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1.
J Clin Med ; 11(20)2022 Oct 18.
Article in English | MEDLINE | ID: mdl-36294446

ABSTRACT

An outbreak of a potentially fatal form of pneumonia in 1976 and in the annual convention of the American Legion was the first time that Legionella spp. was identified. Thereafter, the term Legionnaires' disease (LD) was established. The infection in humans is transmitted by the inhalation of aerosols that contain the microorganisms that belong to the Legionellaceae family and the genus Legionella. The genus Legionella contains genetically heterogeneous species and serogroups. The Legionella pneumophila serogroup 1 (Lp1) is the most often detected strain in outbreaks of LD. The pathogenesis of LD infection initiates with the attachment of the bacterial cells to the host cells, and subsequent intracellular replication. Following invasion, Legionella spp. activates its virulence mechanisms: generation of specific compartments of Legionella-containing vacuole (LCV), and expression of genes that encode a type IV secretion system (T4SS) for the translocation of proteins. The ability of L. pneumophila to transmigrate across the lung's epithelium barrier leads to bacteremia, spread, and invasion of many organs with subsequent manifestations, complications, and septic shock. The clinical manifestations of LD depend on the bacterial load in the aerosol, the virulence factors, and the immune status of the patient. The infection has two distinct forms: the non- pneumatic form or Pontiac fever, which is a milder febrile flu-like illness, and LD, a more severe form, which includes pneumonia. In addition, the extrapulmonary involvement of LD can include heart, brain, abdomen, and joints.

2.
Int J Mol Sci ; 22(10)2021 May 20.
Article in English | MEDLINE | ID: mdl-34065210

ABSTRACT

Previous studies have shown that COVID-19 leads to thrombotic complications, which have been associated with high morbidity and mortality rates. Neutrophils are the largest population of white blood cells and play a pivotal role in innate immunity. During an infection, neutrophils migrate from circulation to the infection site, contributing to killing pathogens. This mechanism is regulated by chemokines such as IL-8. Moreover, it was shown that neutrophils play an important role in thromboinflammation. Through a diverse repertoire of mechanisms, neutrophils, apart from directly killing pathogens, are able to activate the formation of thrombi. In COVID-19 patients, neutrophil activation promotes neutrophil extracellular trap (NET) formation, platelet aggregation, and cell damage. Furthermore, neutrophils participate in the pathogenesis of endothelitis. Overall, this review summarizes recent progress in research on the pathogenesis of COVID-19, highlighting the role of the prothrombotic action of neutrophils in NET formation.


Subject(s)
COVID-19/immunology , Extracellular Traps/immunology , Immunity, Innate , Lung/immunology , Neutrophils/immunology , Thrombosis/immunology , COVID-19/complications , COVID-19/pathology , COVID-19/therapy , Cytokine Release Syndrome/metabolism , Cytokine Release Syndrome/virology , Extracellular Traps/virology , Humans , Inflammation/immunology , Inflammation/pathology , Kidney/cytology , Kidney/immunology , Kidney/pathology , Kidney/virology , Lung/cytology , Lung/pathology , Lung/virology , Mucocutaneous Lymph Node Syndrome/complications , Mucocutaneous Lymph Node Syndrome/immunology , Mucocutaneous Lymph Node Syndrome/virology , SARS-CoV-2 , Thrombosis/complications , Thrombosis/pathology , Thrombosis/virology
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