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Title: Gold nanoparticles attenuates bacterial sepsis in cecal ligation and puncture mouse model through the induction of M2 macrophage polarization
Authors: Sujittra Taratummarat
Naunpun Sangphech
Chau Tran Bao Vu
Tanapat Palaga
Thunnicha Ondee
Saowapha Surawut
Amornpun Sereemaspun
Patcharee Ritprajak
Asada Leelahavanichkul
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Other author: Chulalongkorn University. Faculty of Science
Chulalongkorn University. Faculty of Medicine
Issue Date: 17-Aug-2018
Publisher: BioMed Central
Citation: BMC Microbiology. Vol.18, Article No. 85 (2018), 10 pages
Abstract: Background : Gold nanoparticles (AuNP) have several biochemical advantageous properties especially for a candidate of drug carrier. However, the non-conjugated AuNP has a higher rate of cellular uptake than the conjugated ones. Spherical AuNP in a proper size (20–30 nm) is non-toxic to mice and shows anti-inflammatory properties. We tested if the administration of AuNP, as an adjuvant to antibiotics, could attenuate bacterial sepsis in cecal ligation and puncture (CLP) mouse model with antibiotic (imipenem/cilastatin). Results : Indeed, AuNP administration at the time of CLP improved the survival, blood bacterial burdens, kidney function, liver injury and inflammatory cytokines (TNF-α, IL-6, IL-1β and IL-10). AuNP also decreased M1 macrophages (CD86 + ve in F4/80 + ve cells) and increased M2 macrophages (CD206 + ve in F4/80 + ve cells) in the spleens of sepsis mice. The weak antibiotic effect of AuNP was demonstrated as the reduction of E. coli colony after 4 h incubation. In addition, AuNP altered cytokine production of bone-marrow-derived macrophages including reduced TNF-α, IL-6 and IL-1β but increased IL-10 at 6 and 24 h. Moreover, AuNP induced macrophage polarization toward anti-inflammatory responses (M2) as presented by increased Arg1 (Arginase 1) and PPARγ with decreased Nos2 (inducible nitric oxide synthase, iNos) and Nur77 at 3 h after incubation in vitro. Conclusions : The adjuvant therapy of AuNP, with a proper antibiotic, attenuated CLP-induced bacterial sepsis in mice, at least in part, through the antibiotic effect and the induction of macrophage function toward the anti-inflammatory responses.
ISSN: 1471-2180
metadata.dc.identifier.DOI: 10.1186/s12866-018-1227-3
Type: Article
Appears in Collections:Chula Scholars - 2018

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