabinoids in palliative care of patients with advanced cancer. Currently, he is working on how intestinal microbial dysbiosis controls mucosal immune microenvironment and contributes to the pathogenesis of DGBI, including irritable bowel syndrome (IBS) and functional dyspepsia (FD).

“I started a career in biomedical research because of my deep curiosity about the way in which the human body works. Now, I am working to understand the contribution of different cytokines in human pathology, which will allow me to devise the causes behind the origin of inflammatory diseases and develop effective therapies to serve the community.”

Qualifications

  • Doctor of Philosophy, The University of Queensland, Australia
  • Master of Pharmacy, Dongguk University, South Korea
  • Bachelor of Pharmacy (Hons), Stamford University Bangladesh

Research Interests

  • Immune regulation in mucosal inflammation
    Mucosal inflammation is a complex process that occurs in various tissues, including the respiratory, gastrointestinal, and genitourinary tracts. It plays a crucial role in host defence against pathogens but can also contribute to the development of chronic inflammatory diseases including inflammatory bowel diseases (IBD). Immune regulation is essential to maintain a balance between protective immune responses and tissue homeostasis. In mucosal inflammation, the immune system employs a range of mechanisms to regulate the inflammatory process. One key aspect is the presence of specialized immune cells, such as regulatory T cells (Tregs), which help suppress excessive inflammation. Tregs modulate immune responses by releasing anti-inflammatory molecules and inhibiting the activation of other immune cells. Furthermore, mucosal tissues have unique immunological characteristics that contribute to immune regulation. For instance, the presence of secretory IgA antibodies helps prevent pathogens from invading epithelial cells and triggering an inflammatory response. Additionally, epithelial cells in mucosal tissues produce various antimicrobial peptides and cytokines that contribute to immune regulation and barrier integrity. The gut microbiota also plays a critical role in mucosal immune regulation. The microbiota interacts with the immune system and helps shape its development and function. Dysbiosis, an imbalance in the gut microbial composition, can lead to impaired immune regulation and contribute to mucosal inflammation. Understanding the mechanisms of immune regulation in mucosal inflammation is crucial for developing therapeutic interventions. Targeting Tregs, modulating the microbiota, and promoting barrier integrity are potential strategies for restoring immune balance and alleviating mucosal inflammation-related diseases.
  • Epithelial function in mucosal inflammatory diseases
    Mucosal epithelial cells line the mucosal surfaces, play a crucial role in the inflammatory diseases including inflammatory bowel diseases (IBD) and asthma. Epithelial cells form a physical barrier that separates the internal environment from the external milieu and participate in immune responses and tissue repair. Understanding epithelial function in mucosal inflammatory diseases is key to unravelling the underlying mechanisms and developing effective treatments. In mucosal inflammatory diseases, epithelial cells undergo significant alterations in their function. These changes include impaired barrier function, increased production of inflammatory mediators, and altered interactions with immune cells. The disruption of epithelial barrier integrity allows the entry of pathogens, allergens, and toxins, triggering inflammatory responses. Epithelial cells also actively participate in immune responses by sensing and responding to microbial and inflammatory signals. Upon activation, epithelial cells release cytokines, chemokines, and antimicrobial peptides, contributing to the recruitment and activation of immune cells. Moreover, dysregulation of epithelial cell function can lead to chronic inflammation and tissue damage. Inflammatory bowel diseases and asthma are most common examples of mucosal inflammatory diseases characterized by dysfunctional epithelial cells. A comprehensive understanding of epithelial function in mucosal inflammatory diseases may lead to the development of targeted therapies. Strategies to restore epithelial barrier integrity, modulate immune responses, and promote tissue repair could potentially alleviate symptoms and improve patient outcomes.
  • Intestinal microbial dysbiosis in Disorders of Gut-Brain Interaction (DGBI)
    Gut-brain interactions refer to the bidirectional communication and connection between the gut (digestive system) and the brain (central nervous system). The gut-brain axis is a complex network involving various pathways and signalling mechanisms that facilitate communication between these two systems. The enteric nervous system, also known as the "second brain," is a network of neurons within the gut that can function independently and communicate with the central nervous system. The vagus nerve, a major nerve connecting the gut and the brain, plays a crucial role in transmitting signals and information between these two systems. Gut-brain interactions are involved in regulating a wide range of functions, including digestion, appetite, mood, stress response, and immune function. The gut microbiota, the collection of microorganisms residing in the gut, also influences gut-brain interactions through the production of neurotransmitters and other signalling molecules. However, any disturbance in communication could lead to a variety of symptoms and conditions, called disorders of gut-brain interaction (DGBI) which includes motility disturbance, visceral hypersensitivity, altered mucosal and immune function, altered gut microbiota, and altered CNS processing. Therefore, understanding and studying gut-brain interactions is essential for gaining insights into various disorders and developing potential treatments. This project will span our understanding on the involvement of small intestinal microbial dysbiosis in the pathogenesis of DGBI, whether antimicrobial therapy is effective in all subtypes or if specific subgroups of patients would benefit more, and the bidirectional interactions between mucosal immune function and small intestinal microenvironment; and develop new therapeutics targeting gut microbiota.

Qualifications

  • Doctoral (Research) of Biochemistry and Cell Biology, The University of Queensland
  • Masters (Research) of Pharmacy, Dongguk University
  • Bachelor (Honours) of Pharmacy, Stamford University Bangladesh

Publications

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Grants

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Supervision

  • Designer Nanoparticles for Oral and Targeted Delivery of Protein Therapeutics

    Doctor Philosophy

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Publications

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PhD and MPhil Supervision

Current Supervision

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Links

ResearcherID: J-4482-2017

ORCID: 0000-0002-3905-8627

Scopus ID: 56392674200

Personal Profile: Link

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