Dr Tufael Ahmed completed his PhD in Respiratory Immunology at the QIMR Berghofer Medical Research Institute/QUT in 2024. During his PhD, he identified a novel role for the alarmin IL-33 in inducing neutrophil-mediated NETosis during rhinovirus (RV)-induced asthma exacerbations. These findings highlight the potential of IL-33 as a therapeutic target in asthma, particularly in neutrophilic inflammation and asthma subtypes where eosinophils are less prominent, in addition to T2-high/eosinophilic asthma. He also investigated the molecular mechanisms underlying how a poor maternal diet induces microbial dysbiosis in the infant gut. Tufael has expertise in isolating and transplanting potential pathobiont gut bacteria to study their role in inducing low-grade systemic inflammation and severe lower respiratory tract infections.
Currently, he is working as a senior research assistant under Dr. Adi Idris. His primary focus is on establishing in vivo mouse models to evaluate the efficacy of intranasally delivered small interfering RNAs (siRNAs) encapsulated in novel lipid nanoparticle (LNP) formulations against RSV and hMPV.
Publications:
– Ahmed T*, Curren B, , Rashid RB, Sebina I, Al Amin Sikder M, Howard DR, Alorro M, Ullah MA, Bissell A, Rahman MM, Pearen MA, Ramm GA, Varelias A, Rose-John S, MacDonald KPA, Hoelzle R, Ó Cuív P, Spann KM, Dennis PG, Phipps S. A maternal high-fat diet predisposes to infant lung disease via increased neutrophil-mediated IL-6 trans-signaling. Cell Reports. 2024 Nov 26;43(11):114974. doi: 10.1016/j.celrep.2024.114974. Epub 2024 Nov 12. PMID: 39535919. Joint first author.
– Ahmed T*, Curren B*, Howard DR, Ullah MA, Sebina I, Rashid RB, Sikder MA, Namubiru P, Bissell A, Ngo S, Jackson DJ. IL-33-induced neutrophilic inflammation and NETosis underlie rhinovirus-triggered exacerbations of asthma. Mucosal Immunology. 2023 Aug 15. * Joint first author.
– Sikder MA, Rashid RB, Ahmed T, Sebina I, Howard DR, Ullah MA, Rahman MM, Lynch JP, Curren B, Werder RB, Simpson J. The maternal microbiome regulates infant respiratory disease susceptibility via intestinal Flt3L e