Nicotine therapeutic benefits: Difference between revisions

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='''Multiple Sclerosis - Humans / Experimental Autoimmune Encephalomyelitis (EAE) - Animals'''=

~~=== 2023: [https://www.medscape.com/viewarticle/995075?form=fpf Oral Tobacco Use Linked to Slower MS Progression] ===~~

* Jing Wu, Tomas Olsson, Jan Hillert, Lars Alfredsson, Anna Karin Hedström

* Corresponding author Jing Wu, Karolinska Institute, 171 77 Stockholm, Stockholm, Sweden; Email: jing.wu [at] ki.se [Please demangle the email address; spam prevention ed.]

* [https://jnnp.bmj.com/content/94/8/589 Full Text]

* Oral tobacco use, also known as moist snuff, is associated with slower progression of multiple sclerosis (MS), a new study shows.

* Jing Wu, PhD candidate "Our finding that snuff use is not associated with worse disease progression indicates that nicotine replacement therapy could be an attractive way to increase the chance of quitting smoking post diagnosis,"

* To investigate, the researchers analyzed data from 9089 patients with MS who were participants in two case-control studies from the Swedish MS registry, mean age 37.6 years and 72% female. At baseline, current cigarette smokers had significantly higher Expanded Disability Status Scale (EDSS) scores compared with nonsmokers.

* All analyses controlled for age at diagnosis, sex, disease phenotype, disease duration, baseline EDSS, and use of disease-modifying therapy.

* Compared with never smoking, current smoking was associated with an increased risk of clinical disease worsening (CDW) (adjusted hazard ratio [aHR] 1.13; 95% CI 1.06-1.21), of reaching EDSS 3 (aHR 1.21, 95% CI 1.09-1.34), and EDSS 4 (aHR 1.31, 95% CI 1.14-1.51). In addition, compared with never smokers, current smoking was associated with a higher risk of physical and psychological worsening as determined by the MS Impact Scale-29 (MSIS-29), and worsening cognitive performance measured by the Symbol Digit Modalities Test (SDMT).

* The study revealed a dose-dependent relationship between smoking and negative MS-related outcomes.

* Current snuff use was significantly associated with lower risk of reaching EDSS 4 (aHR 0.73, 95% CI 0.58-0.92), but not CDW or EDSS 3. It was not significantly associated with the risk of worsening health-related quality of life or cognition.

* In a perplexing turn of events study co-author Anna Karin Hedström, MD, PhD said "Physicians should not recommend smoking MS patients switch to snuff, as snuff may have other negative health consequences." [Why not? if the alternative is continued smoking? ed.] Particularly considering she also said this "This indicates that nicotine is not the substance that leads to worse prognosis and that nicotine replacement therapy is probably harmless — at least with respect to disease progression."

===2016 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/ Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis]===

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* This study provides evidence that nicotine alters the infiltration of proinflammatory monocytes and neutrophils into the CNS of [[Special:MyLanguage/Abbreviations|'''EAE''']] mice via multiple [[Special:MyLanguage/Abbreviations|'''nAChRs''']], including the α7 and α9 subtypes. Nicotine appears to achieve these effects by inhibiting the expression of CCL2 and CXCL2, two cytokines involved in the chemotaxis of proinflammatory monocytes and neutrophils, respectively. The use of ligands that are selective for one or both of these nAChR subtypes may offer a beneficial clinical outcome, and thus provide a valuable therapeutic strategy for neuroinflammatory disorders such as MS.

*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/pdf/1501613.pdf PDF Version]

*Citation: Jiang W, St-Pierre S, Roy P, Morley BJ, Hao J, Simard AR. Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. 2016 Mar 1;196(5):2095-108. doi: 10.4049/jimmunol.1501613. Epub 2016 Jan 25. PMID: 26810225; PMCID: PMC4760232.

**Citation: Jiang W, St-Pierre S, Roy P, Morley BJ, Hao J, Simard AR. Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. 2016 Mar 1;196(5):2095-108. doi: 10.4049/jimmunol.1501613. Epub 2016 Jan 25. PMID: 26810225; PMCID: PMC4760232.

*Acknowledgements: This work was supported by grants from the Multiple Sclerosis Society of Canada (to A.R.S.), the New Brunswick Health Research Foundation (to A.R.S.), the New Brunswick Innovation Foundation (to A.R.S.), the Nebraska Tobacco Settlement Biomedical Research Fund (to B.J.M.), and the National Institutes of Health (Grant R01DC006907 to B.J.M.). Salary support was provided by the Centre de Formation Médicale du Nouveau-Brunswick (to W.J.) and the New Brunswick Innovation Foundation (to S.S-P. and P.R.).

***Acknowledgements: This work was supported by grants from the Multiple Sclerosis Society of Canada (to A.R.S.), the New Brunswick Health Research Foundation (to A.R.S.), the New Brunswick Innovation Foundation (to A.R.S.), the Nebraska Tobacco Settlement Biomedical Research Fund (to B.J.M.), and the National Institutes of Health (Grant R01DC006907 to B.J.M.). Salary support was provided by the Centre de Formation Médicale du Nouveau-Brunswick (to W.J.) and the New Brunswick Innovation Foundation (to S.S-P. and P.R.).

*See Also - Related article: [https://mssociety.ca/research-news/article/ms-society-funded-study-shows-that-nicotine-reduces-the-invasion-of-harmful-immune-cells-into-the-brain-in-mice-with-an-ms-like-disease MS Society-funded study shows that nicotine reduces the invasion of harmful immune cells into the brain in mice with an MS-like disease]

===2015 [https://pubmed.ncbi.nlm.nih.gov/25813705/ Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis]===

*Amimal study

*We found that reduction of ependymal cell proliferation correlated with inflammation in the same area, which was relieved by the administration of nicotine. Further, increased numbers of oligodendrocytes (OLs) were observed after nicotine treatment. These findings give a new insight into the mechanism of how nicotine functions to attenuate EAE.

*[https://sci-hub.st/10.1016/j.neuroscience.2015.03.031 PDF Full Study]

**Citation: Gao Z, Nissen JC, Legakis L, Tsirka SE. Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis. Neuroscience. 2015 Jun 25;297:11-21. doi: 10.1016/j.neuroscience.2015.03.031. Epub 2015 Mar 23. PMID: 25813705; PMCID: PMC4428965.

***Acknowledgement: The work was supported by NMSS PP1815, NIH R01NS42168, NIH IRACDA K12GM102778.

===2015 [https://pubmed.ncbi.nlm.nih.gov/26209886/ Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients]===

*The data obtained highlight the role of α7 receptor subtype in the modulation of anti-inflammatory cytokines also in MS. Moreover the ability of nicotine to up-regulate the expression of α7 receptor subtype in RR-MS patients, indicates that nicotinic receptor stimulation may contribute to down-modulate the inflammation occurred in MS by a positive feedback control of its expression.

*[https://sci-hub.st/10.1016/j.intimp.2015.06.034 PDF Full paper]

**Citation: Reale M, Di Bari M, Di Nicola M, D'Angelo C, De Angelis F, Velluto L, Tata AM. Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients. Int Immunopharmacol. 2015 Nov;29(1):152-7. doi: 10.1016/j.intimp.2015.06.034. Epub 2015 Jul 23. PMID: 26209886.

***Acknowledgement: This work was supported by FISM – Fondazione Italiana Sclerosi Multipla – Cod. 2013/R/25. MDB was supported by fellowship on FISM project 2013/R/25.

===2014 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/ The Experimental Autoimmune Encephalomyelitis Disease Course Is Modulated by Nicotine and Other Cigarette Smoke Components]===

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*Our results show that nicotine reduces the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an [[Special:MyLanguage/Abbreviations|'''EAE/MS''']] therapeutic. In contrast, the remaining components of cigarette smoke, delivered as cigarette smoke condensate (CSC), accelerated and increased adverse clinical symptoms during the early stages of EAE.

*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/pdf/pone.0107979.pdf PDF Version]

*Citation: Gao Z, Nissen JC, Ji K, Tsirka SE. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. 2014 Sep 24;9(9):e107979. doi: 10.1371/journal.pone.0107979. PMID: 25250777; PMCID: PMC4176721.

**Citation: Gao Z, Nissen JC, Ji K, Tsirka SE. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. 2014 Sep 24;9(9):e107979. doi: 10.1371/journal.pone.0107979. PMID: 25250777; PMCID: PMC4176721.

*Acknowledgements: This work was supported by National Multiple Sclerosis Society awards CA1044A1 and PP181, National Aeronautics and Space Administration NNA14AB04A and National Institutes of Health R01NS42168 (ST), and National Institutes of Health K12GM102778 to JN.

***Acknowledgements: This work was supported by National Multiple Sclerosis Society awards CA1044A1 and PP181, National Aeronautics and Space Administration NNA14AB04A and National Institutes of Health R01NS42168 (ST), and National Institutes of Health K12GM102778 to JN.

===2013 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/ Novel Therapeutic Approach by Nicotine in Experimental Model of Multiple Sclerosis]===

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*Due to the proven therapeutic effect of nicotine on AD (Alzheimer’s Disease) and PD (Parkinson’s Disease), we decided to study the role of nicotine in [[Special:MyLanguage/Abbreviations|'''EAE''']] as an animal model of MS. Our treatment group showed less inflammation in histopathological evaluation along with myelin sheet protection. Moreover, prevention group showed less inflammation compared with treatment group. Thus, nicotine might be recommended as a promising drug for [[Special:MyLanguage/Abbreviations|MS]] therapy.

*[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/pdf/icns_10_4_20.pdf PDF Version]

*Citation: Naddafi F, Reza Haidari M, Azizi G, Sedaghat R, Mirshafiey A. Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. 2013 Apr;10(4):20-5. PMID: 23696955; PMCID: PMC3659034.

**Citation: Naddafi F, Reza Haidari M, Azizi G, Sedaghat R, Mirshafiey A. Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. 2013 Apr;10(4):20-5. PMID: 23696955; PMCID: PMC3659034.

***Acknowledgement: No funding was provided for the preparation of this article.

<br>

@@ Line 955: / Line 955: @@
 ='''Multiple Sclerosis - Humans / Experimental Autoimmune Encephalomyelitis (EAE) - Animals'''=
-=== 2023: [https://www.medscape.com/viewarticle/995075?form=fpf Oral Tobacco Use Linked to Slower MS Progression] ===
-* Jing Wu, Tomas Olsson, Jan Hillert, Lars Alfredsson, Anna Karin Hedström
-* Corresponding author Jing Wu, Karolinska Institute, 171 77 Stockholm, Stockholm, Sweden; Email: jing.wu [at] ki.se [Please demangle the email address; spam prevention ed.]
-* [https://jnnp.bmj.com/content/94/8/589 Full Text]
-* Oral tobacco use, also known as moist snuff, is associated with slower progression of multiple sclerosis (MS), a new study shows.
-* Jing Wu, PhD candidate "Our finding that snuff use is not associated with worse disease progression indicates that nicotine replacement therapy could be an attractive way to increase the chance of quitting smoking post diagnosis,"
-* To investigate, the researchers analyzed data from 9089 patients with MS who were participants in two case-control studies from the Swedish MS registry, mean age 37.6 years and 72% female. At baseline, current cigarette smokers had significantly higher Expanded Disability Status Scale (EDSS) scores compared with nonsmokers.
-* All analyses controlled for age at diagnosis, sex, disease phenotype, disease duration, baseline EDSS, and use of disease-modifying therapy.
-* Compared with never smoking, current smoking was associated with an increased risk of clinical disease worsening (CDW) (adjusted hazard ratio [aHR] 1.13; 95% CI 1.06-1.21), of reaching EDSS 3 (aHR 1.21, 95% CI 1.09-1.34), and EDSS 4 (aHR 1.31, 95% CI 1.14-1.51). In addition, compared with never smokers, current smoking was associated with a higher risk of physical and psychological worsening as determined by the MS Impact Scale-29 (MSIS-29), and worsening cognitive performance measured by the Symbol Digit Modalities Test (SDMT).
-* The study revealed a dose-dependent relationship between smoking and negative MS-related outcomes.
-* Current snuff use was significantly associated with lower risk of reaching EDSS 4 (aHR 0.73, 95% CI 0.58-0.92), but not CDW or EDSS 3. It was not significantly associated with the risk of worsening health-related quality of life or cognition.
-* In a perplexing turn of events study co-author Anna Karin Hedström, MD, PhD said "Physicians should not recommend smoking MS patients switch to snuff, as snuff may have other negative health consequences." [Why not? if the alternative is continued smoking? ed.] Particularly considering she also said this "This indicates that nicotine is not the substance that leads to worse prognosis and that nicotine replacement therapy is probably harmless — at least with respect to disease progression."<!--T:186-->
 ===2016 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/ Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis]===
@@ Line 974: / Line 960: @@
 * This study provides evidence that nicotine alters the infiltration of proinflammatory monocytes and neutrophils into the CNS of [[Special:MyLanguage/Abbreviations|'''EAE''']] mice via multiple [[Special:MyLanguage/Abbreviations|'''nAChRs''']], including the α7 and α9 subtypes. Nicotine appears to achieve these effects by inhibiting the expression of CCL2 and CXCL2, two cytokines involved in the chemotaxis of proinflammatory monocytes and neutrophils, respectively. The use of ligands that are selective for one or both of these nAChR subtypes may offer a beneficial clinical outcome, and thus provide a valuable therapeutic strategy for neuroinflammatory disorders such as MS.
 *[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760232/pdf/1501613.pdf PDF Version]
-*Citation: Jiang W, St-Pierre S, Roy P, Morley BJ, Hao J, Simard AR. Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. 2016 Mar 1;196(5):2095-108. doi: 10.4049/jimmunol.1501613. Epub 2016 Jan 25. PMID: 26810225; PMCID: PMC4760232.
+**Citation: Jiang W, St-Pierre S, Roy P, Morley BJ, Hao J, Simard AR. Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis. J Immunol. 2016 Mar 1;196(5):2095-108. doi: 10.4049/jimmunol.1501613. Epub 2016 Jan 25. PMID: 26810225; PMCID: PMC4760232.
-*Acknowledgements: This work was supported by grants from the Multiple Sclerosis Society of Canada (to A.R.S.), the New Brunswick Health Research Foundation (to A.R.S.), the New Brunswick Innovation Foundation (to A.R.S.), the Nebraska Tobacco Settlement Biomedical Research Fund (to B.J.M.), and the National Institutes of Health (Grant R01DC006907 to B.J.M.). Salary support was provided by the Centre de Formation Médicale du Nouveau-Brunswick (to W.J.) and the New Brunswick Innovation Foundation (to S.S-P. and P.R.).
+***Acknowledgements: This work was supported by grants from the Multiple Sclerosis Society of Canada (to A.R.S.), the New Brunswick Health Research Foundation (to A.R.S.), the New Brunswick Innovation Foundation (to A.R.S.), the Nebraska Tobacco Settlement Biomedical Research Fund (to B.J.M.), and the National Institutes of Health (Grant R01DC006907 to B.J.M.). Salary support was provided by the Centre de Formation Médicale du Nouveau-Brunswick (to W.J.) and the New Brunswick Innovation Foundation (to S.S-P. and P.R.).
 *See Also - Related article: [https://mssociety.ca/research-news/article/ms-society-funded-study-shows-that-nicotine-reduces-the-invasion-of-harmful-immune-cells-into-the-brain-in-mice-with-an-ms-like-disease MS Society-funded study shows that nicotine reduces the invasion of harmful immune cells into the brain in mice with an MS-like disease]
+===2015 [https://pubmed.ncbi.nlm.nih.gov/25813705/ Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis]===
+*Amimal study
+*We found that reduction of ependymal cell proliferation correlated with inflammation in the same area, which was relieved by the administration of nicotine. Further, increased numbers of oligodendrocytes (OLs) were observed after nicotine treatment. These findings give a new insight into the mechanism of how nicotine functions to attenuate EAE.
+*[https://sci-hub.st/10.1016/j.neuroscience.2015.03.031 PDF Full Study]
+**Citation: Gao Z, Nissen JC, Legakis L, Tsirka SE. Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis. Neuroscience. 2015 Jun 25;297:11-21. doi: 10.1016/j.neuroscience.2015.03.031. Epub 2015 Mar 23. PMID: 25813705; PMCID: PMC4428965.
+***Acknowledgement: The work was supported by NMSS PP1815, NIH R01NS42168, NIH IRACDA K12GM102778.
+===2015 [https://pubmed.ncbi.nlm.nih.gov/26209886/ Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients]===
+*The data obtained highlight the role of α7 receptor subtype in the modulation of anti-inflammatory cytokines also in MS. Moreover the ability of nicotine to up-regulate the expression of α7 receptor subtype in RR-MS patients, indicates that nicotinic receptor stimulation may contribute to down-modulate the inflammation occurred in MS by a positive feedback control of its expression.
+*[https://sci-hub.st/10.1016/j.intimp.2015.06.034 PDF Full paper]
+**Citation: Reale M, Di Bari M, Di Nicola M, D'Angelo C, De Angelis F, Velluto L, Tata AM. Nicotinic receptor activation negatively modulates pro-inflammatory cytokine production in multiple sclerosis patients. Int Immunopharmacol. 2015 Nov;29(1):152-7. doi: 10.1016/j.intimp.2015.06.034. Epub 2015 Jul 23. PMID: 26209886.
+***Acknowledgement: This work was supported by FISM – Fondazione Italiana Sclerosi Multipla – Cod. 2013/R/25. MDB was supported by fellowship on FISM project 2013/R/25.
 ===2014 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/ The Experimental Autoimmune Encephalomyelitis Disease Course Is Modulated by Nicotine and Other Cigarette Smoke Components]===
@@ Line 982: / Line 981: @@
 *Our results show that nicotine reduces the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an [[Special:MyLanguage/Abbreviations|'''EAE/MS''']] therapeutic. In contrast, the remaining components of cigarette smoke, delivered as cigarette smoke condensate (CSC), accelerated and increased adverse clinical symptoms during the early stages of EAE.
 *[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4176721/pdf/pone.0107979.pdf PDF Version]
-*Citation: Gao Z, Nissen JC, Ji K, Tsirka SE. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. 2014 Sep 24;9(9):e107979. doi: 10.1371/journal.pone.0107979. PMID: 25250777; PMCID: PMC4176721.
+**Citation: Gao Z, Nissen JC, Ji K, Tsirka SE. The experimental autoimmune encephalomyelitis disease course is modulated by nicotine and other cigarette smoke components. PLoS One. 2014 Sep 24;9(9):e107979. doi: 10.1371/journal.pone.0107979. PMID: 25250777; PMCID: PMC4176721.
-*Acknowledgements: This work was supported by National Multiple Sclerosis Society awards CA1044A1 and PP181, National Aeronautics and Space Administration NNA14AB04A and National Institutes of Health R01NS42168 (ST), and National Institutes of Health K12GM102778 to JN.
+***Acknowledgements: This work was supported by National Multiple Sclerosis Society awards CA1044A1 and PP181, National Aeronautics and Space Administration NNA14AB04A and National Institutes of Health R01NS42168 (ST), and National Institutes of Health K12GM102778 to JN.
 ===2013 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/ Novel Therapeutic Approach by Nicotine in Experimental Model of Multiple Sclerosis]===
@@ Line 989: / Line 988: @@
 *Due to the proven therapeutic effect of nicotine on AD (Alzheimer’s Disease) and PD (Parkinson’s Disease), we decided to study the role of nicotine in [[Special:MyLanguage/Abbreviations|'''EAE''']] as an animal model of MS. Our treatment group showed less inflammation in histopathological evaluation along with myelin sheet protection. Moreover, prevention group showed less inflammation compared with treatment group. Thus, nicotine might be recommended as a promising drug for [[Special:MyLanguage/Abbreviations|MS]] therapy.
 *[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659034/pdf/icns_10_4_20.pdf PDF Version]
-*Citation: Naddafi F, Reza Haidari M, Azizi G, Sedaghat R, Mirshafiey A. Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. 2013 Apr;10(4):20-5. PMID: 23696955; PMCID: PMC3659034.
+**Citation: Naddafi F, Reza Haidari M, Azizi G, Sedaghat R, Mirshafiey A. Novel therapeutic approach by nicotine in experimental model of multiple sclerosis. Innov Clin Neurosci. 2013 Apr;10(4):20-5. PMID: 23696955; PMCID: PMC3659034.
+***Acknowledgement: No funding was provided for the preparation of this article.
 <br>