Rapid lung cytokine accumulation and neutrophil recruitment after lipopolysaccharide inhalation by cigarette smokers and nonsmokers

Wesselius, Lewis; Nelson, M. E.; Bailey, Kirstin; O’Brien-Ladner, Amy

doi:10.1016/s0022-2143(97)90167-0

Cited by 49 publications

(37 citation statements)

References 22 publications

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“…There are thus factors which support the idea that smokers may respond more strongly to LPS exposure than nonsmokers, thereby contradicting the hypothesis of LPS adaptation in smokers. These observations are supported by the finding by WESSELIUS et al [37], who showed that the recovery of neutrophils and IL-1b concentration in BAL fluid from smokers exceeded that of nonsmokers after LPS inhalation.…”

Section: Occupational and Environmental Lung Diseasesupporting

confidence: 83%

Repeated exposure to organic material alters inflammatory and physiological airway responses

Sundblad¹,

Schéele²,

Palmberg³

et al. 2009

European Respiratory Journal

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Farmers and smokers are repeatedly exposed to airborne organic material. We hypothesised that farmers and smokers show altered airway responses to inhaled organic, proinflammatory agents.A total of 11 farmers, 12 smokers and 12 controls underwent lipopolysaccharide (LPS) bronchial challenge and spent 3 h in a pig barn. Lung function, exhaled nitric oxide and bronchial responsiveness were assessed and nasal lavage fluid and induced sputum were also collected. Symptoms and body temperature were recorded before and after exposures.Following exposure to the pig barn, bronchial responsiveness, exhaled nitric oxide, sputum interleukin (IL)-6, nasal lavage cell count and IL-8 were increased to a greater extent in controls compared to farmers. The sputum IL-6 response was also attenuated in farmers after LPS challenge. The response shown by smokers following exposure to the pig barn was similar to that of controls regarding measurements of exhaled nitric oxide, IL-8 in nasal lavage and IL-6 in sputum, but more similar to farmers concerning bronchial responsiveness and the cell numbers present in nasal lavage. Sputum IL-8 showed a greater increase in smokers than in the other groups following LPS challenge.We conclude that individuals who are repeatedly exposed to organic material develop an adaptation to the effects of acute exposure to inhaled organic material.

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Section: Occupational and Environmental Lung Diseasesupporting

confidence: 83%

Repeated exposure to organic material alters inflammatory and physiological airway responses

Sundblad¹,

Schéele²,

Palmberg³

et al. 2009

European Respiratory Journal

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“…Furthermore, in the ex vivo blood-perfused flooded rat lung, there was no significant increase in alveolar leukocytes in TNF-treated lungs compared with the saline control (21). Although we observed increased neutrophil BALF counts in the TNF-treated animals in vivo at 8 h after treatment, we cannot exclude that their infiltration already occurs at much earlier time points, as was reported in other inflammation models (38,39) and a human endotoxin inhalation study (40). Therefore, we propose that the negative TNF action on edema reabsorption in vivo could at least partially be caused by the presence of infiltrating neutrophils.…”

Section: Discussionmentioning

confidence: 50%

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Braun

Hamacher

Morel³

et al. 2005

The Journal of Immunology

109

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Distinct from its receptor binding sites, TNF carries a lectin-like domain, situated at the tip of the molecule, which specifically binds oligosaccharides, such as N,N′-diacetylchitobiose. In view of the apparently conflicting data concerning TNF actions in pulmonary edema, we investigated the contribution of, on the one hand, the receptor binding sites and, in contrast, the lectin-like domain of the cytokine on pulmonary fluid reabsorption in in situ and in vivo flooded rat lungs. Receptor binding sites were blocked with the human soluble TNFR type 1 construct (sTNFR1), whereas the lectin-like domain was blunted with the oligosaccharide N,N′-diacetylchitobiose. We observed that in situ, TNF failed to stimulate alveolar liquid clearance, but did so together with the sTNFR1, and this activity was neutralized by N,N′-diacetylchitobiose. In vivo TNF inhibited liquid clearance, but activated it when complexed with the sTNFR1. A TNF-derived peptide mimic of the lectin-like domain activated fluid reabsorption in flooded lungs, and this activity was blunted by cotreatment with TNF. Our results thus indicate that in these models the receptor binding sites of TNF inhibit, whereas its lectin-like domain activates, edema reabsorption.

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“…1994; Wesselius et al. 1997) versus nonsmokers. However, we saw a decrease in the secretion of a range of other cytokines including TNF α , IL‐6, MIP‐1 α , MIP‐1 β , MCP‐1, IL‐1 β , and IP‐10 when treated with E‐liquid ± nicotine, nicotine, or cigarette smoke extract.…”

Section: Discussionmentioning

confidence: 99%

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

et al. 2017

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E‐cigarettes are perceived as harmless; however, evidence of their safety is lacking. New data suggests E‐cigarettes discharge a range of compounds capable of physiological damage to users. We previously established that cigarette smoke caused defective alveolar macrophage phagocytosis. The present study compared the effect E‐cigarette of components; E‐liquid flavors, nicotine, vegetable glycerine, and propylene glycol on phagocytosis, proinflammatory cytokine secretion, and phagocytic recognition molecule expression using differentiated THP‐1 macrophages. Similar to CSE, phagocytosis of NTHi bacteria was significantly decreased by E‐liquid flavoring (11.65–15.75%) versus control (27.01%). Nicotine also decreased phagocytosis (15.26%). E‐liquid, nicotine, and E‐liquid+ nicotine reduced phagocytic recognition molecules; SR‐A1 and TLR‐2. IL‐8 secretion increased with flavor and nicotine, while TNF α, IL‐1β, IL‐6, MIP‐1α, MIP‐1β, and MCP‐1 decreased after exposure to most flavors and nicotine. PG, VG, or PG:VG mix also induced a decrease in MIP‐1α and MIP‐1β. We conclude that E‐cigarettes can cause macrophage phagocytic dysfunction, expression of phagocytic recognition receptors and cytokine secretion pathways. As such, E‐cigarettes should be treated with caution by users, especially those who are nonsmokers.

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Rapid lung cytokine accumulation and neutrophil recruitment after lipopolysaccharide inhalation by cigarette smokers and nonsmokers

Cited by 49 publications

References 22 publications

Repeated exposure to organic material alters inflammatory and physiological airway responses

Repeated exposure to organic material alters inflammatory and physiological airway responses

Dichotomal Role of TNF in Experimental Pulmonary Edema Reabsorption

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

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