haidut

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If the truly wonder-drug properties of aspirin were considered lacking by some medical authorities, now we can add curing sepsis to that list. Sepsis is the leading cause of death in hospitalized patients, regardless of age, condition, treatment, etc. It is largely considered a lost cause once organ failure starts to develop. There have been many attempts to develop drugs that treat it, and most of those attempts had focused on blocking the TLR4 receptor. However, as the study says, those clinical trials failed to show life-saving benefit even though they did find reduced inflammatory burden.
Anyways, it has been recently discovered that an enzyme called caspase may be the true cause for a cell to succumb to sepsis. So, inhibiting this enzyme sufficiently is likely to prevent the multiple organ failure and death commonly associated with sepsis. The study confirmed the life-saving effects of NSAID drugs like aspirin in an in-vivo model as well, so the likelihood of this working in humans is pretty high.
I don't have access to the full study, so I can't see what the effective dose/concentration for aspirin was. So, if somebody has access to the article please share so I can look at it in more detail.

http://www.cell.com/cell-chemical-biology/fulltext/S2451-9456(17)30033-8
Common drugs similar to ibuprofen could help treat sepsis, study suggests
"...But Yin’s research found that a subgroup of NSAIDs also act strongly and independently on another family of enzymes, caspases, which reside deep within the cell and have recently been found to play a key role in aggressive immune responses, like sepsis. “For instance, some chemicals derived from bacteria actually penetrate the cell and trigger the caspase response, prompting the cell to commit suicide. This also is known as apoptosis,” said Yin. “Such activation, in turn, potentially causes inflammation.”"

"...After the disappointing failure of late-stage clinical trials of anti-sepsis drugs targeting an immune receptor called toll-like receptor 4 (TLR4), located on the surface of cells, Yin and other scientists began to wonder if the key to halting the disease was to develop an antiseptic therapy that simultaneously targets caspases."

"...“It was a complete surprise,” said Yin. He and study co-author Ding Xue, a professor in the department of Molecular Cellular and Developmental Biology, then used biochemical and biophysical assays in the lab, as well as experiments with roundworms to test the theory further. “We showed that NSAIDs were effective in delaying cell death in worms, presumably by blocking caspase activity.”
 
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It's a bold claim. I think it will vary upon each bacteria species.
 
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tyw

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Aspirin and NSAIDs in general do nothing to kill the bacteria actually causing sepsis.

First, this is a worm study. There are other studies on animal tissue that reveal different effects.

Before getting to those studies, it is important to note caspases are enzymes that "slice up the cell" during the apoptotic mechanism. Forcible caspase inhibition is a tool to (temporarily) remove the knife from the hand of the cell, which has already decided to kill itself. There is nothing to stop the cell from trying to kill itself again if the stressor that caused the issue is not resolved.

This means that the mechanics by which the stressor causes harm must be understood, to know if caspase inhibition is buying life-saving time, or just delaying the inevitable.

eg: in the case of free radical induced cell death, it is usually the case whereby the cell has lost significant amounts of its cytochrome c oxidase activity, usually through detachment of the actual protein from mitochondria (for details, see Nick Lane's books). This is usually not a case where the cell can be saved.

Regarding pathogen induced sepsis, it depends on the exact mechanism by which the invading pathogen is functioning upon. In bacterial cases, whereby we have over expression of inflammatory signalling molecules, inhibiting caspase activity, and then getting rid of the bacteria, and then calming the cell down to stop responding to those inflammatory signals, are all necessary steps to prevent cell death. In viral cases where the Lytic cycle has already taken hold, the cell is doomed. More details here -- Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

Again, NSAIDs do not kill the pathogen. At best, they buy time for using other methods to kill the pathogen.

Then we have animal cell models.

- Gastric Cancer cells. NSAIDs activate caspase-3 and cause apoptosis. In this case, this is a good thing -- Non-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak | Carcinogenesis | Oxford Academic

- Case of Gastric ulcers. NSAIDs activate caspase-3, and can cause these potentially healthy cells to die. In this case, this is a bad thing -- Nonsteroidal Anti-Inflammatory Drug-Activated Gene-1 Plays a Role in the Impairing Effects of Cyclooxygenase Inhibitors on Gastric Ulcer Healing | Journal of Pharmacology and Experimental Therapeutics

- Effects of NSAIDs (aspirin included) on caspase activity in animal cells is complex as hell, and has many potential signalling pathways. Activation in caspase 8 and 9 frequently seen. Details here -- https://www.hindawi.com/journals/omcl/2013/504230/

No simple answer. Aspirin may help or hurt, and in the case of sepsis, does not kill the pathogen, and must therefore always be used with another anti-pathogen strategy.

......
 

paymanz

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If I understanded correctly, at least in this case it doesn't claim it aspirin has anti pathogenic activity, it just softens the inflammatory reaction of body,so it doesn't turn into a sepsis shock.
 

haidut

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It's a bold claim. I think it will vary upon each bacteria species.

The sepsis from bacteria relies largely upon the same mechanism. This study did not look at anti-bacterial effects but of effect on that general mechanism (caspase inhibition) so it should apply to any bacteria species.
 

haidut

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Aspirin and NSAIDs in general do nothing to kill the bacteria actually causing sepsis.

First, this is a worm study. There are other studies on animal tissue that reveal different effects.

Before getting to those studies, it is important to note caspases are enzymes that "slice up the cell" during the apoptotic mechanism. Forcible caspase inhibition is a tool to (temporarily) remove the knife from the hand of the cell, which has already decided to kill itself. There is nothing to stop the cell from trying to kill itself again if the stressor that caused the issue is not resolved.

This means that the mechanics by which the stressor causes harm must be understood, to know if caspase inhibition is buying life-saving time, or just delaying the inevitable.

eg: in the case of free radical induced cell death, it is usually the case whereby the cell has lost significant amounts of its cytochrome c oxidase activity, usually through detachment of the actual protein from mitochondria (for details, see Nick Lane's books). This is usually not a case where the cell can be saved.

Regarding pathogen induced sepsis, it depends on the exact mechanism by which the invading pathogen is functioning upon. In bacterial cases, whereby we have over expression of inflammatory signalling molecules, inhibiting caspase activity, and then getting rid of the bacteria, and then calming the cell down to stop responding to those inflammatory signals, are all necessary steps to prevent cell death. In viral cases where the Lytic cycle has already taken hold, the cell is doomed. More details here -- Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

Again, NSAIDs do not kill the pathogen. At best, they buy time for using other methods to kill the pathogen.

Then we have animal cell models.

- Gastric Cancer cells. NSAIDs activate caspase-3 and cause apoptosis. In this case, this is a good thing -- Non-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak | Carcinogenesis | Oxford Academic

- Case of Gastric ulcers. NSAIDs activate caspase-3, and can cause these potentially healthy cells to die. In this case, this is a bad thing -- Nonsteroidal Anti-Inflammatory Drug-Activated Gene-1 Plays a Role in the Impairing Effects of Cyclooxygenase Inhibitors on Gastric Ulcer Healing | Journal of Pharmacology and Experimental Therapeutics

- Effects of NSAIDs (aspirin included) on caspase activity in animal cells is complex as hell, and has many potential signalling pathways. Activation in caspase 8 and 9 frequently seen. Details here -- https://www.hindawi.com/journals/omcl/2013/504230/

No simple answer. Aspirin may help or hurt, and in the case of sepsis, does not kill the pathogen, and must therefore always be used with another anti-pathogen strategy.

......

Agreed, the mechanisms are complex and far from proven. But it is a very promising development for a drug that has shown so much systemic benefit. Actually, aspirin actually does seem to have anti-bacterial infection or at least protect people from dying from some bacterial infections.
Aspirin As A "novel" Potent Anti-bacterial Agent

The study I posted above did not look at such direct antibacterial activity and I don't think I implied that anywhere in my post. But evidence for antibacterial effects of aspirin is out there. Maybe this is in indeed the real mechanism for the protection the new study saw, and not the caspase mechanism since in some studies (as you pointed out) aspirin actually activates some caspase isoforms. Btw, there is another study somewhere on the forum where aspirin also showed potent antifungal activity and antibacterial activity even against Clostridium species. The EC50 was 1mM, which is achievable in humans with about 2g-3g single dose aspirin.
Finally, given the role of estrogen, serotonin, and histamine in promoting bacterial virulence and the damage the pathogen it does, at least some of the protection by aspirin is probably due to inhibiting the synthesis of estrogen, and the release of serotonin and histamine in the blood.
 

tyw

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Agreed, the mechanisms are complex and far from proven. But it is a very promising development for a drug that has shown so much systemic benefit. Actually, aspirin actually does seem to have anti-bacterial infection or at least protect people from dying from some bacterial infections.
Aspirin As A "novel" Potent Anti-bacterial Agent

The study I posted above did not look at such direct antibacterial activity and I don't think I implied that anywhere in my post. But evidence for antibacterial effects of aspirin is out there. Maybe this is in indeed the real mechanism for the protection the new study saw, and not the caspase mechanism since in some studies (as you pointed out) aspirin actually activates some caspase isoforms. Btw, there is another study somewhere on the forum where aspirin also showed potent antifungal activity and antibacterial activity even against Clostridium species. The EC50 was 1mM, which is achievable in humans with about 2g-3g single dose aspirin.
Finally, given the role of estrogen, serotonin, and histamine in promoting bacterial virulence and the damage the pathogen it does, at least some of the protection by aspirin is probably due to inhibiting the synthesis of estrogen, and the release of serotonin and histamine in the blood.

No, that study showed reduced mortality in people who were already taking aspirin, and happened to get infected. This was the study -- Low-Dose Acetylsalicylic Acid Treatment and Impact on Short-Term Mortality in Staphylococcus aureus Bloodstream Infection: A Propensity Score-Match... - PubMed - NCBI

This is a comparison of Aspirin + Antibacterial treatment vs only Antibacterial treatment. What we find is:

In S. aureus bloodstream infection cases, at day 30, 12.1% of cases and 27.4% of controls had died (hazard ratio, 0.40; p < 0.001).

Although ASA users were significantly more likely than nonusers to be on statins (61% vs. 20%), the two groups' other characteristics were similar, including length of hospital stay after BSI onset, time to adequate antibiotic therapy, and antimicrobial treatment duration.

In contrast, low-dose acetylsalicylic acid use was not associated with the primary endpoint in patients with E. coli bloodstream infection.​


At best, we can say that aspirin helped to potentiate the antibacterial treatment protocol. The massive difference in statin use is a huge factor as well, since cholesterol is an active immune compound.

Aspirin did nothing for E. coli infection.

A test for aspirins effect on pathogens would be simple. Take a set of cells:

- treat one group with aspirin / salicylic acid before pathogen infection
- treat one group with aspirin / salicylic acid after pathogen infection
- one control group without treatment

Compare actual pathogen colony growth before and after.

In fact, there was a recent study that showed the exact opposite -- The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

Treatment of mice with SAL induced a significant increase of S aureus colonization. It is suggested that the elevated PIA expression induced by SAL might be responsible for the high nasal colonization observed in mice.​

It was very clear that the more aspirin was given, the thicker the biofilms of MRSA (see figure 3).

Even this study, which claims aspirin to be effective on inhibiting Pseudomonas aeruginosa growth, used very very high doses, showed only partial inhibition at those high doses, and showed no effect in live animal experiments -- Salicylic Acid Reduces the Production of Several Potential Virulence Factors of Pseudomonas aeruginosa Associated with Microbial Keratitis | IOVS | ARVO Journals

Figure 1 demonstrates the effect on growth of 30 mM salicylic acid by strain 6294. After 24 hours of growth, the number of colony-forming units per milliliter of cells grown in the absence of salicylic acid was 4.98 × 10^9 cfu/mL ± 2.02 × 10^8 for strain 6294 or 4.43 × 10^9 cfu/mL ± 3.55 × 10^8 for strain 6206, and 3.62 × 10^9 cfu/mL ± 2.93 × 10^8 for strain 6294 or 4.42 × 10^9 cfu/mL ± 1.53 × 10^8 for strain 6206 grown in the presence of salicylic acid.
Reduction of 1 - (3.62 / 4.98) = 27.3% in strain 6294. No change in strain 6206.

Dosage is tens of times more than levels achievable through supplementation. Direct application of aspirin to affected tissues is needed (in this case, the eyes)

Reading through the paper, one will see anywhere from 30-50% reduction in the various measures of bacterial activity. The real question, is "Does this actually work in practice?"

However, it is the continued presence of inflammation, particularly PMNs in the cornea, that contributes to a large extent to the corneal destruction associated with keratitis.

Perhaps the addition of salicylic acid on presentation of a patient with Pseudomonas keratitis would benefit from the combined anti-virulence factor and anti-inflammatory functions of salicylic acid. If 1 mg/mL sodium salicylate is applied to the corneas of guinea pigs 4 hours after initiation of P. aeruginosa infection and subsequently every hour for 6 hours, there is no apparent reduction in the number of PMNs.​

In other words, likely no effect, but we don't know.

----

SIDENOTE: if we want to bring up the fact that in plants, salicylic acid is a "anti-pathogenic substance", this is irrelevant to humans.

Plants react specifically to salicylic acid stimulates the production of Pathogenesis-related (PR) proteins. It is these proteins that are responsible for the anti-pathogen response. In animals and humans, such proteins are not produced, and any mechanism of salicylic acid as anti-pathogen cannot be attributed to the plant-based mechanism.

I have also speculated that long chain polysaccharides may be part of this immune response in plants. It is clear that polysaccharides like PSK (found in Turkey Tail mushrooms) inhibit viral activity, but only if present before the onset of viral infection. Again, this is irrelevant to animals and humans, since we cannot make such polysaccharides.

....
 
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haidut

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No, that study showed reduced mortality in people who were already taking aspirin, and happened to get infected. This was the study -- Low-Dose Acetylsalicylic Acid Treatment and Impact on Short-Term Mortality in Staphylococcus aureus Bloodstream Infection: A Propensity Score-Match... - PubMed - NCBI

This is a comparison of Aspirin + Antibacterial treatment vs only Antibacterial treatment. What we find is:

In S. aureus bloodstream infection cases, at day 30, 12.1% of cases and 27.4% of controls had died (hazard ratio, 0.40; p < 0.001).

Although ASA users were significantly more likely than nonusers to be on statins (61% vs. 20%), the two groups' other characteristics were similar, including length of hospital stay after BSI onset, time to adequate antibiotic therapy, and antimicrobial treatment duration.

In contrast, low-dose acetylsalicylic acid use was not associated with the primary endpoint in patients with E. coli bloodstream infection.​


At best, we can say that aspirin helped to potentiate the antibacterial treatment protocol. The massive difference in statin use is a huge factor as well, since cholesterol is an active immune compound.

Aspirin did nothing for E. coli infection.

A test for aspirins effect on pathogens would be simple. Take a set of cells:

- treat one group with aspirin / salicylic acid before pathogen infection
- treat one group with aspirin / salicylic acid after pathogen infection
- one control group without treatment

Compare actual pathogen colony growth before and after.

In fact, there was a recent study that showed the exact opposite -- The Active Component of Aspirin, Salicylic Acid, Promotes Staphylococcus aureus Biofilm Formation in a PIA-dependent Manner

Treatment of mice with SAL induced a significant increase of S aureus colonization. It is suggested that the elevated PIA expression induced by SAL might be responsible for the high nasal colonization observed in mice.​

It was very clear that the more aspirin was given, the thicker the biofilms of MRSA (see figure 3).

Even this study, which claims aspirin to be effective on inhibiting Pseudomonas aeruginosa growth, used very very high doses, showed only partial inhibition at those high doses, and showed no effect in live animal experiments -- Salicylic Acid Reduces the Production of Several Potential Virulence Factors of Pseudomonas aeruginosa Associated with Microbial Keratitis | IOVS | ARVO Journals

Figure 1 demonstrates the effect on growth of 30 mM salicylic acid by strain 6294. After 24 hours of growth, the number of colony-forming units per milliliter of cells grown in the absence of salicylic acid was 4.98 × 10^9 cfu/mL ± 2.02 × 10^8 for strain 6294 or 4.43 × 10^9 cfu/mL ± 3.55 × 10^8 for strain 6206, and 3.62 × 10^9 cfu/mL ± 2.93 × 10^8 for strain 6294 or 4.42 × 10^9 cfu/mL ± 1.53 × 10^8 for strain 6206 grown in the presence of salicylic acid.
Reduction of 1 - (3.62 / 4.98) = 27.3% in strain 6294. No change in strain 6206.

Dosage is tens of times more than levels achievable through supplementation. Direct application of aspirin to affected tissues is needed (in this case, the eyes)

Reading through the paper, one will see anywhere from 30-50% reduction in the various measures of bacterial activity. The real question, is "Does this actually work in practice?"

However, it is the continued presence of inflammation, particularly PMNs in the cornea, that contributes to a large extent to the corneal destruction associated with keratitis.

Perhaps the addition of salicylic acid on presentation of a patient with Pseudomonas keratitis would benefit from the combined anti-virulence factor and anti-inflammatory functions of salicylic acid. If 1 mg/mL sodium salicylate is applied to the corneas of guinea pigs 4 hours after initiation of P. aeruginosa infection and subsequently every hour for 6 hours, there is no apparent reduction in the number of PMNs.​

In other words, likely no effect, but we don't know.

----

SIDENOTE: if we want to bring up the fact that in plants, salicylic acid is a "anti-pathogenic substance", this is irrelevant to humans.

Plants react specifically to salicylic acid stimulates the production of Pathogenesis-related (PR) proteins. It is these proteins that are responsible for the anti-pathogen response. In animals and humans, such proteins are not produced, and any mechanism of salicylic acid as anti-pathogen cannot be attributed to the plant-based mechanism.

I have also speculated that long chain polysaccharides may be part of this immune response in plants. It is clear that polysaccharides like PSK (found in Turkey Tail mushrooms) inhibit viral activity, but only if present before the onset of viral infection. Again, this is irrelevant to animals and humans, since we cannot make such polysaccharides.

....

I beg to disagree. There are multiple studies showing direct anti-bacterial effect of aspirin, both in cultures and in vivo. I am not saying "aspirin is the new antibiotic" kind of thing, but there is plenty of evidence doing pretty much what you suggested with the set of pre-infected, post-infected and control cells. I read some of these studies long time ago, and are not near my main computer right now to look into the details, but here are some of the most notable ones. One of the studies is on Candida, but I thought to include it anyways given the discussion of biofilms.

The assessment of the antibacterial and antifungal activities of aspirin, EDTA and aspirin-EDTA combination and their effectiveness as antibiofilm ... - PubMed - NCBI
"...METHODS AND RESULTS: Minimal inhibitory concentrations (MIC) and minimal biocidal concentrations (MBC) were determined using twofold broth microdilution and viable counting methods, respectively. Aspirin's recorded MIC values ranged from 1.2 to 2.7 mg ml(-1). Checkerboard assay demonstrated a synergism in antimicrobial activity upon combination. Aspirin's minimal biofilm eradication concentration values (MBEC) against the established biofilms ranged between 1.35 and 3.83 mg ml(-1). A complete eradication of bacterial biofilms was achieved after a 4-h treatment with the A-EDTA combination.
CONCLUSION: Both aspirin and EDTA possess broad-spectrum antimicrobial activity for both planktonic and biofilm cultures. Aspirin used at the MBEC for 24 h was successful in eradicating P. aeruginosa, E. coli and C. albicans biofilms established on abiotic surfaces. Moreover, the exposure to the A-EDTA combination (4 h) effected complete bacterial biofilm eradication."

Antibacterial effect of NSAIDS on clinical isolates of urinary tract infection and diabetic foot infection. - PubMed - NCBI
"...Antibacterial effect of Aspirin and Tylenol were tested against 100 clinical isolates by Replica plate method, Agar well diffusion method and tube dilution method. Concentrations of Aspirin and Tylenol (10 microg, 50 microg, 100 microg, 500 microg, 1000 microg) were made in Muller Hinton media. Bacteria isolated from urine samples were Escherichia coli 30%, Staphylococcus aureus 20%, Enterococcus faecalis 10%, S. saprophyticus 10%, Proteus spp. 6%, Pseudomonas spp. 6%, S. pyogenes 6%, S. agalactiae 6%, S. epidermidis 4%, and Klebsiella spp. 2%. Bacteria isolated from pus samples were S. aureus 30%, Pseudomonas aeruginosa 18%, S. epidermidis 14%, Klebsiella pneumonia 12%, Proteus mirabilis 12%, E. coli 10%, P. vulgaris 4%. Aspirin was effective at 100-500 microg concentration against all isolates. Tylenol has marked effect on pathogens at 100 microg concentration. Aspirin and Tylenol along with analgesic, anti-pyretic, anti-inflammatory properties also have marked anti bacterial effect on isolates from UTI and Diabetic foot infections and inhibits the growth of both gram negative and gram positive bacteria, and both can be used synergistically with antibiotics for effective treatment."

Effects of Aspirin and Other Nonsteroidal Anti-Inflammatory Drugs on Biofilms and Planktonic Cells of Candida albicans
"...Prostaglandins are now known to be produced by Candida albicans and may play an important role in fungal colonization. Their synthesis in mammalian cells is decreased by inhibitors of the cyclooxygenase isoenzymes required for prostaglandin formation. In the present study, a catheter disk model system was used to investigate the effects of nonsteroidal anti-inflammatory drugs (all cyclooxygenase inhibitors) on biofilm formation by three strains of C. albicans. Seven of nine drugs tested at a concentration of 1 mM inhibited biofilm formation. Aspirin, etodolac, and diclofenac produced the greatest effects, with aspirin causing up to 95% inhibition. Celecoxib, nimesulide, ibuprofen, and meloxicam also inhibited biofilm formation, but to a lesser extent. Aspirin was active against growing and fully mature (48-h) biofilms; its effect was dose related, and it produced significant inhibition (20 to 80%) at pharmacological concentrations. Simultaneous addition of prostaglandin E2 abolished the inhibitory effect of 25 or 50 μM aspirin. At 1 mM, aspirin reduced the viability of biofilm organisms to 1.9% of that of controls. Surviving cells had a wrinkled appearance, as judged by scanning electron microscopy, and consisted of both yeasts and hyphae. Treatment with other cyclooxygenase inhibitors, such as etodolac, resulted in biofilms that consisted almost entirely of yeast cells. In conventional assays for germ tube formation, these drugs produced significant inhibition, whereas aspirin had little effect. Our findings suggest that cyclooxygenase-dependent synthesis of fungal prostaglandin(s) is important for both biofilm development and morphogenesis in C. albicans and may act as a regulator in these physiological processes. Our results also demonstrate that aspirin possesses potent antibiofilm activity in vitro and could be useful in combined therapy with conventional antifungal agents in the management of some biofilm-associated Candidainfections."

Finally, a study discussing one novel pathway through which aspirin (and possible niacinamide) act against bacteria - inhbition of fatty acid metabolism.
Aspirin: the anti-inflammatory, antifungal, antibacterial agent?
"...The article talks about acetylsalicylic acid or aspirin, which lessens inflammation in humans and also hampers yeast reproduction through the inhibition of 3-hydroxy fatty acid (3-OH FA) metabolism. Since 3-OH FAs are also found in Gramnegative bacteria as a crucial component of inflammatory, disease-causing endotoxin production, the possibility to control Gram-negative bacterial infections, as well as yeast infestations, with aspirin or other non-steroidal anti-inflammatory drugs is hypothesized. Latest research suggests that aside from broad anti-inflammatory actions, aspirin also has profound effects on budding yeasts. More information on the subject matter is given."

Again, too early to say is aspirin would be effective for sepsis but to chalk it up completely to the category of "we just don't know" is not warranted in my opinion. Maybe a better category would be "sounds promising but more in vivo (and especially human studies) are needed". But to me the last study is too coherent with what we know about the role fatty acid oxidation and a host of diseases to ascribe to coincidence.
 

tyw

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@haidut The first two studies did not use cell culture. The second two studies used yeast cells (of fungi kingdom, not animal).

The two studies I quoted were done on animal tissue, with some in vivo treatment, and yielded minor to no result.

I should qualify my statement then: We don't know if aspirin works as an anti-pathogenic aid in animals, nor on what types of pathogens it is effective against, nor in what ways it works synergistically (or not) with other treatment protocols.

....
 

Jarman

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@haidut The first two studies did not use cell culture. The second two studies used yeast cells (of fungi kingdom, not animal).

The two studies I quoted were done on animal tissue, with some in vivo treatment, and yielded minor to no result.

I should qualify my statement then: We don't know if aspirin works as an anti-pathogenic aid in animals, nor on what types of pathogens it is effective against, nor in what ways it works synergistically (or not) with other treatment protocols.

....

@tyw I really like your posts and enjoy them very much. Thank you for your sharing your great knowledge to the community. Take care
 

haidut

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MB50

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Thats what separates this forum from many others: the ability to engage in objective discussion (most of the time) without getting overly emotional. These discussions are helpful to all of us, so thanks for that.
 

haidut

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@haidut The first two studies did not use cell culture. The second two studies used yeast cells (of fungi kingdom, not animal).

The two studies I quoted were done on animal tissue, with some in vivo treatment, and yielded minor to no result.

I should qualify my statement then: We don't know if aspirin works as an anti-pathogenic aid in animals, nor on what types of pathogens it is effective against, nor in what ways it works synergistically (or not) with other treatment protocols.

....

OK, then here is an in-vivo study, with a low dose aspirin (HED 3.3mg/kg) showing the greatest effectiveness in inhibiting development of infection. The only drawback is that the aspirin-only group was given the aspirin as preventative and not as treatment. The actual tratment group was antibiotic + aspirin. In both cases aspirin showed benefit. It would have been great if there was an aspirin-only treatment group :-(
http://aac.asm.org/content/39/8/1748.full.pdf
"...Ninety-three animals successfully completed this portion of the protocol (control [n 5 18], and 2.5 [n 5 18]-, 10 [n 5 20]-, 20 [n 5 18]-, and 50 [n 5 19]-mg/kg ASA groups]. There were no differences in the concentrations of the initial inoculum between treatment groups. The relationships between vegetation weight (in milligrams) and bacterial density (log10 CFU per gram) versus the ASA dosage are shown in Table 1. The 2.5- and 10-mg/kg treatment groups had a statistically significant reduction in vegetative weight compared with the untreated controls (P 5 0.0001). In addition, the 2.5-mg/kg dose also resulted in a statistically significant reduction in weight compared with the 20-mg/kg group (P 5 0.0001). The 20- and the 50-mg/kg groups showed a reduction; however, this was not statistically significant. Regarding the bacterial density, the 10-mg/kg dose resulted in a significant decrease compared with untreated controls (P 5 0.0084). Although reductions were also evident in the other treatment groups compared with controls, these reductions did not reach statistical significance."
"...The treatment study also reveals that when ASA is combined with vancomycin, it not only reduces the vegetation weight but also improves the sterilization rate of aortic valve vegetations infected with S. aureus. The increased sterilization rate may be explained because ASA reduces the bacterial density and size of the vegetation and therefore not only lowers the total microbial load within the vegetation but also increases the potential exposure of organism to the antimicrobial agent via improved penetration and distribution throughout the infection site. Although the exact mechanism for these observations has not been fully elucidated, the dose-dependent effect suggests that the mechanism involves more than just the prevention of platelet aggregation, for this can be accomplished with a variety of doses (14). Although these observations may be due in part to ASA’s direct effect on platelets, it is likely that this agent’s effect on prostacyclin and mediators of adherence, such as thrombospondin and fibronection, also contributes to the observed reduction in both bacterial density and vegetation weight. In addition, the reduction in vegetation weight observed with ASA therapy may have other important clinical implications, such as decreasing the incidence of embolic phenomena that are commonly experienced with endocarditis (13). Although many questions remain and other investigations are required to determine the mechanism responsible for our observations, this study provides encouraging data regarding the role of ASA therapy in the treatment of infective endocarditis."


And two human studies.
Aspirin treatment is associated with a significantly decreased risk of Staphylococcus aureus bacteremia in hemodialysis patients with tunneled cath... - PubMed - NCBI
Aspirin treatment for neonatal infectious endocarditis. - PubMed - NCBI
 
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lollipop

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Thats what separates this forum from many others: the ability to engage in objective discussion (most of the time) without getting overly emotional. These discussions are helpful to all of us, so thanks for that.
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