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Pivot Concepts:
Gene/Protein
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Target Concepts:
Gene/Protein
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Query: UMLS:C0023241 (
Legionella
)
6,990
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Mycobacterium tuberculosis is one of the intracellular parasitic bacteria escaping the intracellular killing inside macrophages. The aim of this symposium was to get some insight into the mechanism of pathogenicity and host defense in M. tuberculosis infection, which has not yet been elucidated well, by the presentation of up-to-date knowledge on these aspect in infection with different intracellular parasitic microbes. Dr. Yoshikai (Nagoya Univ.) indicated that TLR is involved in the initial response of host against S. choleraesuis. Among the cytokines contributing to the induction of specific immunity, the importance of IL-15 was emphasized, based on their own experimental data using IL-15 transgenic mice and the application of anti-IL-15 antibody in vivo. Dr. Yoshida (Kyushu Univ.) reviewed the mechanisms of intracellular growth of Legionellae. Several genes so far identified as essential genes in intra-macrophage growth appeared to be similar to those encoding type 3 secretion system observed in Shigellae. There is a significant strain difference in the growth of L. pneumophila inside macrophages and such difference seemed to be under the control of a gene at chromosome 13, Lgn 1. The investigation of difference in the mode of escape among various
Legionella
. spp. may provide a novel mechansim in bacterial invasion and escape. Dr. Kawamura (Kyoto Univ.) summarized some new reports on the molecular mechanism of the inhibition of P-L fusion by M. tuberculosis. He emphasized the importance of the alteration in phagosomal maturation as indicated by the accumulation of
TACO
protein. The possible involvement of TLR in the recognition of Mycobacterial cells and its LAM was discussed. Dr. Kawakami (Ryukyu Univ.) first discussed the possibility that Cryptococcus neoformans, a fungal pathogen, could be regarded as one of the intracellular parasitic microbes. His presentation mainly focused on the TH1-Th2 balance in the expression of host defense against C. neoformans in mice. From their experimental infection using attenuated strain TC-13 in various cytokine-knock out mice, the pivotal role of both IL-12 and IL-18 was clearly indicated.
...
PMID:[Mechanisms of pathogenicity and host defense in infections by intracellular parasitic microbes]. 1106 72
Legionella
pneumophila, the causative agent of
Legionnaires' disease
, is a human pathogen that multiplies within alveolar macrophages. L. pneumophila establishes specialized phagosomes in which it evades the host defense through largely unknown mechanisms. Here we analyzed the role of an actin-binding protein, p57/
coronin-1
, a member of the coronin protein family, during Legionella infection. On fluorescence microscopy, p57/
coronin-1
and F-actin were found to be co-localized at the sites on the plasma membrane where L. pneumophila adhered to U937 human macrophage-like cells. The localization of p57/
coronin-1
at the sites of bacterial adherence was inhibited by treatment with cytochalasin D (an inhibitor of actin polymerization), suggesting that p57/
coronin-1
is involved in the actin-dependent uptake of L. pneumophila into U937 cells. In addition, we showed that p57/
coronin-1
was excluded from phagosomes containing live L. pneumophila throughout the infection, whereas transient accumulation of p57/
coronin-1
was observed on phagosomes containing Texas-Red-labeled opsonized zymosan (TROpZ) or heat-killed L. pneumophila at an early stage of phagocytosis. The exclusion of p57/
coronin-1
from phagosomes containing live another
Legionella
species
Legionella
gratiana at an early stage of infection was also observed. Taken together, these results suggest that the endocytic pathways of live
Legionella
species are distinct from general phagocytic pathways, which lead to lysosomal degradation.
...
PMID:Exclusion of actin-binding protein p57/coronin-1 from bacteria-containing phagosomes in macrophages infected with Legionella. 1845 8