Effects of cigarette smoke on the immune response: II. Chronic exposure to cigarette smoke inhibits surface immunoglobulin-mediated responses in B cells☆
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Cited by (43)
Autoimmune pre-disease
2023, Autoimmunity ReviewsCitation Excerpt :In addition to development and differentiation, the function of T and B cells is also altered by exposure to cigarette smoke. For example, exposure to cigarette smoke inhibits the surface immunoglobulin-mediated responses of B cells and impairs antigen receptor-mediated signaling in T cells [354,355]. In summary, CS affects the immune system in multiple ways that overall seem permissive for the induction of the autoimmune response and/or lead to clinical disease manifestation.
Association between chronic psychoactive substances use and systemic inflammation: A systematic review and meta-analysis
2021, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Another review conducted by (Piao et al., 2009) suggested that chronic tobacco use alters immune responses through a reduction in (1) antibody-forming cell response in the spleen, (2) a decrease in the proliferation of peripheral blood mononuclear cells, regulating lymphocytes, macrophages and (3) by affecting the secretion of cytokines and lymphocytes (Piao et al., 2009). On the other hand, chronic tobacco use also promotes neuroinflammatory processes by the activation of epithelial and immune cells that release pro-inflammatory factors and promote the recruitment of neutrophils, macrophages, T cells, and dendritic cells (Kohno et al., 2019; Savage et al., 1991; Sopori, 2002; Sopori and Kozak, 1998). Despite the fact that chronic use of substances such as alcohol, tobacco, cannabis, and cocaine might lead to inflammation (including neuro-inflammation) (Imhof et al., 2004; McEvoy et al., 2015; Strzelak et al., 2018), there is as yet no meta-analysis testing the effect of chronic substance use on different inflammatory biomarkers (e.g. C-Reactive Proteins (CRP), Interleukins (e.g. IL-6), Tumor Necrosis Factor (TNF)).
Neuroinflammation in addiction: A review of neuroimaging studies and potential immunotherapies
2019, Pharmacology Biochemistry and BehaviorCitation Excerpt :Nicotine, in contrast, is thought to be a significant contributor to the inhibition of the antibody response and the immunosuppressive effects of chronic smoking (Geng et al., 1995; Geng et al., 1996). Animal studies show that smoking can increase reactive oxygen species and decrease levels of antioxidants (Savage et al., 1991; Sopori, 2002; Sopori and Kozak, 1998). Increases in inflammatory markers associated with cigarette smoking are also shown to be dose-dependent and related to smoking intensity and time since smoking cessation (Sopori, 2002).
Extracts from presumed "reduced harm" cigarettes induce equivalent or greater toxicity in antigen-presenting cells
2015, ToxicologyCitation Excerpt :That study was also performed with condensate prepared using a technique that potentially eliminates a number of transient but potent cigarette smoke chemicals relevant to tobacco-induced diseases. Cigarette smoke constituents profoundly alter immune functions required for control of tumor development and spread (Barton et al., 1988; Ginns et al., 1985; Lu et al., 2007; Mian et al., 2008; Savage et al., 1991; Sopori, 2002; Tollerud et al., 1989; Vassallo et al., 2005). We and others have demonstrated that cigarette smoke exposure in vivo and CSE exposure in vitro profoundly suppress the function of DCs (Kroening et al., 2008; Nouri-Shirazi and Guinet, 2003; Nouri-Shirazi et al., 2007; Vassallo et al., 2008, 2005).
Impact of cigarette smoke on T and B cell responsiveness
2008, Cellular ImmunologyCitation Excerpt :Lymphocytes express the nicotinic acetylcholine receptor [31], and in a smoke-exposed environment, nicotine binding to these receptors may result in constitutive activation of their signal cascades, and consequent IP3-mediated release of intracellular Ca2+[24]. The B- and T-cell receptors (BCR and TCR, respectively) rely on the same downstream messengers, and early experimental studies have demonstrated that cells taken from nicotine- or smoke-exposed animals have reduced numbers of antibody secreting cells, are unable to mount a Ca2+ flux in response to antigen receptor ligation, and have a reduced proliferative capacity [24,25]. These studies have been performed principally in rat models, using levels of cigarette smoke up to three times those seen in most human smokers [24,32].
Nicotinic receptors regulate B lymphocyte activation and immune response
2005, European Journal of Pharmacology
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This work was supported in part by grants from NIH (AI 31386) and the Council for Tobacco Research, USA (CTR-1957).