Oxidative Stress Response in Pseudomonas aeruginosa

Abstract

Pseudomonas aeruginosa is a Gram-negative environmental and human opportunistic pathogen highly adapted to many different environmental conditions. It can cause a wide range of serious infections, including wounds, lungs, the urinary tract, and systemic infections. The high versatility and pathogenicity of this bacterium is attributed to its genomic complexity, the expression of several virulence factors, and its intrinsic resistance to various antimicrobials. However, to thrive and establish infection, P. aeruginosa must overcome several barriers. One of these barriers is the presence of oxidizing agents (e.g., hydrogen peroxide, superoxide, and hypochlorous acid) produced by the host immune system or that are commonly used as disinfectants in a variety of different environments including hospitals. These agents damage several cellular molecules and can cause cell death. Therefore, bacteria adapt to these harsh conditions by altering gene expression and eliciting several stress responses to survive under oxidative stress. Here, we used PubMed to evaluate the current knowledge on the oxidative stress responses adopted by P. aeruginosa. We will describe the genes that are often differently expressed under oxidative stress conditions, the pathways and proteins employed to sense and respond to oxidative stress, and how these changes in gene expression influence pathogenicity and the virulence of P. aeruginosa. Understanding these responses and changes in gene expression is critical to controlling bacterial pathogenicity and developing new therapeutic agents.

Exposure to the Pseudomonas aeruginosa secretome alters the proteome and secondary metabolite production of Aspergillus fumigatus

“…The glyoxylate shunt (GS) is a metabolic process whereby bacteria metabolize acetate and fatty acids as carbon sources, and which may be used as an alternative to the TCA cycle [55,56]. This two-step pathway involves isocitrate lyase and malate synthase, and is upregulated under conditions of oxidative stress [55,56]. Both enzymes involved in this pathway were detected in the P. aeruginosa CuF.…”

The Pseudomonas aeruginosa DksA1 protein is involved in H2O2 tolerance and within-macrophages survival and can be replaced by DksA2

“…As mentioned in the introduction, the oxidative burst is the first microbicidal mechanism activated by macrophages to kill engulfed bacteria 5 , 6 . Thus, we analysed the role of DksA1 and DksA2 in counteracting oxidative stress within macrophages.…”

“…H 2 O 2 can be further converted to hydroxyl free radical via Fenton reaction or halogenated ROS. This quick ROS production in the phagosome, a process known as oxidative burst, plays a key role in the host innate immune response 5 , 6 . Bacteria must also cope with extracellular ROS.…”

“…In addition to a wide arsenal of virulence factors, P . aeruginosa expresses an array of ROS-scavenging enzymes to counteract endogenous and exogenous ROS, including the four catalases KatA, KatB, KatE and KatN 5 , 6 , 10 – 12 . The KatA and KatB catalases are crucial for P. aeruginosa adaptation to the high levels of H 2 O 2 encountered in the host 11 , 13 , 14 .…”

Interrelation between Stress Management and Secretion Systems of Ralstonia solanacearum: An In Silico Assessment

“…Similarly, PINs were also recorded among the GSPS cluster (representing nine genes: secA, secB, secD, secE, sceF, secG, secY, ftsY, and ffh), MSR cluster, and OxSR cluster. Interestingly, interactions between Sec and MSR in Escherichia coli and the Sec secretion system and OxSR in Pseudomonas aeruginosa were also reported [ 71 , 72 ]. As in most bacteria, the Sec pathway is the main route by which secretory proteins are exported across the cytoplasmic membrane in Rs [ 73 ].…”