Acute LPS inhalation in healthy volunteers induces dendritic cell maturation in vivo

Alexis, Neil E.; Lay, John C.; Almond, Martha; Bromberg, Philip A.; Patel, Dhavalkumar D.; Peden, David B.

doi:10.1016/j.jaci.2004.11.040

Cited by 61 publications

(29 citation statements)

References 25 publications

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“…The indication of a more antigen presentation phenotype of the macrophages (elevated level of CD86)22 in the present study resemble patterns observed after LPS inhalation challenge 8. After 6 h of inhaled LPS, markers of dendritic cell maturation were upregulated and discrete populations of mature dendritic cell were observed.…”

Section: Discussionsupporting

confidence: 83%

“…Studies involving LPS challenge in healthy volunteers and in vitro exposure to organic dust have shown that the cell surface phenotypes on airway cells have been modified 7 8. Cell surface phenotypes, such as the Fcγ receptors CD16/FcγRIII and CD64/FcγRI, are involved in neutrophil activation and are upregulated in proinflammatory environments 9.…”

Section: Introductionmentioning

confidence: 99%

“…Cell surface phenotypes, such as the Fcγ receptors CD16/FcγRIII and CD64/FcγRI, are involved in neutrophil activation and are upregulated in proinflammatory environments 9. CD11b/CR3, which mediates complement-associated phagocytosis, plays a role in airway response to pathogens and is important in neutrophil migration, and CD80 and CD86 are costimulatory molecules that are involved in dendritic cell maturation and antigen presentation to T cells 7 8. All these cell surface phenotypes mediate innate and acquired immune responses that are of interest in bacterial endotoxin-induced inflammation.…”

Section: Introductionmentioning

confidence: 99%

“…First, we sought to determine whether airway inflammation had changed 1 year after cessation of exposure, and second, since it had been shown that cell surface phenotypes on airway cells were modified in environments where pathogenic/bacterial material are present,7 8 we wanted to test if prolonged exposure to BSCP (containing LPS) induced similar effects.…”

Section: Introductionmentioning

confidence: 99%

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Recovery from workplace-induced airway inflammation 1 year after cessation of exposure

et al. 2012

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Recovery from workplace-induced airway inflammation 1 year after cessation of exposure

et al. 2012

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“…All volunteers had normal lung function, normal methacholine challenge and negative skin tests and were genotyped only after challenge and assessment of samples was completed, thus avoiding selection bias. Venipuncture, induced sputum, spirometry, cytokine measurements in sputum and genotyping for GSTM1 were performed as previously described 8 9. Circulating total WBCs, PMNs and platelet counts, sputum PMNs and mediators in recovered sputum samples, spirometry measures and symptom scores were assessed at baseline (pre-challenge) and 4 h after CCRE challenge was complete in GSTM1 null and sufficient cohorts.…”

Section: Methodsmentioning

confidence: 99%

Enhancement of systemic and sputum granulocyte response to inhaled endotoxin in people with the GSTM1 null genotype: Figure 1

et al. 2011

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Objective To determine if the GSTM1 null genotype is a risk factor for increased inflammatory response to inhaled endotoxin. Methods 35 volunteers who had undergone inhalation challenge with a 20 000 endotoxin unit dose of Clinical Center Reference Endotoxin (CCRE) were genotyped for the GSTM1 null polymorphism. Parameters of airway and systemic inflammation observed before and after challenge were compared in GSTM1 null (n=17) and GSTM1 (n=18) sufficient volunteers. Results GSTM1 null volunteers had significantly increased circulating white blood cells (WBCs), polymorphonuclear neutrophils (PMNs), platelets and sputum PMNs (% sputum PMNs and PMNs/mg sputum) after CCRE challenge. GSTM1 sufficient volunteers had significant, but lower increases in circulating WBCs, PMNs and % sputum PMNs, and no increase in platelets or PMNs/mg sputum. Linear regression analysis adjusted for baseline values of the entire cohort revealed that the GSTM1 null genotype significantly increased circulating WBCs, platelets and % sputum PMNs after challenge Conclusion These data support the hypothesis that the GSTM1 null genotype is a risk factor for increased acute respiratory and systemic inflammatory response to inhaled CCRE. These data are consistent with other observations that the GSTM1 null genotype is associated with increased respiratory, systemic and cardiovascular effects linked to ambient air particulate matter exposure and indicate that the GSTM1 null genotype should be considered a risk factor for adverse health effects associated with exposure to environmental endotoxin.

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Occupational endotoxin‐exposure and possible health effects on humans (review)

Liebers

Brüning

Raulf‐Heimsoth

2006

American J Industrial Med

131

101

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Acute LPS inhalation in healthy volunteers induces dendritic cell maturation in vivo

Cited by 61 publications

References 25 publications

Recovery from workplace-induced airway inflammation 1 year after cessation of exposure

Recovery from workplace-induced airway inflammation 1 year after cessation of exposure

Enhancement of systemic and sputum granulocyte response to inhaled endotoxin in people with the GSTM1 null genotype: Figure 1

Occupational endotoxin‐exposure and possible health effects on humans (review)

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