» Articles » PMID: 28264910

Expanding Role of Type II Secretion in Bacterial Pathogenesis and Beyond

Overview
Journal Infect Immun
Date 2017 Mar 8
PMID 28264910
Citations 105
Authors
Affiliations
Soon will be listed here.
Abstract

Type II secretion (T2S) is one means by which Gram-negative pathogens secrete proteins into the extracellular milieu and/or host organisms. Based upon recent genome sequencing, it is clear that T2S is largely restricted to the , occurring in many, but not all, genera in the , , , and classes. Prominent human and/or animal pathogens that express a T2S system(s) include , , , , , , , , , and T2S-expressing plant pathogens include , , , , , , and T2S also occurs in nonpathogenic bacteria, facilitating symbioses, among other things. The output of a T2S system can range from only one to dozens of secreted proteins, encompassing a diverse array of toxins, degradative enzymes, and other effectors, including novel proteins. Pathogenic processes mediated by T2S include the death of host cells, degradation of tissue, suppression of innate immunity, adherence to host surfaces, biofilm formation, invasion into and growth within host cells, nutrient assimilation, and alterations in host ion flux. The reach of T2S is perhaps best illustrated by those bacteria that clearly use it for both environmental survival and virulence; e.g., employs T2S for infection of amoebae, growth within lung cells, dampening of cytokines, and tissue destruction. This minireview provides an update on the types of bacteria that have T2S, the kinds of proteins that are secreted via T2S, and how T2S substrates promote infection.

Citing Articles

IrsA, a novel, iron-regulated exoprotein that facilitates growth in low-iron conditions and modulates biofilm formation.

Lopez A, Mayoral J, Zheng H, Cianciotto N Microbiol Spectr. 2024; 13(1):e0231324.

PMID: 39612475 PMC: 11705809. DOI: 10.1128/spectrum.02313-24.


Microalgae and cyanobacteria as microbial substrate and their influence on the potential postbiotic capability of a bacterial probiotic.

Dominguez-Maqueda M, Perez-Gomez O, Garcia-Marquez J, Espinosa-Ruiz C, Cuesta A, Esteban M Microb Biotechnol. 2024; 17(11):e70046.

PMID: 39573896 PMC: 11582085. DOI: 10.1111/1751-7915.70046.


Holliday junction resolvase RuvC targets biofilm eDNA and confers plant resistance to vascular pathogens.

Du X, Li P, Fan C, Tian J, Lin Y, Xie J Nat Plants. 2024; 10(11):1710-1723.

PMID: 39384943 DOI: 10.1038/s41477-024-01817-6.


A decade of dinoflagellate genomics illuminating an enigmatic eukaryote cell.

Lin S BMC Genomics. 2024; 25(1):932.

PMID: 39367346 PMC: 11453091. DOI: 10.1186/s12864-024-10847-5.


T6SS in plant pathogens: unique mechanisms in complex hosts.

Matte L, Genal A, Landolt E, Danka E Infect Immun. 2024; 92(9):e0050023.

PMID: 39166846 PMC: 11385963. DOI: 10.1128/iai.00500-23.


References
1.
Liles M, Edelstein P, Cianciotto N . The prepilin peptidase is required for protein secretion by and the virulence of the intracellular pathogen Legionella pneumophila. Mol Microbiol. 1999; 31(3):959-70. DOI: 10.1046/j.1365-2958.1999.01239.x. View

2.
Hales L, Shuman H . Legionella pneumophila contains a type II general secretion pathway required for growth in amoebae as well as for secretion of the Msp protease. Infect Immun. 1999; 67(7):3662-6. PMC: 116561. DOI: 10.1128/IAI.67.7.3662-3666.1999. View

3.
Deshazer D, Brett P, Burtnick M, Woods D . Molecular characterization of genetic loci required for secretion of exoproducts in Burkholderia pseudomallei. J Bacteriol. 1999; 181(15):4661-4. PMC: 103600. DOI: 10.1128/JB.181.15.4661-4664.1999. View

4.
Dharmapuri S, Sonti R . A transposon insertion in the gumG homologue of Xanthomonas oryzae pv. oryzae causes loss of extracellular polysaccharide production and virulence. FEMS Microbiol Lett. 1999; 179(1):53-9. DOI: 10.1111/j.1574-6968.1999.tb08707.x. View

5.
Stabb E, Reich K, Ruby E . Vibrio fischeri genes hvnA and hvnB encode secreted NAD(+)-glycohydrolases. J Bacteriol. 2000; 183(1):309-17. PMC: 94880. DOI: 10.1128/JB.183.1.309-317.2001. View