While not exhaustive, this list includes recent publications (2019 onwards) that outline the types of experimentation to which animals are subjected in Australian laboratories. More detailed profiles of Australian animal research can be found in our case studies.
1.
Matt D. Johansen, Stefan Miemczyk, Duc H. Nguyen, Guanshu Zhao, Catherine J. M. Stapledon, Ravi Krishnan, Philip M. Hansbro
Pentosan polysulfate sodium limits pulmonary inflammation in a SARS-CoV-2 mouse model Journal Article
In: Microbiology Spectrum, pp. 21, 2026, (University of Technology Sydney Centenary Institute Paradigm Biopharmaceuticals Ltd).
Abstract | Links | BibTeX | Tags: COVID-19, Mice, pulmonary inflammation, SARS-CoV-2
@article{nokey,
title = {Pentosan polysulfate sodium limits pulmonary inflammation in a SARS-CoV-2 mouse model},
author = {Matt D. Johansen, Stefan Miemczyk, Duc H. Nguyen, Guanshu Zhao, Catherine J. M. Stapledon, Ravi Krishnan, Philip M. Hansbro},
editor = {Junki Maruyama, The University of Texas Medical Branch at Galveston, Galveston, Texas, USA},
url = {https://pubmed.ncbi.nlm.nih.gov/42872814/},
doi = {10.1128/spectrum.01990-26},
year = {2026},
date = {2026-10-13},
urldate = {2026-10-13},
journal = {Microbiology Spectrum},
pages = {21},
abstract = {Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection remains prevalent globally, causing severe pulmonary inflammation and mortality in up to 10% of patients. While the introduction of effective vaccines has substantially reduced the number of severe coronavirus disease 2019 (COVID-19) cases, there are currently few available therapeutics that have been developed. Pentosan polysulfate sodium (PPS) has been shown to possess potent anti-inflammatory activity in influenza infection and allergen-induced rhinitis models and was recently demonstrated to inhibit SARSCoV-2 infection in vitro. As such, we hypothesized that PPS may represent an attractive therapeutic that could be utilized for SARS-CoV-2 infection and COVID-19. Using the K18-hACE2 mouse model of SARS-CoV-2 infection, we administered PPS (6 mg/kg) from either 1 (early) or 3 (late) days post-infection via intranasal instillation and then examined the efficacy in mitigating viral-induced inflammation and severe disease outcomes. We found that the early administration of PPS was accompanied by significant improvements in weight loss, clinical disease presentation, and neutrophilic airway inflammation. Early PPS administration also significantly reduced pro-inflammatory cytokine production at both the mRNA and protein levels while having no impact on viral titers or interferon and antiviral gene expression. Histologically, early treatment significantly prevented severe pulmonary inflammation and tissue remodeling. Comparatively, late administration of PPS worsened weight loss and clinical disease presentation following SARS-CoV-2 infection. Moreover, late administration was unable to prevent significant increases in pro-inflammatory cytokines and was further associated with significantly downregulated antiviral-associated genes. Histological examination also showed no protection in the late PPS administered groups. Taken together, these findings underscore the significance of time-dependent administration and demonstrate the therapeutic potential of PPS for treatment of SARS-CoV-2-induced inflammation.},
note = {University of Technology Sydney
Centenary Institute
Paradigm Biopharmaceuticals Ltd},
keywords = {COVID-19, Mice, pulmonary inflammation, SARS-CoV-2},
pubstate = {published},
tppubtype = {article}
}
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection remains prevalent globally, causing severe pulmonary inflammation and mortality in up to 10% of patients. While the introduction of effective vaccines has substantially reduced the number of severe coronavirus disease 2019 (COVID-19) cases, there are currently few available therapeutics that have been developed. Pentosan polysulfate sodium (PPS) has been shown to possess potent anti-inflammatory activity in influenza infection and allergen-induced rhinitis models and was recently demonstrated to inhibit SARSCoV-2 infection in vitro. As such, we hypothesized that PPS may represent an attractive therapeutic that could be utilized for SARS-CoV-2 infection and COVID-19. Using the K18-hACE2 mouse model of SARS-CoV-2 infection, we administered PPS (6 mg/kg) from either 1 (early) or 3 (late) days post-infection via intranasal instillation and then examined the efficacy in mitigating viral-induced inflammation and severe disease outcomes. We found that the early administration of PPS was accompanied by significant improvements in weight loss, clinical disease presentation, and neutrophilic airway inflammation. Early PPS administration also significantly reduced pro-inflammatory cytokine production at both the mRNA and protein levels while having no impact on viral titers or interferon and antiviral gene expression. Histologically, early treatment significantly prevented severe pulmonary inflammation and tissue remodeling. Comparatively, late administration of PPS worsened weight loss and clinical disease presentation following SARS-CoV-2 infection. Moreover, late administration was unable to prevent significant increases in pro-inflammatory cytokines and was further associated with significantly downregulated antiviral-associated genes. Histological examination also showed no protection in the late PPS administered groups. Taken together, these findings underscore the significance of time-dependent administration and demonstrate the therapeutic potential of PPS for treatment of SARS-CoV-2-induced inflammation.