The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

Dotto, Cristián; Serrat, Andrea Lombarte; Cattelan, Natalia; Barbagelata, María Sol; Yantorno, Osvaldo; Sordelli, Daniel O.; Ehling‐Schulz, Monika; Grunert, Tom; Buzzola, Fernanda R.

doi:10.3389/fmicb.2017.00004

Cited by 34 publications

(42 citation statements)

References 72 publications

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“…A recent study demonstrated that salicylic acid (SAL) reduced bacterial adhesion, affected biofilm structural development, reduced viable biomass, extracellular proteins and polysaccharides, and promoted biofilm detachment (12). However, it was observed that the presence of SAL, the active component of aspirin, exhibited moderate iron-chelating capacity, which markedly promoted Staphylococcus aureus biofilm production (13). These different observations may have been due to differences in the experiment design, model use and aspirin concentrations.…”

Section: Discussionmentioning

confidence: 99%

Aspirin alleviates orthopedic implant‑associated infection

Jiang

Wang

et al. 2019

Int J Mol Med

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Implant-associated infection (IAI), a common condition marked by progressive inflammation and bone destruction, is mentally and financially devastating to those it affects, causing severe morbidity, prolonged hospital admissions, significant hospital costs and, in certain cases, mortality. Aspirin, a popular synthetic compound with a history of >100 years, is antipyretic, anti-inflammatory and analgesic. It is the most active component of non-steroidal anti-inflammatory drugs. However, the effects of aspirin on IAI remain unknown. In the present study, an IAI animal model was used, in which a stainless steel pin coated with Staphylococcus aureus was implanted through the left shaft of the tibia in mice. The animals were then randomized into five groups and subjected respectively to IAI, IAI + 15 mg aspirin treatment, IAI + 30 mg aspirin treatment, IAI + 60 mg aspirin treatment and IAI + 120 mg aspirin treatment groups. Aspirin was injected intraperitoneally twice daily for 11 days. Micro-CT and histological assays were performed to assess the effects of aspirin on IAI. It was found that aspirin reduced osteolysis and periosteal reaction, inhibited the activation of osteoclasts, promoted the activation of osteoblasts and facilitated healing of the infected fracture.

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Section: Discussionmentioning

confidence: 99%

Aspirin alleviates orthopedic implant‑associated infection

Jiang

Wang

et al. 2019

Int J Mol Med

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“…Ethanolic extracts of the carotenoid pigment from bacterial suspensions with equal optical density (OD) at 600 nm were quantified spectrophotometrically at 450 nm 63 . The quantitative assessment of biofilm formation was performed as previously described with modifications 64 . Briefly, S. aureus strains were grown for 18 h and diluted 1:100 in TSB supplemented with 0.25% of glucose (TSBg).…”

Section: Methodsmentioning

confidence: 99%

“…Three independent experiments were performed in sixtuplicate measurements. PIA production was assessed by ELISA according to a protocol described elsewhere 64 . Briefly, the procedure was similar to that described above for biofilm except that, after blocking solution removal,100 μl per well was added of a 75 ng/ml wheat germ agglutinin (WGA)-HRP conjugate, a lectin that binds to PIA sugar residues.…”

Section: Methodsmentioning

confidence: 99%

Acapsular Staphylococcus aureus with a non-functional agr regains capsule expression after passage through the bloodstream in a bacteremia mouse model

Suligoy

Díaz

Gehrke

et al. 2020

Sci Rep

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Selection pressures exerted on Staphylococcus aureus by host factors during infection may lead to the emergence of regulatory phenotypes better adapted to the infection site. traits convenient for persistence may be fixed by mutation thus turning these mutants into microevolution endpoints. The feasibility that stable, non-encapsulated S. aureus mutants can regain expression of key virulence factors for survival in the bloodstream was investigated. S. aureus agr mutant HU-14 (IS256 insertion in agrC) from a patient with chronic osteomyelitis was passed through the bloodstream using a bacteriemia mouse model and derivative P3.1 was obtained. Although IS256 remained inserted in agrC, P3.1 regained production of capsular polysaccharide type 5 (CP5) and staphyloxanthin. Furthermore, P3.1 expressed higher levels of asp23/SigB when compared with parental strain HU-14. Strain P3.1 displayed decreased osteoclastogenesis capacity, thus indicating decreased adaptability to bone compared with strain HU-14 and exhibited a trend to be more virulent than parental strain HU-14. Strain P3.1 exhibited the loss of one IS256 copy, which was originally located in the HU-14 noncoding region between dnaG (DNA primase) and rpoD (sigA). this loss may be associated with the observed phenotype change but the mechanism remains unknown. in conclusion, S. aureus organisms that escape the infected bone may recover the expression of key virulence factors through a rapid microevolution pathway involving SigB regulation of key virulence factors. Staphylococcus aureus is a transient, sometimes permanent member of the human microbiota in the nares and skin of a significant number of healthy individuals. As predisposing conditions emerge in the host, this opportunistic species may cause infections with different severity, ranging from mild skin and soft tissue infection to severe disseminated disease 1,2. Treatment of S. aureus infections is hampered by widespread dissemination of methicillin-resistant S. aureus (MRSA) 3 and by the frequent emergence of S. aureus with low level resistance to vancomycin 4. Whereas MRSA was primarily considered a nosocomial pathogen 5 , it is now unanimously accepted that MRSA also affects individuals of the general community with no previous exposure to health care settings 6,7. Up to 1.5-2% of patients receiving an orthopedic prosthetic device becomes infected and a significant number of these infections are caused by S. aureus. Most osteomyelitis caused by S. aureus become refractory to antibiotic treatment soon after bacteria settles on the prosthetic device surface and in bone tissue 1 .

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“…Biofilm formation was quantitatively assessed according to a procedure routinely performed in our laboratory (Dotto et al, 2017 ). Briefly, S. aureus suspensions were placed in sterile 96-well polystyrene microtiter plates.…”

Section: Methodsmentioning

confidence: 99%

Mutation of Agr Is Associated with the Adaptation of Staphylococcus aureus to the Host during Chronic Osteomyelitis

Suligoy

Lattar

Llana

et al. 2018

Front. Cell. Infect. Microbiol.

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Selection pressures exerted on Staphylococcus aureus by host factors may lead to the emergence of mutants better adapted to the evolving conditions at the infection site. This study was aimed at identifying the changes that occur in S. aureus exposed to the host defense mechanisms during chronic osteomyelitis and evaluating whether these changes affect the virulence of the organism. Genome assessment of two S. aureus isolates collected 13 months apart (HU-85a and HU-85c) from a host with chronic osteomyelitis was made by whole genome sequencing. Agr functionality was assessed by qRT-PCR. Isolates were tested in a rat model of osteomyelitis and the bacterial load (CFU/tibia) and the morphometric osteomyelitic index (OI) were determined. The ability of the isolates to trigger the release of proinflammatory cytokines was determined on macrophages in culture. Persistence of S. aureus within the host resulted in an agrC frameshift mutation that likely led to the observed phenotype. The capacity to cause bone tissue damage and trigger proinflammatory cytokines by macrophages of the agr-deficient, unencapsulated derivative (HU-85c) was decreased when compared with those of the isogenic CP8-capsulated parental strain (HU-85a). By comparison, no significant differences were found in the bacterial load or the OI from rats challenged with isogenic Reynolds strains [CP5, CP8, and non-typeable (NT)], indicating that lack of CP expression alone was not likely responsible for the reduced capacity to cause tissue damage in HU-85c compared with HU-85a. The production of biofilm was significantly increased in the isogenic derivative HU-85c. Lack of agr-dependent factors makes S. aureus less virulent during chronic osteomyelitis and alteration of the agr functionality seems to permit better adaptation of S. aureus to the chronically infected host.

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The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

Cited by 34 publications

References 72 publications

Aspirin alleviates orthopedic implant‑associated infection

Aspirin alleviates orthopedic implant‑associated infection

Acapsular Staphylococcus aureus with a non-functional agr regains capsule expression after passage through the bloodstream in a bacteremia mouse model

Mutation of Agr Is Associated with the Adaptation of Staphylococcus aureus to the Host during Chronic Osteomyelitis

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