Re: RESEARCH - Anti-inflammatory fish-oil EPA product resolvin is blocked by COX-2 inhibitors

[Guest guest]

,

If I'm reading this right, the resolvin in fish oil helps decrease

inflammation but when we take cox-2's it counteracts the resolvin and

we loose the benefits of fish oil. If so this may explain why some

people get relief from fish oil and others don't. But then I think

I'm reading that aspirin increases the resolvin, so that means if

aspirin and fish oil were taken together, the anti-inflammatory

properties of the fish oil would increase. Is this your take on this

article?

a

On Thu, 10 Mar 2005 07:43:38 -0600, <Matsumura_Clan@...> wrote:

> Anti-inflammatory fish-oil EPA product resolvin is blocked by COX-2

> inhibitors

>

>

> Rheumawire

> Mar 7, 2005

> Janis

>

> Boston, MA - The anti-inflammatory effect of fish oils appears to be due to

> a powerful anti-inflammatory compound called resolvin (resolution-phase

> interaction product) E1, which is produced from eicosapentaenoic acid

> (EPA),

> Dr Makoto Arita (Brigham and Women's Hospital and Harvard Medical School,

> Boston, MA) and colleagues report in the March 7, 2005 issue of the Journal

> of Experimental Medicine [1]. Arita writes, " At nanomolar levels, resolvin

> E1 dramatically reduced dermal inflammation, peritonitis, dendritic cell

> migration, and interleukin (IL)-12 production. "

>

> Senior author Dr N Serhan (Brigham and Women's Hospital, Harvard

> Medical School) tells rheumawire that the resolvin E1 pathway might also

> explain some of the untoward cardiovascular effects of the COX-2

> inhibitors.

>

> " In vitro, we found that inhibiting vascular endothelial cells' COX-2

> blocks

> the biosynthesis of resolvin E1. In humans, in vivo evidence is needed, and

> this would require a clinical trial. Maybe our findings can serve as the

> base for such future clinical studies, " says Serhan.

>

> Aspirin increases, coxibs decrease resolvin E1 biosynthesis

> In contrast to the coxib effect, Serhan's group had previously found that

> aspirin triggers the conversion of EPA to various resolvins and had

> identified resolvin E1 in the plasma of human subjects given omega-3 fatty

> acids and aspirin.

>

> Resolvin E1 was discovered in vivo during the resolution phase of

> inflammation in exudates from inflamed tissues in a mouse model. The main

> task of resolvin E1 appears to be to serve as a counterregulator to

> proinflammatory mediators and turn down acute inflammatory processes before

> too much damage is done to normal tissue.

>

> " The resolution of inflammation is an active process controlled in part by

> endogenous chemical mediators that counterregulate proinflammatory gene

> expression and cell trafficking as well as stimulate inflammatory cell

> clearance, " the authors write.

>

> The current study showed that as little as 100 ng/mouse of synthetic

> resolvin E1 could decrease leukocyte infiltration into inflammatory loci by

> 50% to 60% in a mouse model of tumor-necrosis-factor (TNF)--induced

> inflammation. By comparison, local administration of dexamethasone produced

> 60% inhibition in this model, aspirin produced 70% inhibition, and

> indomethacin gave 25% inhibition.

>

> Resolvin counteracts the effect of TNF-

> The investigators found that the resolvin E1 anti-inflammatory effect is

> mediated via the ChemR23 receptor, activation of which inhibits NF-B

> activation. Resolvin E1 thus acts as a selective agonist that

> counterregulates TNF-. The ChemR23 receptor was mapped in cardiovascular,

> brain, kidney, gastrointestinal, and myeloid tissues.

>

> " It is possible that loss of resolvin pathways like the one we documented

> here could give rise to ongoing chronic inflammatory phenotypesas being

> unable to actively turn off acute responses, rather then [as suggested by]

> the current thinking that chronic inflammatory diseases arise by enhanced

> inflammation, " Serhan says. He adds that resolvin E1 and its receptor

> present possible targets for therapeutic intervention.

>

> The researchers conclude, " Together, our findings offer an endogenous

> agonist-driven molecular mechanism that can underlie some of the beneficial

> actions of omega-3 EPA observed in many clinical situations, as well as

> identify novel components in endogenous anti-inflammation/resolution,

> namely

> resolvin E1 and its receptor, that are of interest as new checkpoint

> regulators that may be involved in the pathogenesis of a wide range of

> human

> diseases. "

>

>

> Source

>

> Arita M, Bianchini F, Aliberti J, et al. Stereochemical

> assignment, anti-inflammatory properties, and receptor for the omega-3

> lipid

> mediator resolving E1. J Exp Med 2005; 201: DOI:10.1084/jem.20042031.

> Available at: http://www.jem.org.

>

>

>

>

>

>

> Not an MD

>

> I'll tell you where to go!

>

> Mayo Clinic in Rochester

> http://www.mayoclinic.org/rochester

>

> s Hopkins Medicine

> http://www.hopkinsmedicine.org

>

>

>

>

[Guest guest]

,

If I'm reading this right, the resolvin in fish oil helps decrease

inflammation but when we take cox-2's it counteracts the resolvin and

we loose the benefits of fish oil. If so this may explain why some

people get relief from fish oil and others don't. But then I think

I'm reading that aspirin increases the resolvin, so that means if

aspirin and fish oil were taken together, the anti-inflammatory

properties of the fish oil would increase. Is this your take on this

article?

a

On Thu, 10 Mar 2005 07:43:38 -0600, <Matsumura_Clan@...> wrote:

> Anti-inflammatory fish-oil EPA product resolvin is blocked by COX-2

> inhibitors

>

>

> Rheumawire

> Mar 7, 2005

> Janis

>

> Boston, MA - The anti-inflammatory effect of fish oils appears to be due to

> a powerful anti-inflammatory compound called resolvin (resolution-phase

> interaction product) E1, which is produced from eicosapentaenoic acid

> (EPA),

> Dr Makoto Arita (Brigham and Women's Hospital and Harvard Medical School,

> Boston, MA) and colleagues report in the March 7, 2005 issue of the Journal

> of Experimental Medicine [1]. Arita writes, " At nanomolar levels, resolvin

> E1 dramatically reduced dermal inflammation, peritonitis, dendritic cell

> migration, and interleukin (IL)-12 production. "

>

> Senior author Dr N Serhan (Brigham and Women's Hospital, Harvard

> Medical School) tells rheumawire that the resolvin E1 pathway might also

> explain some of the untoward cardiovascular effects of the COX-2

> inhibitors.

>

> " In vitro, we found that inhibiting vascular endothelial cells' COX-2

> blocks

> the biosynthesis of resolvin E1. In humans, in vivo evidence is needed, and

> this would require a clinical trial. Maybe our findings can serve as the

> base for such future clinical studies, " says Serhan.

>

> Aspirin increases, coxibs decrease resolvin E1 biosynthesis

> In contrast to the coxib effect, Serhan's group had previously found that

> aspirin triggers the conversion of EPA to various resolvins and had

> identified resolvin E1 in the plasma of human subjects given omega-3 fatty

> acids and aspirin.

>

> Resolvin E1 was discovered in vivo during the resolution phase of

> inflammation in exudates from inflamed tissues in a mouse model. The main

> task of resolvin E1 appears to be to serve as a counterregulator to

> proinflammatory mediators and turn down acute inflammatory processes before

> too much damage is done to normal tissue.

>

> " The resolution of inflammation is an active process controlled in part by

> endogenous chemical mediators that counterregulate proinflammatory gene

> expression and cell trafficking as well as stimulate inflammatory cell

> clearance, " the authors write.

>

> The current study showed that as little as 100 ng/mouse of synthetic

> resolvin E1 could decrease leukocyte infiltration into inflammatory loci by

> 50% to 60% in a mouse model of tumor-necrosis-factor (TNF)--induced

> inflammation. By comparison, local administration of dexamethasone produced

> 60% inhibition in this model, aspirin produced 70% inhibition, and

> indomethacin gave 25% inhibition.

>

> Resolvin counteracts the effect of TNF-

> The investigators found that the resolvin E1 anti-inflammatory effect is

> mediated via the ChemR23 receptor, activation of which inhibits NF-B

> activation. Resolvin E1 thus acts as a selective agonist that

> counterregulates TNF-. The ChemR23 receptor was mapped in cardiovascular,

> brain, kidney, gastrointestinal, and myeloid tissues.

>

> " It is possible that loss of resolvin pathways like the one we documented

> here could give rise to ongoing chronic inflammatory phenotypesas being

> unable to actively turn off acute responses, rather then [as suggested by]

> the current thinking that chronic inflammatory diseases arise by enhanced

> inflammation, " Serhan says. He adds that resolvin E1 and its receptor

> present possible targets for therapeutic intervention.

>

> The researchers conclude, " Together, our findings offer an endogenous

> agonist-driven molecular mechanism that can underlie some of the beneficial

> actions of omega-3 EPA observed in many clinical situations, as well as

> identify novel components in endogenous anti-inflammation/resolution,

> namely

> resolvin E1 and its receptor, that are of interest as new checkpoint

> regulators that may be involved in the pathogenesis of a wide range of

> human

> diseases. "

>

>

> Source

>

> Arita M, Bianchini F, Aliberti J, et al. Stereochemical

> assignment, anti-inflammatory properties, and receptor for the omega-3

> lipid

> mediator resolving E1. J Exp Med 2005; 201: DOI:10.1084/jem.20042031.

> Available at: http://www.jem.org.

>

>

>

>

>

>

> Not an MD

>

> I'll tell you where to go!

>

> Mayo Clinic in Rochester

> http://www.mayoclinic.org/rochester

>

> s Hopkins Medicine

> http://www.hopkinsmedicine.org

>

>

>

>

[Guest guest]

This one is very cool, a.

When they talk about the " resolvin E1 pathway, " they are referring to a

chain

of events where certain things have to happen before the resolvin is

synthesized.

They don't know for sure since they didn't study it in humans (in vivo),

but, in the lab (in vitro), there is evidence that blocking COX-2 might

interfere with the production of resolvin.

So, you start out with EPA which is needed for the synthesis of resolvin.

Blocking COX-2 interferes with the process, but, in another study, adding

aspirin was shown to enhance it.

Even traditional NSAIDs block COX-2, so this is something interesting to

think about.

A side note: I remember asking my first rheumatologist in 1996 about the

value of fish oil. He told me that I would have to eat so much before I

noticed any relief that I would smell like a fish. I used it anyway and

still do. Nobody has told me yet that I stink, LOL.

Not an MD

I'll tell you where to go!

Mayo Clinic in Rochester

http://www.mayoclinic.org/rochester

s Hopkins Medicine

http://www.hopkinsmedicine.org

Re: [ ] RESEARCH - Anti-inflammatory fish-oil EPA product

resolvin is blocked by COX-2 inhibitors

>

> ,

> If I'm reading this right, the resolvin in fish oil helps decrease

> inflammation but when we take cox-2's it counteracts the resolvin and

> we loose the benefits of fish oil. If so this may explain why some

> people get relief from fish oil and others don't. But then I think

> I'm reading that aspirin increases the resolvin, so that means if

> aspirin and fish oil were taken together, the anti-inflammatory

> properties of the fish oil would increase. Is this your take on this

> article?

> a

>

>

>

> On Thu, 10 Mar 2005 07:43:38 -0600, <Matsumura_Clan@...>

> wrote:

>> Anti-inflammatory fish-oil EPA product resolvin is blocked by COX-2

>> inhibitors

>>

>>

>> Rheumawire

>> Mar 7, 2005

>> Janis

>>

>> Boston, MA - The anti-inflammatory effect of fish oils appears to be due

>> to

>> a powerful anti-inflammatory compound called resolvin (resolution-phase

>> interaction product) E1, which is produced from eicosapentaenoic acid

>> (EPA),

>> Dr Makoto Arita (Brigham and Women's Hospital and Harvard Medical

>> School,

>> Boston, MA) and colleagues report in the March 7, 2005 issue of the

>> Journal

>> of Experimental Medicine [1]. Arita writes, " At nanomolar levels,

>> resolvin

>> E1 dramatically reduced dermal inflammation, peritonitis, dendritic cell

>> migration, and interleukin (IL)-12 production. "

>>

>> Senior author Dr N Serhan (Brigham and Women's Hospital, Harvard

>> Medical School) tells rheumawire that the resolvin E1 pathway might also

>> explain some of the untoward cardiovascular effects of the COX-2

>> inhibitors.

>>

>> " In vitro, we found that inhibiting vascular endothelial cells' COX-2

>> blocks

>> the biosynthesis of resolvin E1. In humans, in vivo evidence is needed,

>> and

>> this would require a clinical trial. Maybe our findings can serve as the

>> base for such future clinical studies, " says Serhan.

>>

>> Aspirin increases, coxibs decrease resolvin E1 biosynthesis

>> In contrast to the coxib effect, Serhan's group had previously found

>> that

>> aspirin triggers the conversion of EPA to various resolvins and had

>> identified resolvin E1 in the plasma of human subjects given omega-3

>> fatty

>> acids and aspirin.

>>

>> Resolvin E1 was discovered in vivo during the resolution phase of

>> inflammation in exudates from inflamed tissues in a mouse model. The

>> main

>> task of resolvin E1 appears to be to serve as a counterregulator to

>> proinflammatory mediators and turn down acute inflammatory processes

>> before

>> too much damage is done to normal tissue.

>>

>> " The resolution of inflammation is an active process controlled in part

>> by

>> endogenous chemical mediators that counterregulate proinflammatory gene

>> expression and cell trafficking as well as stimulate inflammatory cell

>> clearance, " the authors write.

>>

>> The current study showed that as little as 100 ng/mouse of synthetic

>> resolvin E1 could decrease leukocyte infiltration into inflammatory loci

>> by

>> 50% to 60% in a mouse model of tumor-necrosis-factor (TNF)--induced

>> inflammation. By comparison, local administration of dexamethasone

>> produced

>> 60% inhibition in this model, aspirin produced 70% inhibition, and

>> indomethacin gave 25% inhibition.

>>

>> Resolvin counteracts the effect of TNF-

>> The investigators found that the resolvin E1 anti-inflammatory effect is

>> mediated via the ChemR23 receptor, activation of which inhibits NF-B

>> activation. Resolvin E1 thus acts as a selective agonist that

>> counterregulates TNF-. The ChemR23 receptor was mapped in

>> cardiovascular,

>> brain, kidney, gastrointestinal, and myeloid tissues.

>>

>> " It is possible that loss of resolvin pathways like the one we

>> documented

>> here could give rise to ongoing chronic inflammatory phenotypesas being

>> unable to actively turn off acute responses, rather then [as suggested

>> by]

>> the current thinking that chronic inflammatory diseases arise by

>> enhanced

>> inflammation, " Serhan says. He adds that resolvin E1 and its receptor

>> present possible targets for therapeutic intervention.

>>

>> The researchers conclude, " Together, our findings offer an endogenous

>> agonist-driven molecular mechanism that can underlie some of the

>> beneficial

>> actions of omega-3 EPA observed in many clinical situations, as well as

>> identify novel components in endogenous anti-inflammation/resolution,

>> namely

>> resolvin E1 and its receptor, that are of interest as new checkpoint

>> regulators that may be involved in the pathogenesis of a wide range of

>> human

>> diseases. "

>>

>>

>> Source

>>

>> Arita M, Bianchini F, Aliberti J, et al. Stereochemical

>> assignment, anti-inflammatory properties, and receptor for the omega-3

>> lipid

>> mediator resolving E1. J Exp Med 2005; 201: DOI:10.1084/jem.20042031.

>> Available at: http://www.jem.org.

>>

>>

>>

>>

>>

>>

>> Not an MD

>>

>> I'll tell you where to go!

>>

>> Mayo Clinic in Rochester

>> http://www.mayoclinic.org/rochester

>>

>> s Hopkins Medicine

>> http://www.hopkinsmedicine.org

>>

>>

>>

>>

[Guest guest]

This one is very cool, a.

When they talk about the " resolvin E1 pathway, " they are referring to a

chain

of events where certain things have to happen before the resolvin is

synthesized.

They don't know for sure since they didn't study it in humans (in vivo),

but, in the lab (in vitro), there is evidence that blocking COX-2 might

interfere with the production of resolvin.

So, you start out with EPA which is needed for the synthesis of resolvin.

Blocking COX-2 interferes with the process, but, in another study, adding

aspirin was shown to enhance it.

Even traditional NSAIDs block COX-2, so this is something interesting to

think about.

A side note: I remember asking my first rheumatologist in 1996 about the

value of fish oil. He told me that I would have to eat so much before I

noticed any relief that I would smell like a fish. I used it anyway and

still do. Nobody has told me yet that I stink, LOL.

Not an MD

I'll tell you where to go!

Mayo Clinic in Rochester

http://www.mayoclinic.org/rochester

s Hopkins Medicine

http://www.hopkinsmedicine.org

Re: [ ] RESEARCH - Anti-inflammatory fish-oil EPA product

resolvin is blocked by COX-2 inhibitors

>

> ,

> If I'm reading this right, the resolvin in fish oil helps decrease

> inflammation but when we take cox-2's it counteracts the resolvin and

> we loose the benefits of fish oil. If so this may explain why some

> people get relief from fish oil and others don't. But then I think

> I'm reading that aspirin increases the resolvin, so that means if

> aspirin and fish oil were taken together, the anti-inflammatory

> properties of the fish oil would increase. Is this your take on this

> article?

> a

>

>

>

> On Thu, 10 Mar 2005 07:43:38 -0600, <Matsumura_Clan@...>

> wrote:

>> Anti-inflammatory fish-oil EPA product resolvin is blocked by COX-2

>> inhibitors

>>

>>

>> Rheumawire

>> Mar 7, 2005

>> Janis

>>

>> Boston, MA - The anti-inflammatory effect of fish oils appears to be due

>> to

>> a powerful anti-inflammatory compound called resolvin (resolution-phase

>> interaction product) E1, which is produced from eicosapentaenoic acid

>> (EPA),

>> Dr Makoto Arita (Brigham and Women's Hospital and Harvard Medical

>> School,

>> Boston, MA) and colleagues report in the March 7, 2005 issue of the

>> Journal

>> of Experimental Medicine [1]. Arita writes, " At nanomolar levels,

>> resolvin

>> E1 dramatically reduced dermal inflammation, peritonitis, dendritic cell

>> migration, and interleukin (IL)-12 production. "

>>

>> Senior author Dr N Serhan (Brigham and Women's Hospital, Harvard

>> Medical School) tells rheumawire that the resolvin E1 pathway might also

>> explain some of the untoward cardiovascular effects of the COX-2

>> inhibitors.

>>

>> " In vitro, we found that inhibiting vascular endothelial cells' COX-2

>> blocks

>> the biosynthesis of resolvin E1. In humans, in vivo evidence is needed,

>> and

>> this would require a clinical trial. Maybe our findings can serve as the

>> base for such future clinical studies, " says Serhan.

>>

>> Aspirin increases, coxibs decrease resolvin E1 biosynthesis

>> In contrast to the coxib effect, Serhan's group had previously found

>> that

>> aspirin triggers the conversion of EPA to various resolvins and had

>> identified resolvin E1 in the plasma of human subjects given omega-3

>> fatty

>> acids and aspirin.

>>

>> Resolvin E1 was discovered in vivo during the resolution phase of

>> inflammation in exudates from inflamed tissues in a mouse model. The

>> main

>> task of resolvin E1 appears to be to serve as a counterregulator to

>> proinflammatory mediators and turn down acute inflammatory processes

>> before

>> too much damage is done to normal tissue.

>>

>> " The resolution of inflammation is an active process controlled in part

>> by

>> endogenous chemical mediators that counterregulate proinflammatory gene

>> expression and cell trafficking as well as stimulate inflammatory cell

>> clearance, " the authors write.

>>

>> The current study showed that as little as 100 ng/mouse of synthetic

>> resolvin E1 could decrease leukocyte infiltration into inflammatory loci

>> by

>> 50% to 60% in a mouse model of tumor-necrosis-factor (TNF)--induced

>> inflammation. By comparison, local administration of dexamethasone

>> produced

>> 60% inhibition in this model, aspirin produced 70% inhibition, and

>> indomethacin gave 25% inhibition.

>>

>> Resolvin counteracts the effect of TNF-

>> The investigators found that the resolvin E1 anti-inflammatory effect is

>> mediated via the ChemR23 receptor, activation of which inhibits NF-B

>> activation. Resolvin E1 thus acts as a selective agonist that

>> counterregulates TNF-. The ChemR23 receptor was mapped in

>> cardiovascular,

>> brain, kidney, gastrointestinal, and myeloid tissues.

>>

>> " It is possible that loss of resolvin pathways like the one we

>> documented

>> here could give rise to ongoing chronic inflammatory phenotypesas being

>> unable to actively turn off acute responses, rather then [as suggested

>> by]

>> the current thinking that chronic inflammatory diseases arise by

>> enhanced

>> inflammation, " Serhan says. He adds that resolvin E1 and its receptor

>> present possible targets for therapeutic intervention.

>>

>> The researchers conclude, " Together, our findings offer an endogenous

>> agonist-driven molecular mechanism that can underlie some of the

>> beneficial

>> actions of omega-3 EPA observed in many clinical situations, as well as

>> identify novel components in endogenous anti-inflammation/resolution,

>> namely

>> resolvin E1 and its receptor, that are of interest as new checkpoint

>> regulators that may be involved in the pathogenesis of a wide range of

>> human

>> diseases. "

>>

>>

>> Source

>>

>> Arita M, Bianchini F, Aliberti J, et al. Stereochemical

>> assignment, anti-inflammatory properties, and receptor for the omega-3

>> lipid

>> mediator resolving E1. J Exp Med 2005; 201: DOI:10.1084/jem.20042031.

>> Available at: http://www.jem.org.

>>

>>

>>

>>

>>

>>

>> Not an MD

>>

>> I'll tell you where to go!

>>

>> Mayo Clinic in Rochester

>> http://www.mayoclinic.org/rochester

>>

>> s Hopkins Medicine

>> http://www.hopkinsmedicine.org

>>

>>

>>

>>