Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals

Holt, P. G.; Keast, David

doi:10.1128/br.41.1.205-216.1977

Cited by 112 publications

(14 citation statements)

References 96 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[ 4 ] Leukocytosis is a well-known effect of cigarette smoking though the function of these cells is greatly reduced. [ 5 6 ] Eichel et al . [ 7 ] reported that a single cigarette provided enough toxic material that completely inhibited the function of oral salivary neutrophils in situ .…”

Section: Introductionmentioning

confidence: 99%

Salivary immunoglobulin classes in Nigerian cigarette smokers: Indication for increased risk of oral diseases

Olayanju¹,

Rahamon²,

Arinola³

2012

Dent Res J

View full text Add to dashboard Cite

Background:Cigarette smoking is a worldwide social epidemic and it is one of the main causes of preventable death and disability. Gingivitis, periodontitis, pocket depth, attachment loss, alveolar bone loss, and tooth loss are some of oral pathologies commonly found in cigarette smokers. The aim of this study was to explore, for the first time among Nigerians, the interplay between components of cigarette smoke and salivary levels of immunoglobulin classes so as to provide oral immunological based reasons for oral diseases in cigarette smokers.Materials and Methods:In this case-control study, 5 mL of unstimulated saliva was collected in plain sample bottles from 24 active smokers who smoke at least 6 sticks of cigarette per day and 21 sex and age-matched non-smokers who were apparently healthy. The samples were spun and supernatant stored at -20°C until assayed. The immunoglobulin levels of the samples were estimated using enzyme-linked immunosorbent assay (ELISA). Student's t-test (unpaired) was used to determine significant differences between the two groups. P values less than 0.05 was considered significant.Results:No significant differences were observed in the mean salivary levels of IgG, IgA, and IgE. Only IgM was significantly lower in smokers compared with non-smokers (P = 0.038). The proportion of smokers with detectable level of salivary IgE was lower compared with controls.Conclusion:Our study showed that there is decreased salivary IgM in smokers. This observation suggests that reduced salivary immunoglobulin level of IgM might be involved in the pathogenesis of oral diseases in cigarette smokers.

show abstract

Section: Introductionmentioning

confidence: 99%

Salivary immunoglobulin classes in Nigerian cigarette smokers: Indication for increased risk of oral diseases

Olayanju¹,

Rahamon²,

Arinola³

2012

Dent Res J

View full text Add to dashboard Cite

show abstract

“…Moreover, being a current or former smoker decreases the chances of response to biologics. Smoke acts on both cellular and humoral immunity that leads to a systemic proinflammatory state [38,39]. Chronic cigarette smoking appears to trigger various morphological, physiological, and enzymatic changes that impairs inflammatory responses [38][39][40].…”

Section: Discussionmentioning

confidence: 99%

Predictors of remission in rheumatoid arthritis patients treated with biologics: a systematic review and meta-analysis

et al. 2022

View full text Add to dashboard Cite

Biologics have emerged as an effective treatment of rheumatoid arthritis (RA). However, there is a significant proportion of patients who fail to respond to biologics. Identifying the predictors that affect the response to biologics remains challenging. A comprehensive literature search of PubMed, Embase, and Web of Science databases was conducted through May 1, 2022. We included all studies that used a multivariate model to assess for the predictors of remission in RA patients treated with biologics. We calculated pooled odds ratios (OR) with 95% confidence intervals (CI) for risk factors reported in ≥ 3 studies using a random-effects model. A total of 16,934 patients with RA who were treated with biologics were included in twenty-one studies. Our study showed that old age (OR 0.98 (0.97, 0.99), P < 0.00001), female gender (OR 0.66 (0.56, 0.77), P < 0.00001), smoking history (OR 0.86 (0.75, 0.99), P 0.04), obesity (OR 0.95 (0.91, 0.99), P 0.02), poor functional status (OR 0.62 (0.48, 1.27), P < 0.00001), high disease activity (OR 0.90 (0.85, 0.96), P 0.0005), and elevated erythrocyte sedimentation rate (OR 0.99 (0.98, 1.00), P 0.009) were poor predictors of remission. On the other hand, positive anti-citrullinated protein antibodies (OR 2.52 (1.53, 4.12), P 0.0003) was associated with high remission rate. Old age, female gender, obesity, smoking history, poor functional status, high disease activity, and elevated ESR at the time of diagnosis have been associated with poor response to biologics. Our findings could help establish a risk stratification model for predicting the remission rate in RA patients receiving biologics.

show abstract

“…The possibility that the increase in the prevalence of diseases associated with cigarette smoke may, in part, be due to changes induced by tobacco smoke in the immune and inflammatory processes was recognized for the first time in the 1960s 26 . However, recent reviews recognize that the influence of cigarette smoke on the immune system is complex due to its chemical heterogeneity and dual nature, pro-inflammatory and immunosuppressive 6 , 7 .…”

Section: Discussionmentioning

confidence: 99%

Chronic exposure to cigarette smoke transiently worsens the disease course in a mouse model of pulmonary paracoccidioidomycosis

Buccheri

Duarte‐Neto

Silva

et al. 2022

Rev. Inst. Med. trop. S. Paulo

View full text Add to dashboard Cite

Paracoccidioidomycosis (PCM) may present as an acute/subacute clinical form, characterized by a progressive disease arising from the airborne initial infection, or, most often, as an asymptomatic or subclinical infection that may manifest later during an individual's life, the chronic form. Epidemiological studies show the existence of a strong association between smoking and the development of the chronic form. Current evidence demonstrates that cigarette smoke (CS) has immunosuppressive properties that could be implicated in the increasing susceptibility to the chronic form of PCM. To address this issue, we developed a murine model of a non-progressive pulmonary form of PCM that was exposed to CS at a magnitude that mimicked a moderate smoker. The chronic CS exposure started after 2 weeks and lasted up until 20 weeks post-infection, with the aim of mimicking human natural history, since it is estimated that individuals from endemic areas are infected early in life. The control group consisted of infected but not CS-exposed mice. We assessed the lung fungal burden (colony forming units [CFU]) and the area affected by the granulomatous inflammatory response, fungal dissemination to spleen and liver, and, by immunohistochemistry, the presence of CD4 and CD8 lymphocytes, CD68 and MAC-2 macrophages, and IFN-γ, IL-10 and TNF expressing cells within the granulomatous response. We detected a CS effect as early as 2 weeks after exposure (four weeks post-infection) when the lung CFU of exposed animals was significantly higher than in their non-exposed counterparts. At 12 weeks, the CS-exposed animals presented a more severe disease, as witnessed by the persistent higher lung fungal load (although it did not reach statistical significance [p = 0.054]), greater dissemination to other organs, greater affected area of the lung, decreased IFN-γ/IL-10 ratio, and higher TNF expression within the granulomas, compared with CS-non-exposed mice. The number of CD4 and CD8 lymphocytes infiltrating the granulomas was similar between both mice groups, but there was a decrease in the number of MAC-2+ macrophages. No difference was noted in the CD68+ macrophage number. However, the follow-up in week 20 showed that the immunological effects of exposure to CS ceased, with both CS and NCS mice showing the same infectious features, i.e., a trend for resolution of the infection. In conclusion, we show that chronic CS-exposure alters the course of the disease in an experimental model of subclinical pulmonary PCM, confirming the epidemiological link between CS-exposure and the chronic form of PCM. However, we also show that this effect is transitory, being detected between 4-and 12-weeks post-infection but not thereafter. The possible immune mechanisms that mediate this effect and the reasons for its transitory effect are discussed.

show abstract

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals

Cited by 112 publications

References 96 publications

Salivary immunoglobulin classes in Nigerian cigarette smokers: Indication for increased risk of oral diseases

Salivary immunoglobulin classes in Nigerian cigarette smokers: Indication for increased risk of oral diseases

Predictors of remission in rheumatoid arthritis patients treated with biologics: a systematic review and meta-analysis

Chronic exposure to cigarette smoke transiently worsens the disease course in a mouse model of pulmonary paracoccidioidomycosis

Contact Info

Product

Resources

About