Rab32 restriction of intracellular bacterial pathogens

Research output: Contribution to journalArticle

7 Citations (Scopus)
3 Downloads (Pure)

Abstract

Our immune system is engaged in a continuous battle against invading pathogens, many of which have evolved to survive in intracellular niches of mammalian hosts. A variety of cellular processes are involved in preventing bacterial invasion or in killing bacteria that successfully invade host cells. Recently, the Rab GTPase Rab32 emerged as critical regulator of a host defense pathway that can eliminate bacterial pathogens. Salmonella enterica is an intracellular bacterium and a major cause of infections and deaths in humans. Rab32 and its guanine nucleotide exchange factor BLOC-3 are essential to prevent the growth of the human-restricted Salmonella enterica serovar Typhi (S. Typhi) in mice, a non-susceptible host. The importance of the Rab32/BLOC-3 pathway has been recently confirmed by the finding that broad-host Salmonella enterica serovars deliver two bacterial effectors to neutralize this pathway and infect mice. Rab32 has also been shown to control infection by Listeria monocytogenes, another medically relevant intracellular pathogen. In addition, genetic evidence indicate a possible role of Rab32 in controlling leprosy, a disease caused by Mycobacterium leprae in humans, suggesting that a Rab32-dependent pathway can also act as a host defense pathway in humans. The Rab32 role in bacterial pathogen restriction is discussed here and compared to the function of this GTPase in other cellular processes.
Original languageEnglish
Pages (from-to)216-223
Number of pages8
JournalSmall GTPases
Volume9
Issue number3
Early online date20 Sep 2016
DOIs
Publication statusPublished - 2018

Keywords

  • salmonella
  • Rab GTPases
  • Hermansky– Pudlak syndrome
  • lysosome-related organelles
  • host-pathogen interactions
  • bacterial pathogens
  • typhoid fever
  • innate immunity

Fingerprint Dive into the research topics of 'Rab32 restriction of intracellular bacterial pathogens'. Together they form a unique fingerprint.

Cite this