TY - JOUR
T1 - Innate immunity against Legionella pneumophila during pulmonary infections in mice
AU - Park, Bonggoo
AU - Park, Gayoung
AU - Kim, Jiyoung
AU - Lim, Seon Ah
AU - Lee, Kyung Mi
N1 - Funding Information:
This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT, and Future Planning (Grants NRF-2013M3A9D3045719). B. Park is also supported by a Grant from the National Research Foundation of Korea (2014R1A1A2057068).
Publisher Copyright:
© 2017, The Pharmaceutical Society of Korea.
PY - 2017/2/1
Y1 - 2017/2/1
N2 - Legionella pneumophila is an etiological agent of the severe pneumonia known as Legionnaires’ disease (LD). This gram-negative bacterium is thought to replicate naturally in various freshwater amoebae, but also replicates in human alveolar macrophages. Inside host cells, legionella induce the production of non-endosomal replicative phagosomes by injecting effector proteins into the cytosol. Innate immune responses are first line defenses against legionella during early phases of infection, and distinguish between legionella and host cells using germline-encoded pattern recognition receptors such as Toll-like receptors , NOD-like receptors, and RIG-I-like receptors, which sense pathogen-associated molecular patterns that are absent in host cells. During pulmonary legionella infections, various inflammatory cells such as macrophages, neutrophils, natural killer (NK) cells, large mononuclear cells, B cells, and CD4+ and CD8+ T cells are recruited into infected lungs, and predominantly occupy interstitial areas to control legionella. During pulmonary legionella infections, the interplay between distinct cytokines and chemokines also modulates innate host responses to clear legionella from the lungs. Recognition by NK cell receptors triggers effector functions including secretion of cytokines and chemokines, and leads to lysis of target cells. Crosstalk between NK cells and dendritic cells, monocytes, and macrophages provides a major first-line defense against legionella infection, whereas activation of T and B cells resolves the infection and mounts legionella-specific memory in the host.
AB - Legionella pneumophila is an etiological agent of the severe pneumonia known as Legionnaires’ disease (LD). This gram-negative bacterium is thought to replicate naturally in various freshwater amoebae, but also replicates in human alveolar macrophages. Inside host cells, legionella induce the production of non-endosomal replicative phagosomes by injecting effector proteins into the cytosol. Innate immune responses are first line defenses against legionella during early phases of infection, and distinguish between legionella and host cells using germline-encoded pattern recognition receptors such as Toll-like receptors , NOD-like receptors, and RIG-I-like receptors, which sense pathogen-associated molecular patterns that are absent in host cells. During pulmonary legionella infections, various inflammatory cells such as macrophages, neutrophils, natural killer (NK) cells, large mononuclear cells, B cells, and CD4+ and CD8+ T cells are recruited into infected lungs, and predominantly occupy interstitial areas to control legionella. During pulmonary legionella infections, the interplay between distinct cytokines and chemokines also modulates innate host responses to clear legionella from the lungs. Recognition by NK cell receptors triggers effector functions including secretion of cytokines and chemokines, and leads to lysis of target cells. Crosstalk between NK cells and dendritic cells, monocytes, and macrophages provides a major first-line defense against legionella infection, whereas activation of T and B cells resolves the infection and mounts legionella-specific memory in the host.
KW - Legionella pneumophila
KW - Natural killer cells
KW - NOD-like receptor
KW - Pattern recognition receptor
KW - Pulmonary infection
KW - Toll-like receptor
UR - http://www.scopus.com/inward/record.url?scp=85008481805&partnerID=8YFLogxK
U2 - 10.1007/s12272-016-0859-9
DO - 10.1007/s12272-016-0859-9
M3 - Review article
C2 - 28063015
AN - SCOPUS:85008481805
SN - 0253-6269
VL - 40
SP - 131
EP - 145
JO - Archives of Pharmacal Research
JF - Archives of Pharmacal Research
IS - 2
ER -