Jun-Hong Ch’ng

National University of Singapore

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Mats Wahlgren

Karolinska Institutet

Kevin S. W. Tan

Guangxi Medical University

Kirsten Moll

Karolinska Institutet

María del Pilar Quintana

University of Copenhagen

Kimberly Kline

Nanyang Technological University

Kelvin Kian Long Chong

Singapore Centre for Environmental Life Sciences Engineering

Martin J. Lear

University of Lincoln

François Nosten

Shoklo Malaria Research Unit

Santosh R. Kotturi

National University of Singapore

Jun Jie Wong

Singapore Centre for Environmental Life Sciences Engineering

Cooperative Institutions

National University of Singapore

Karolinska Institutet

Nanyang Technological University

Karolinska University Hospital

Singapore Centre for Environmental Life Sciences Engineering

Science for Life Laboratory

Singapore Immunology Network

Uppsala University

Agency for Science, Technology and Research

Centre National de la Recherche Scientifique

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Biofilm-associated infection by enterococci

Nature Reviews Microbiology (2018)

Jun-Hong Ch’ng Kelvin Kian Long Chong Ling Ning Lam Jun Jie Wong Kimberly Kline

10.1038/s41579-018-0107-z

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Citations (365)

Author Correction: Biofilm-associated infection by enterococci

Nature Reviews Microbiology (2018)

Jun-Hong Ch’ng Kelvin Kian Long Chong Ling Ning Lam Jun Jie Wong Kimberly Kline

Confusion

Section (typography)

Surface protein

10.1038/s41579-018-0128-7

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Citations (9)

Heme cross-feeding can augment Staphylococcus aureus and Enterococcus faecalis dual species biofilms

The ISME Journal (2022)

Jun-Hong Ch’ng Mugil Muthu Kelvin Kian Long Chong Jun Jie Wong Casandra Ai Zhu Tan

The contribution of biofilms to virulence and as a barrier to treatment is well-established for Staphylococcus aureus and Enterococcus faecalis, both nosocomial pathogens frequently isolated from biofilm-associated infections. Despite frequent co-isolation, their interactions in biofilms have not been well-characterized. We report that in combination, these two species can give rise to augmented biofilms biomass that is dependent on the activation of E. faecalis aerobic respiration. In E. faecalis, respiration requires both exogenous heme to activate the cydAB-encoded heme-dependent cytochrome bd, and the availability of O2. We determined that the ABC transporter encoded by cydDC contributes to heme import. In dual species biofilms, S. aureus provides the heme to activate E. faecalis respiration. S. aureus mutants deficient in heme biosynthesis were unable to augment biofilms whereas heme alone is sufficient to augment E. faecalis mono-species biofilms. Our results demonstrate that S. aureus-derived heme, likely in the form of released hemoproteins, promotes E. faecalis biofilm formation, and that E. faecalis gelatinase activity facilitates heme extraction from hemoproteins. This interspecies interaction and metabolic cross-feeding may explain the frequent co-occurrence of these microbes in biofilm-associated infections.

Enterococcus faecalis

Augment

10.1038/s41396-022-01248-1

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Citations (46)

Correction: Evasion of Immunity to Plasmodium falciparum: Rosettes of Blood Group A Impair Recognition of PfEMP1

PLoS ONE (2016)

Kirsten Moll Mia Palmkvist Jun-Hong Ch’ng Mpungu Steven Kiwuwa Mats Wahlgren

Evasion (ethics)

10.1371/journal.pone.0149765

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Citations (1)

Antibodies in children with malaria to PfEMP1, RIFIN and SURFIN expressed at the Plasmodium falciparum parasitized red blood cell surface

Scientific Reports (2018)

María del Pilar Quintana Jun-Hong Ch’ng Kirsten Moll Arash Zandian Peter Nilsson

Naturally acquired antibodies to proteins expressed on the Plasmodium falciparum parasitized red blood cell (pRBC) surface steer the course of a malaria infection by reducing sequestration and stimulating phagocytosis of pRBC. Here we have studied a selection of proteins representing three different parasite gene families employing a well-characterized parasite with a severe malaria phenotype (FCR3S1.2). The presence of naturally acquired antibodies, impact on rosetting rate, surface reactivity and opsonization for phagocytosis in relation to different blood groups of the ABO system were assessed in a set of sera from children with mild or complicated malaria from an endemic area. We show that the naturally acquired immune responses, developed during malaria natural infection, have limited access to the pRBCs inside a blood group A rosette. The data also indicate that SURFIN4.2 may have a function at the pRBC surface, particularly during rosette formation, this role however needs to be further validated. Our results also indicate epitopes differentially recognized by rosette-disrupting antibodies on a peptide array. Antibodies towards parasite-derived proteins such as PfEMP1, RIFIN and SURFIN in combination with host factors, essentially the ABO blood group of a malaria patient, are suggested to determine the outcome of a malaria infection.

Rosette (schizont appearance)

10.1038/s41598-018-21026-4

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Citations (22)

Development of drug-loaded immunoliposomes for the selective targeting and elimination of rosetting Plasmodium falciparum- infected red blood cells

Journal of Controlled Release (2016)

Ernest Moles Kirsten Moll Jun-Hong Ch’ng Paolo Parini Mats Wahlgren

Polyclonal antibodies

10.1016/j.jconrel.2016.09.006

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Citations (26)

A programmed cell death pathway in the malaria parasite Plasmodium falciparum has general features of mammalian apoptosis but is mediated by clan CA cysteine proteases

Cell Death and Disease (2010)

Jun-Hong Ch’ng Santosh R. Kotturi Akhilesh Chong Martin J. Lear Kevin S. W. Tan

Several recent discoveries of the hallmark features of programmed cell death (PCD) in Plasmodium falciparum have presented the possibility of revealing novel targets for antimalarial therapy. Using a combination of cell-based assays, flow cytometry and fluorescence microscopy, we detected features including mitochondrial dysregulation, activation of cysteine proteases and in situ DNA fragmentation in parasites induced with chloroquine (CQ) and staurosporine (ST). The use of the pan-caspase inhibitor, z-Val-Ala-Asp-fmk (zVAD), and the mitochondria outer membrane permeabilization (MOMP) inhibitor, 4-hydroxy-tamoxifen, enabled the characterization of a novel CQ-induced pathway linking cysteine protease activation to downstream mitochondrial dysregulation, amplified protease activity and DNA fragmentation. The PCD features were observed only at high (μM) concentrations of CQ. The use of a new synthetic coumarin-labeled chloroquine (CM-CQ) showed that these features may be associated with concentration-dependent differences in drug localization. By further using cysteine protease inhibitors z-Asp-Glu-Val-Asp-fmk (zDEVD), z-Phe-Ala-fmk (zFA), z-Phe-Phe-fmk (zFF), z-Leu-Leu-Leu-fmk (zLLL), E64d and CA-074, we were able to implicate clan CA cysteine proteases in CQ-mediated PCD. Finally, CQ induction of two CQ-resistant parasite strains, 7G8 and K1, reveals the existence of PCD features in these parasites, the extent of which was less than 3D7. The use of the chemoreversal agent verapamil implicates the parasite digestive vacuole in mediating CQ-induced PCD.

Cysteine protease

10.1038/cddis.2010.2

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Citations (82)

Frequent GU wobble pairings reduce translation efficiency in Plasmodium falciparum

Scientific Reports (2017)

Sherwin Chan Jun-Hong Ch’ng Mats Wahlgren Jessada Thutkawkorapin

Plasmodium falciparum genome has 81% A+T content. This nucleotide bias leads to extreme codon usage bias and culminates in frequent insertion of asparagine homorepeats in the proteome. Using recodonized GFP sequences, we show that codons decoded via G:U wobble pairing are suboptimal codons that are negatively associated to protein translation efficiency. Despite this, one third of all codons in the genome are GU wobble codons, suggesting that codon usage in P. falciparum has not been driven to maximize translation efficiency, but may have evolved as translational regulatory mechanism. Particularly, asparagine homorepeats are generally encoded by locally clustered GU wobble AAT codons, we demonstrated that this GU wobble-rich codon context is the determining factor that causes reduction of protein level. Moreover, insertion of clustered AAT codons also causes destabilization of the transcripts. Interestingly, more frequent asparagine homorepeats insertion is seen in single-exon genes, suggesting transcripts of these genes may have been programmed for rapid mRNA decay to compensate for the inefficiency of mRNA surveillance regulation on intronless genes. To our knowledge, this is the first study that addresses P. falciparum codon usage in vitro and provides new insights on translational regulation and genome evolution of this parasite.

Speed wobble

10.1038/s41598-017-00801-9

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Citations (19)