Mechanisms involved in the evasion of the host defence by Pseudomonas aeruginosa
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2021, The Cell SurfaceCitation Excerpt :Deposition of C3b and C1q-binding to the bacterial surface of Streptococcus pneumoniae biofilms is impaired, enabling pneumococcal biofilms to avoid the activation of the classical pathway (Domenech et al., 2013). Pseudomonas aeruginosa growing planktonically resulted in a stronger activation of complement than biofilms (Jensen et al., 1993), which could be inactivating the complement system by secreting alkaline protease and elastase (Kharazmi et al., 1991). Biofilms are likely to have a plethora of wide-reaching interactions and effects on the innate immune response.
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2021, Cell ReportsCitation Excerpt :These chronic infections persist even after initiation of highly effective CFTR modulator therapy (Hisert et al., 2017); thus, a better understanding of how P. aeruginosa eludes killing by both host immune factors and antibiotics remains a critical area of research. Physical disruption of P. aeruginosa aggregates in laboratory experiments can restore susceptibility to killing with antibiotics (Alhede et al., 2011) and cells of the immune system (Jensen et al., 1992; Kharazmi, 1991). Thus, understanding mechanisms that promote cellular aggregation is an important focus of research efforts.
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2018, Research in MicrobiologyCitation Excerpt :P. aeruginosa possesses a plethora of virulence factors, including lipopolysaccharides, exopolysaccharides, flagella, pili, pigments, proteases, lipases and exotoxins [21,42]. These molecules enable P. aeruginosa to obtain nutrition, colonize and invade at different locations in the human body, adapt against host defenses and cause damage to the hosts [7,24]. Certain virulence molecules containing the N-terminal signal peptide are secreted by the bacterial type I secretion system (T1SS), the type II secretion system (T2SS) and the type III secretion system (T3SS) [3,16,22].