Biology subjects

Park, S. L.

Publications and source records attributed to Park, S. L..

3 recordsLinked to original sources

bioRxiv2020

Naringenin as an antibacterial reagent controlling of biofilm formation and fatty acid metabolism in MRSA

MRSA is Methicillin-resistant Staphylococcus aureus and they are widespread and making trouble in treatment in communities and surgical areas. MRSA have been adapted to antibiotics so that they can block the access of antibiotics physically or chemically deactivate it or modify the precursor of the target. Flavonoids are secondary metabolites which are naturally produced by plant or fungus and they are acting generally as pigment, quorum sensing molecules, antibiotics to other competitive microorganisms. Their natural origins and multiple activities have drawn much attention to be developed as the potential drugs since flavonoids could be a good candidate to overcome antibiotic resistant bacteria. Among various flavonoids, we found out naringenin has antibacterial activity on MRSA and {Delta}agr mutants which are more resistance than MRSA to beta-lactam antibiotics by decreasing biofilm formation dramatically and decreasing the secretion of fatty acid. It also showed high synergetic activity with oxacillin to both antibacterial activity and biofilm inhibition. Considering the number of flavonoids, our experiments expand the possibility of the use of flavonoids to MRSA.

microbiology↗

bioRxiv2019

Systemic inflammation suppresses lymphoid tissue remodelling and B cell immunity during concomitant local infection

Concurrent infection with multiple pathogens occurs frequently in individuals and can result in exacerbated infections and altered immunity. However, the impact of such coinfections on immune responses remains poorly understood. Here we reveal that systemic infection results in an inflammation-induced suppression of local immunity. During localized infection or vaccination in barrier tissues including the skin or respiratory tract, concurrent systemic infection induced a type I interferon-dependent lymphopenia that impairs lymphocyte recruitment to the draining lymph node (dLN). This leads to suppressed lymphoid stromal cell expansion and dLN remodeling and impaired induction of B cell responses and antibody production. Our data suggest that contemporaneous systemic inflammation constrains the induction of regional immunity.Competing Interest StatementThe authors have declared no competing interest.View Full Text

immunology↗

bioRxiv2019

PTPN2 deletion in T cells promotes anti-tumour immunity and CAR T cell efficacy in solid tumours

Although adoptive T cell therapy has shown remarkable clinical efficacy in hematological malignancies, its success in combating solid tumours has been limited. Here we report that PTPN2 deletion in T cells enhances cancer immunosurveillance and the efficacy of adoptively transferred tumour-specific T cells. T cell-specific PTPN2 deficiency prevented tumours forming in aged mice heterozygous for the tumour suppressor p53. Adoptive transfer of PTPN2-deficient CD8+ T cells markedly repressed tumour formation in mice bearing mammary tumours. Moreover, PTPN2 deletion in T cells expressing a chimeric antigen receptor (CAR) specific for the oncoprotein HER-2 increased the activation of the Src family kinase LCK and cytokine-induced STAT-5 signalling thereby enhancing both CAR T cell activation and homing to CXCL9/10 expressing tumours to eradicate HER-2+ mammary tumours in vivo. Our findings define PTPN2 as a target for bolstering T-cell mediated anti-tumour immunity and CAR T cell therapy against solid tumours.

immunology↗