Naslov
Legionella pneumophila - imunopatogegeza infekcije
(Legionella pneumophila - immunopathogenesis of infection)

Autori
Tićac, Brigita

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
10. hrvatski kongres kliničke mikrobiologije i 7. hrvatski kongres o infektivnim bolestima (CROCMID 2013) : knjiga sažetaka = abstract book / Bradarić, Nikola ; Tambić Andrašević Arjana - Zagreb : Hrvatski liječnički zbor ; Hrvatsko društvo za mikrobiologiju ; Hrvatsko društvo za infektivne bolesti, 2013

Skup
Hrvatski kongres kliničke mikrobiologije (10 ; 2013) ; Hrvatski kongres o infektivnim bolestima (7 ; 2013)

Mjesto i datum
Rovinj, Hrvatska, 24.10.2013. - 27.10.2013

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Domaća recenzija

Ključne riječi
Legionella; immunopathogenesis

Sažetak
Legionella pneumophila, an intracellular bacterial pathogen that causes a serious and often fatal pneumonia in humans (Legionnaires' disease). Intracellular replication of L. pneumophila within environmental protozoa plays a major role in the transmission of Legionnaires' disease (Harb, 1998). The pathogenesis of legionellosis is largely due to the ability of L. pneumophila to grow within alveolar macrophages. Surface structures that enhance infection include LPS, flagella, type IV pili, an outer membrane porin, and the Mip protein. Type II and type IV protein secretion systems are critical for the pathogenesis. Type II system secretes a collection of degradative enzymes while type IV system likely exports effector proteins that are critical for trafficking of the Legionella phagosome. L. pneumophila, utilizes a type IVB secretion system (icm/dot, intracellular multiplication/defect in organelle trafficking genes), to translocate numerous effector proteins into its eukaryotic host. These effectors are important for the intracellular survival. The L. pneumophila containing vacuoles avoid fusion with lysosomes, recruiting rough endoplasmic reticulum and mitochondria. The induction of Dot/Icm- depended, caspase-3 activation apoptosis by L. pneumophila is well documented. Periplasmic and cytosolic infectivity determinants include a catalase- peroxidase and the HtrA and Hsp60 stress- response proteins (Horwitz, 1983 ; Jules, 2007). In vivo studies indicate that the infections result in a humoral and cell-mediated immune response. Macrophages and dendritic cells are able to present microbial antigens on MHC class I and class II molecules, which stimulate antigen- specific T-cell response. Humoral immunity probably plays a role as a second line of defense by reducing intrapulmonary growth of L. pneumophila, while cellular immunity in concert with cytokines could be essential for resolution of a primary infection (Friedman, 1983 ; Susa, 1998). In our earlier work, the influence of T- cell depletion on the pathogenesis of experimental infection was studied. We have shown that L. pneumophila replicated in the lungs of A/J mice reaching the peak at 24-48h . Inflammatory cells were recruited into the lung on the second day of infection, reaching a maximum on the day three. During the first 3 days after inoculation, mainly macrophages, B-cells and NK-cells were attracted into the lung, whereas T-lymphocytes infiltrated subsequently. Furthermore, we confirmed that L. pneumophila infection is indeed ensued by an immediate production of inflammatory cytokines (IFN-, TNF-, IL-6, and IL-1β), and that the control of infection and clearance from the lungs depend on successful recruitment and unimpaired function of CD4 and CD8 T-lymphocytes (Susa, 1998).

Izvorni jezik
Hrvatski, engleski

Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti

POVEZANOST RADA