Pathogenicity and Virulence of Legionella: Intracellular replication and host response

被引:79
作者
Chauhan, Deepika [1 ]
Shames, Stephanie R. [1 ]
机构
[1] Kansas State Univ, Div Biol, Ackert Hall, Manhattan, KS 66506 USA
关键词
Legionella; pathogenicity; virulence; host-response; innate immunity; LEGIONNAIRES-DISEASE BACTERIUM; II PROTEIN SECRETION; PNEUMOPHILA LUNG INFECTION; FORMATION-MEDIATED EGRESS; AMINO-ACID-REQUIREMENTS; OUTER-MEMBRANE PROTEIN; NECROSIS-FACTOR-ALPHA; ACANTHAMOEBA-CASTELLANII; IV SECRETION; STATIONARY-PHASE;
D O I
10.1080/21505594.2021.1903199
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Bacteria of the genus Legionella are natural pathogens of amoebae that can cause a severe pneumonia in humans called Legionnaires' Disease. Human disease results from inhalation of Legionella-contaminated aerosols and subsequent bacterial replication within alveolar macrophages. Legionella pathogenicity in humans has resulted from extensive co-evolution with diverse genera of amoebae. To replicate intracellularly, Legionella generates a replication-permissive compartment called the Legionella-containing vacuole (LCV) through the concerted action of hundreds of Dot/Icm-translocated effector proteins. In this review, we present a collective overview of Legionella pathogenicity including infection mechanisms, secretion systems, and translocated effector function. We also discuss innate and adaptive immune responses to L. pneumophila, the implications of Legionella genome diversity and future avenues for the field.
引用
收藏
页码:1122 / 1144
页数:23
相关论文
共 266 条
[2]   Caspase-7 Activation by the Nlrc4/Ipaf Inflammasome Restricts Legionella pneumophila Infection [J].
Akhter, Anwari ;
Gavrilin, Mikhail A. ;
Frantz, Laura ;
Washington, Songcerae ;
Ditty, Cameron ;
Limoli, Dominique ;
Day, Colby ;
Sarkar, Anasuya ;
Newland, Christie ;
Butchar, Jonathan ;
Marsh, Clay B. ;
Wewers, Mark D. ;
Tridandapani, Susheela ;
Kanneganti, Thirumala-Devi ;
Amer, Amal O. .
PLOS PATHOGENS, 2009, 5 (04)
[3]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[4]   Temporal pore formation-mediated egress from macrophages and alveolar epithelial cells by Legionella pneumophila [J].
Alli, OAT ;
Gao, LY ;
Pedersen, LL ;
Zink, S ;
Radulic, M ;
Doric, M ;
Abu Kwaik, Y .
INFECTION AND IMMUNITY, 2000, 68 (11) :6431-6440
[5]   INTERACTION OF L-PNEUMOPHILA AND A FREE LIVING AMEBA (ACANTHAMOEBA, PALESTINENSIS) [J].
ANAND, CM ;
SKINNER, AR ;
MALIC, A ;
KURTZ, JB .
JOURNAL OF HYGIENE, 1983, 91 (02) :167-178
[6]   Cutting Edge: Pulmonary Legionella pneumophila Is Controlled by Plasmacytoid Dendritic Cells but Not Type I IFN [J].
Ang, Desmond K. Y. ;
Oates, Clare V. L. ;
Schuelein, Ralf ;
Ly, Michelle Kel ;
Sansom, Fiona M. ;
Bourges, Dorothee ;
Boon, Louis ;
Hertzog, Paul J. ;
Hartland, Elizabeth L. ;
van Driel, Ian R. .
JOURNAL OF IMMUNOLOGY, 2010, 184 (10) :5429-5433
[7]   Legionella effector Lpg1137 shuts down ER-mitochondria communication through cleavage of syntaxin 17 [J].
Arasaki, Kohei ;
Mikami, Yumi ;
Shames, Stephanie R. ;
Inoue, Hiroki ;
Wakana, Yuichi ;
Tagaya, Mitsuo .
NATURE COMMUNICATIONS, 2017, 8
[8]   MyD88-dependent responses involving toll-like receptor 2 are important for protection and clearance of Legionella pneumophila in a mouse model of Legionnaires' disease [J].
Archer, Kristina A. ;
Roy, Craig R. .
INFECTION AND IMMUNITY, 2006, 74 (06) :3325-3333
[9]   Multiple MyD88-dependent responses contribute to pulmonary clearance of Legionella pneumophila [J].
Archer, Kristina A. ;
Alexopoulou, Lena ;
Flavell, Richard A. ;
Roy, Craig R. .
CELLULAR MICROBIOLOGY, 2009, 11 (01) :21-36
[10]   RpoS co-operates with other factors to induce Legionella pneumophila virulence in the stationary phase [J].
Bachman, MA ;
Swanson, MS .
MOLECULAR MICROBIOLOGY, 2001, 40 (05) :1201-1214