Professor Teng was a trained veterinarian graduated from National Taiwan University in 1992. He went to Cornell University in U.S.A. to pursue his Ph.D. degree in the field of Comparative Biomedical Sciences in 1996. Right after his Ph. D. study he started his first postdoctoral study at School of Medicine of University of Maryland, U.S.A. for a short period of time in 2002. After that, he worked for his second postdoctoral research at Johns Hopkins University School of Medicine from 2002 to 2005.  From 2005 to present he is an faculty member in the Institute of Molecular Medicine of National Cheng Kung University School of Medicine.

Due to wide use and abuse of antimicrobial agents, the rapid emergence of antimicrobial-resistant pathogenic bacteria becomes a global health concern. It is necessary to develop novel strategies to prevent and treat bacterial infectious diseases. The long term goal of our laboratory is to develop such strategies. The knowledge of the bacterial pathogens required to achieve this goal. Therefore, we proceed from understanding the pathogenic mechanisms of bacterial pathogens. Escherichia coli have been used as the model bacteria for studying the bacterial pathogenesis in our laboratory. Currently, we are mainly focusing on the neonatal meningitis pathogenic E. coli (NMEC) and uropathogenic E. coli (UPEC).

E. coli neonatal meningitis usually develops through several steps of bacteria–host interactions. These include mucosa colonization by the pathogens (usually upper respiratory or gastrointestinal tract), microbial invasion of the intravascular space, and followed by intravascular survival and multiplication resulting in bacteremia. After reaching a threshold level bacteremia (>103 colony forming units per milliliter of blood), NMEC penetrate the blood brain barrier (BBB) and invades central nervous system to cause meningitis. We are investigating the mechanisms by which NMEC survive in the blood- stream and invade the BBB.

UPEC is the most common cause of urinary tract infections (UTIs), including acute cystitis, pyelonephritis, and urosepsis. It is widely accepted that UPEC mainly emerges from the distal gut microbiota. To cause ascending UTI, UPEC needs to overcome and adapt to different distinct host environments, such as the bladder, the kidneys, and even the blood stream Accordingly, UPEC tends to be distinct from the commensal E. coli strains in the intestinal tract in having extra virulence genes allowing their successful transition from the intestinal tract to the urinary tract. We are currently investigating the uropathogenic roles of E. coli genes that exhibit significantly higher frequencies among UPEC strains than the fecal commensal strains.