Low-Tar and High-Tar Cigaretters

Holt, Patrick G.; Chalmer, Jane E.; Roberts, L; Papadimitriou, John; Thomas, Wayne R.; Keast, David

doi:10.1080/00039896.1976.10667230

Cited by 20 publications

(5 citation statements)

References 17 publications

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“…Several studies (45)(46)(47)(48) showed no changes, whereas others (5,13,49,50) showed decreased mitogen-induced T cell proliferation. We reported that nicotine did not affect T cell proliferation induced by anti-CD3/CD28 Abs (19).…”

Section: Discussionmentioning

confidence: 99%

“…Nicotine, however, is the only agent considered synonymous with smoking in modulating the immune system (5,12). For example, Holt and colleagues (13) observed that exposure to smoke from high-nicotine cigarettes is more immunosuppressive than the smoke from low-nicotine cigarettes. In experiments separating the vapor phase from the particulate phase, the Sopori group (5) found that particulate phase-containing nicotine is necessary for the immunosuppression associated with cigarette smoke.…”

mentioning

confidence: 99%

“…In experiments separating the vapor phase from the particulate phase, the Sopori group (5) found that particulate phase-containing nicotine is necessary for the immunosuppression associated with cigarette smoke. Also, animals treated chronically (3 to 4 wk) with nicotine, in a manner similar to cigarette smoke, have a significant loss of Ab responses and T cell proliferation (13)(14)(15). Altogether, these studies provided the rationale for studying the impact of nicotine on host immunity and host response to vaccination.…”

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confidence: 99%

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Exposure to Nicotine Adversely Affects the Dendritic Cell System and Compromises Host Response to Vaccination

Nouri-Shirazi

Guinet

2012

The Journal of Immunology

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The magnitude of Th1 cells response to vaccination is a critical factor in determining protection from clinical disease. Our previous in vitro studies suggested that exposure to the nicotine component of cigarette smoke skews the differentiation of both human and mouse dendritic cell (DC) precursors into atypical DCs (DCs differentiated ex vivo in the presence of nicotine) lacking parameters essential for the development of Th1-mediated immunity. In this study, we determined the causal relationship between nicotine-induced DC alterations and host response to vaccines. We show that animals exposed to nicotine failed to develop and maintain Ag-specific effector memory Th1 cells and Ab production to protein-based vaccine formulated with Th1 adjuvants. Accordingly, both prophylactic and therapeutic vaccines failed to protect and cure the nicotine-exposed mice from disease. More importantly, we demonstrate the nicotine-induced defects in the biological activities of in vivo DCs as an underlying mechanism. Indeed, i.v. administration of DCs differentiated in the presence of nicotine preferentially promoted the development of Ag-specific IL-4–producing effector cells in the challenged mice. In addition, DC subsets isolated from mice exposed to nicotine produced significantly less cytokines in response to Th1 adjuvants and inadequately supported the development of Ag-specific Th1 cells. Collectively, our studies suggest that nicotine-induced defects in the DC system compromises vaccine efficacy in smokers.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Exposure to Nicotine Adversely Affects the Dendritic Cell System and Compromises Host Response to Vaccination

Nouri-Shirazi

Guinet

2012

The Journal of Immunology

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“…There is increasing evidence that nicotine, the primary constituent among the thousands of chemicals in all tobacco products, is an immune modulator having sole effects on host immunity that reflect the effects of cigarette smoke in its entirety [19][20][21]. Although, our understanding of the mechanisms whereby nicotine affects host immunity is largely incomplete, nicotine is being used in medications (e.g., patch, gum, nasal spray/inhaler) to aid smoking cessation [22] and is being considered as an anti-inflammatory agent for the treatment of diseases such as Alzheimer's disease [23], Parkinson's disease [24], and autoimmune diseases [25].…”

Section: Introductionmentioning

confidence: 99%

Nicotine alters the biological activities of developing mouse bone marrow-derived dendritic cells (DCs)

2007

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“…Finklea and colleagues [4] showed that smokers had lower titers and a decreased t 1/2 of antibodies to influenza virus after natural disease and immunization. In addition, Holt’s group [6, 7] reported that the longevity of the immune response to subunit vaccine was severely depressed 50 weeks post-vaccination in smokers. Reduced protection seen in smokers compared with nonsmokers after vaccination is further supported by a study from Winter et al [5] in which it was found that smokers who received hepatitis B vaccines at 0, 1, and 6 months (standard booster vaccine) had lower Ab levels than nonsmokers after 3, 7, and 13 months.…”

Section: Introductionmentioning

confidence: 99%

Combination of TLR8 and TLR4 agonists reduces the degrading effects of nicotine on DC-NK mediated effector T cell generation

Nouri-Shirazi

Tamjidi

Nourishirazi

et al. 2018

International Immunopharmacology

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The magnitude of immune responses to vaccination is a critical factor in determining protection from disease. It is known that cigarette smoke dampens the immune system and increases the risk of vaccine-preventable diseases. We reported that nicotine, the immunosuppressive component of cigarette smoke, disrupts the differentiation and functional properties of DC, which are pivotal in the initiation of immune response to vaccines. We also reported that TLR agonists act in synergy and boost DC maturation, DC-NK crosstalk and ultimately naïve T cell polarization into effector Th1 and Tc1 cells. Here, we investigated whether the combination of TLR agonists could diminish the degrading effects of nicotine on DC-NK mediated effector T cell generation. We found that none of TLR agonists, single or combined, were able to diminish completely the adverse effects of nicotine on DC. However, TLR3, TLR4, and TLR8 agonists acted as the most effective adjuvants to increase the expression levels of antigen-presenting, costimulatory molecules and production of cytokines by nicotine-exposed DC (nicDC). When combined, TLR3 + 8 and TLR4 + 8 synergistically optimized nicDC maturation and IFN-γ secretion from nicotine-exposed NK (nicNK) during co-cultures. Interestingly, in contrast to DC-NK-T, co-cultures of nicDC-nicNK-T treated with TLR3 + 8 or TLR4 + 8 agonists produced a similar frequency of effector memory Th1 and Tc1 cells. However, the effector cells from TLR4 + 8 followed by TLR3 + 8 treated nicDC-nicNK-T co-cultures produced significantly more IFN-γ when compared with aluminum salt treated co-culture. Our data suggest that addition of appropriate TLR agonists to vaccine formulation could potentially augment the immune response to vaccination in smokers.

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Low-Tar and High-Tar Cigaretters

Cited by 20 publications

References 17 publications

Exposure to Nicotine Adversely Affects the Dendritic Cell System and Compromises Host Response to Vaccination

Exposure to Nicotine Adversely Affects the Dendritic Cell System and Compromises Host Response to Vaccination

Nicotine alters the biological activities of developing mouse bone marrow-derived dendritic cells (DCs)

Combination of TLR8 and TLR4 agonists reduces the degrading effects of nicotine on DC-NK mediated effector T cell generation

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