C‐reactive protein and depressed mood in a sub‐group of smokers during nicotine abstinence

Corwin, Elizabeth J.; Klein, Laura Cousino

doi:10.1002/hup.487

Cited by 12 publications

(9 citation statements)

References 63 publications

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“…Moreover, since C reactive protein is an inflammation marker evaluated to predict several cardiovascular diseases [32], the direct effect of nicotine on this protein may mask in smokers the increased cardiovascular risk associated with smoking. A modification in C-reactive protein levels was detected in humans also during abstinence, although with a split response [33].…”

Section: Discussionmentioning

confidence: 98%

Serum proteomic analysis during nicotine self‐administration, extinction and relapse in rats

et al. 2008

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Nicotine dependence is known to induce long-term neural adaptations in brain. The purpose of this study was to verify whether specific protein patterns related to nicotine self-administration states could also be detected in a peripheral tissue. A serum proteomic analysis was performed by 2-DE on samples taken at six time points: N, naïve; P, priming; S, self-administration; W, withdrawal; E, extinction; R, relapse. After image analysis, spot volume values were submitted to a principal component analysis and relevant comparisons were selected. In N versus S; S versus W; E versus R; S versus R and S versus E comparisons a clear separation between groups could be observed, suggesting that each self-administration state correlates with a specific protein expression pattern. Partial least squares discriminant analysis was adopted to rank proteins by the contribution to the overall separation. A number of spots were identified; among them, C reactive protein and haemopexin displayed a significant reduction after nicotine administration; two haemopexin isoforms were decreased in the S state and antithrombin III was increased in the E phase. This study showed that specific protein patterns related to the nicotine self-administration states exist in serum. Further development of this approach may provide biomarkers to assess dependence states of drug-taking individuals.

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Section: Discussionmentioning

confidence: 98%

Serum proteomic analysis during nicotine self‐administration, extinction and relapse in rats

et al. 2008

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“…Studies have shown that CRP and SAA level are elevated in cocaine abusers, alcohol users and cigarette smokers [19,20,29]. The inflammatory markers CRP and SAA proteins play a major role in chronic inflammation of HIV infection, inducing immune dysfunction, disease progression and subsequently decreased CD4 count [22].…”

Section: Discussionmentioning

confidence: 99%

HIV infection and drugs of abuse: role of acute phase proteins

Samikkannu

Rao

Arias

et al. 2013

J Neuroinflammation

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BackgroundHIV infection and drugs of abuse such as methamphetamine (METH), cocaine, and alcohol use have been identified as risk factors for triggering inflammation. Acute phase proteins such as C-reactive protein (CRP) and serum amyloid A (SAA) are the biomarkers of inflammation. Hence, the interactive effect of drugs of abuse with acute phase proteins in HIV-positive subjects was investigated.MethodsPlasma samples were utilized from 75 subjects with METH use, cocaine use, alcohol use, and HIV-positive alone and HIV-positive METH, cocaine, and alcohol users, and age-matched control subjects. The plasma CRP and SAA levels were measured by ELISA and western blot respectively and the CD4 counts were also measured.ResultsObserved results indicated that the CRP and SAA levels in HIV-positive subjects who are METH, cocaine and alcohol users were significantly higher when compared with either drugs of abuse or HIV-positive alone. The CD4 counts were also dramatically reduced in HIV-positive with drugs of abuse subjects compared with only HIV-positive subjects.ConclusionsThese results suggest that, in HIV-positive subjects, drugs of abuse increase the levels of CRP and SAA, which may impact on the HIV infection and disease progression.

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“…Although tocilizumab has similar efficacy and safety profiles to TNF-α inhibitor for RA treatment, our mechanism suggests that IL-6 and TNF-α act through different pathogenic mechanisms in RA and other inflammatory diseases [19,20]. Actually, studies have reported that increased CRP and SAA levels in alcohol users, abusers of cocaine and methamphetamine (METH), cigarette smokers and HIV-infected patients [21][22][23][24]. It has been well known that alcohol user and drug abusers develop chronic inflammation that leads to immune Citation: Song SNJ, Yoshizaki K (2016) Mechanism and Clinical Significance of IL-6 Combined with TNF-α or IL-1 for the Induction of Acute Phase Proteins SAA and CRP in Chronic Inflammatory Diseases.…”

Section: Clinical Significance Of Il-6 Combined With Il-1 or Tnf-α Inmentioning

confidence: 83%

Mechanism and Clinical Significance of IL-6 Combined with TNF-α or IL-1 for the Induction of Acute Phase Proteins SAA and CRP in Chronic Inflammatory Diseases

Song¹,

Yoshizaki

2016

J Alcohol Drug Depend

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Serum amyloid A (SAA) and C-reactive protein (CRP) are two major acute phase proteins whose serum concentrations increase in response to inflammation, though the exact mechanism underlying this induction remains unknown. Dysregulated production of interleukin (IL)-6 plays a pathogenic role in various inflammatory diseases such as rheumatoid arthritis, Castleman's disease and systemic juvenile idiopathic arthritis. IL-6 blocking therapy with an anti-IL-6 receptor antibody (tocilizumab) can ameliorate clinical symptoms and abnormal laboratory findings, and completely normalize CRP and SAA levels in rheumatoid arthritis patients. Conversely, therapy for blocking tumor necrosis factor (TNF)-α, another key pathogenic factor in rheumatoid arthritis, barely lowers CRP and SAA to within their normal range, suggesting that IL-6 and TNF-α play different roles in the induction of acute phase protein expression. To clarify the different pathogenic roles and mechanisms of IL-6 and TNF-α or IL-1 in the induction of CRP and SAA in chronic inflammatory diseases, we investigated the transcriptional regulation mechanisms of SAA and CRP using hepatoma-derived cell lines in vitro, and related these mechanisms to the different effects of IL-6 and TNF-α blocking therapies on serum SAA and CRP in rheumatoid arthritis patients in vivo. We propose transcriptional regulation models for inflammatory cytokine-induced SAA and CRP expression that explain why IL-6 plays an essential role in the induction of SAA and CRP in the presence of inflammation.

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C‐reactive protein and depressed mood in a sub‐group of smokers during nicotine abstinence

Cited by 12 publications

References 63 publications

Serum proteomic analysis during nicotine self‐administration, extinction and relapse in rats

Serum proteomic analysis during nicotine self‐administration, extinction and relapse in rats

HIV infection and drugs of abuse: role of acute phase proteins

Mechanism and Clinical Significance of IL-6 Combined with TNF-α or IL-1 for the Induction of Acute Phase Proteins SAA and CRP in Chronic Inflammatory Diseases

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