Immunomodulatory effects of human beta-defensin 2 in treating asthma and COPD

Jayaraman, Ranjith

Immunomodulatory effects of human beta-defensin 2 in treating asthma and COPD

Jayaraman, Ranjith

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Publication Type:: Thesis
Issue Date:: 2023

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Field	Value	Language
dc.contributor.author	Jayaraman, Ranjith
dc.date.accessioned	2024-04-23T01:14:48Z
dc.date.available	2024-04-23T01:14:48Z
dc.date.issued	2023
dc.identifier.uri	http://hdl.handle.net/10453/178239
dc.description	University of Technology Sydney. Faculty of Science.	en_US.UTF-8
dc.description.abstract	Background: Asthma and chronic obstructive pulmonary disease (COPD) are debilitating diseases and effective therapies are a priority. Human beta-defensin 2 (hBD2) is an antimicrobial peptide with potential for treating asthma and COPD. Methods: The effects of hBD2 in allergic airway disease (AAD), severe steroid-resistant (SSRAAD), and experimental COPD murine models were assessed. In AAD, faecal microbial transfer (FMT) and flow cytometry were used to assess the role of faecal microbiome and immunomodulation in hBD2-mediated effects. Results: Intranasal hBD2 reduced airway inflammation, but partially suppressed airway hyperresponsiveness (AHR), while oral hBD2 had no effects on airway inflammation and alleviated AHR in SSRAAD. In AAD, oral hBD2 reduced AAD features. FMT from hBD2-donors did not transfer the protective effects of hBD2 in AAD. hBD2 reversed AAD-induced granulocyte depletion in the colon and reduced AAD-induced granulocytes in the lungs to suppress AAD. Intranasal hBD2 did not suppress CS-induced acute airway inflammation. High-dose oral hBD2 reduced CS-induced acute airway inflammation, however failed to suppress disease features in CS-induced experimental COPD. Conclusion: Intranasal and oral hBD2 partially alleviated SSRAAD. Oral hBD2 alleviates AAD, which is associated with the immunomodulation of colon and lung immune cells. Oral hBD2 is not effective in experimental COPD.	en_US.UTF-8
dc.format	Thesis (PhD)
dc.language.iso	en_US	en_US.UTF-8
dc.relation	https://opus.lib.uts.edu.au/bitstream/10453/178239/1/thesis.pdf
dc.rights	info:eu-repo/semantics/embargoedAccess
dc.rights	The author owns the copyright in this thesis including all reproduction and reuse rights for the work. The work may not be altered without the permission of the copyright owner. Attribution is essential when quoting or paraphrasing from this thesis.
dc.rights	© 2023 Ranjith Jayaraman
dc.rights	au.edu.uts.lib/cph
dc.title	Immunomodulatory effects of human beta-defensin 2 in treating asthma and COPD	en_US.UTF-8
dc.type	Thesis
utslib.copyright.status	embargoed	*
utslib.copyright.embargo	2044-12-31T00:00:00+1000

Abstract:

Background: Asthma and chronic obstructive pulmonary disease (COPD) are debilitating diseases and effective therapies are a priority. Human beta-defensin 2 (hBD2) is an antimicrobial peptide with potential for treating asthma and COPD. Methods: The effects of hBD2 in allergic airway disease (AAD), severe steroid-resistant (SSRAAD), and experimental COPD murine models were assessed. In AAD, faecal microbial transfer (FMT) and flow cytometry were used to assess the role of faecal microbiome and immunomodulation in hBD2-mediated effects. Results: Intranasal hBD2 reduced airway inflammation, but partially suppressed airway hyperresponsiveness (AHR), while oral hBD2 had no effects on airway inflammation and alleviated AHR in SSRAAD. In AAD, oral hBD2 reduced AAD features. FMT from hBD2-donors did not transfer the protective effects of hBD2 in AAD. hBD2 reversed AAD-induced granulocyte depletion in the colon and reduced AAD-induced granulocytes in the lungs to suppress AAD. Intranasal hBD2 did not suppress CS-induced acute airway inflammation. High-dose oral hBD2 reduced CS-induced acute airway inflammation, however failed to suppress disease features in CS-induced experimental COPD. Conclusion: Intranasal and oral hBD2 partially alleviated SSRAAD. Oral hBD2 alleviates AAD, which is associated with the immunomodulation of colon and lung immune cells. Oral hBD2 is not effective in experimental COPD.

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http://hdl.handle.net/10453/178239