Circadian variation of sputum inflammatory cells in mild asthma

Panzer, Sarah E.; Dodge, Ann; Kelly, Elizabeth A.; Jarjour, Nizar N.

doi:10.1067/mai.2003.65

Cited by 67 publications

(52 citation statements)

References 35 publications

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“…Furthermore, the night fall in PEF was positively correlated with change in neutrophils and eosinophils, further indicating a relationship between nocturnal inflammation and decline of pulmonary function in nocturnal asthmatics (Martin et al 1991). Another study investigated FEV 1 and sputum inflammatory cells in mild asthmatics at 4 pm and 7 am resulting in similar findings to the previous studies, that is, lower FEV 1 at 7 am with higher numbers of sputum inflammatory cells compared to 4 pm timepoint (Panzer et al 2003).…”

Section: Asthmasupporting

confidence: 73%

“…One of the first studies involving 3000 asthma patients found that asthma episodes during washout from regular maintenance asthma treatment occurred 70-fold more frequently between 4 am and 5 am compared to 2 pm-3 pm (Dethlefsen and Repges 1985). Death from severe asthma attacks is also known to mostly occur during the night or early morning (Smolensky and D' Alonzo 1997;Cochrane and Clark 1975).These times coincide with the times at which lung function is reduced and inflammation and airway hyperreactivity is increased (Spengler and Shea 2000;Kraft et al 1996;Jarjour 1999;Martin et al 1991;Hetzel and Clark 1980;Gervais et al 1977;Bonnet et al 1991;Panzer et al 2003;Kelly et al 2004).…”

Section: Asthmamentioning

confidence: 99%

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A circadian based inflammatory response – implications for respiratory disease and treatment

Comas

Gordon

Oliver

et al. 2017

Sleep Science Practice

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Circadian clocks regulate the daily timing of many of our physiological, metabolic and biochemical functions. The immune system also displays circadian oscillations in immune cell count, synthesis and cytokine release, clock gene expression in cells and organs of the immune system as well as clock-controlled genes that regulate immune function. Circadian disruption leads to dysregulation of immune responses and inflammation which can further disrupt circadian rhythms. The response of organisms to immune challenges, such as allergic reactions also vary depending on time of the day, which can lead to detrimental responses particularly during the rest and early active periods. This review evaluates what is currently known in terms of circadian biology of immune response and the cross-talk between circadian and immune system. We discuss the circadian pattern of three respiratory-related inflammatory diseases, chronic obstructive pulmonary disease, allergic rhinitis and asthma. Increasing our knowledge on circadian patterns of immune responses and developing chronotherapeutic studies in inflammatory diseases with strong circadian patterns will lead to preventive measures as well as improved therapies focussing on the circadian rhythms of symptoms and the daily variation of the patients' responses to medication.

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Section: Asthmasupporting

confidence: 73%

Section: Asthmamentioning

confidence: 99%

A circadian based inflammatory response – implications for respiratory disease and treatment

Comas

Gordon

Oliver

et al. 2017

Sleep Science Practice

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“…These inflammatory changes have been related to airflow limitation and reversibility [98]. Most investigators view the circadian cycles of cortisol, cholinergic tone, histamine and adrenaline as having theoretical relevance to inflammation, but the specific and detailed mechanistic links among these cycling biological processes and the control of inflammation remain incompletely defined [99].…”

Section: Asthmamentioning

confidence: 99%

Night-time symptoms: a forgotten dimension of COPD

Agustí¹,

Hedner²,

Marı́n³

et al. 2011

Eur Respir Rev

197

189

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Sleep quality is often poor in patients with chronic obstructive pulmonary disease (COPD), but these night-time symptoms are frequently unnoticed by physicians and/or not reported by patients themselves. Therefore, the prevalence and clinical impact of sleep disturbances and night-time symptoms in COPD is not well understood and has not been a clinical focus to date. To address this gap, an expert panel meeting was convened in Barcelona, Spain, in March 2011 to discuss the aetiology, evolution, burden, long-term clinical consequences and optimal management of night-time symptoms in COPD. The term ''night-time symptoms'' in COPD has not been distinctly defined in an objective sense but epidemiological data suggests that the prevalence of nocturnal symptoms and symptomatic sleep disturbance may exceed 75% in patients with COPD. The panel concluded that night-time symptoms in COPD are prevalent and bothersome; that their cause(s) are multiple and include demographic factors, such as age and obesity, pharmacotherapy, disease-specific symptoms and the presence of comorbid sleep disorders, and other medical conditions; and that potential long-term consequences can include lung function changes, increased exacerbation frequency, emergence or worsening of cardiovascular disease, cognitive effects, depression, impaired quality of life and increased mortality. To date, few interventional studies have investigated them, but emerging data suggest that bronchodilator therapy can improve them if deployed appropriately. In summary, night-time symptoms in COPD warrant further clinical investigation with validated tools.

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“…Bronchoscopy and bronchial lavage (BL) were conducted as previously described (33,34). Briefly, one bronchopulmonary segment was identified, and the fiberoptic bronchoscope was wedged into that segment.…”

Section: Isolation Of Alveolar Macrophagesmentioning

confidence: 99%

“…Sandwich ELISA for MCP-1 was performed with Abs obtained from Endogen as previously described (33,34). PBS with 0.1% Tween 20 (PBST) was used for all washes.…”

Section: Elisamentioning

confidence: 99%

The Role of p38 MAPK in Rhinovirus-Induced Monocyte Chemoattractant Protein-1 Production by Monocytic-Lineage Cells

Hall

Bates

Guar

et al. 2005

The Journal of Immunology

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Viral respiratory infections are a major cause of asthma exacerbations and can contribute to the pathogenesis of asthma. Major group human rhinovirus enters cells by binding to the cell surface molecule ICAM-1 that is present on epithelial and monocytic lineage cells. The focus of the resulting viral infection is in bronchial epithelia. However, previous studies of the cytokine dysregulation that follows rhinovirus infection have implicated monocytic lineage cells in establishing the inflammatory environment even though productive infection is not a result. We have determined that human alveolar macrophages and human peripheral blood monocytes release MCP-1 upon exposure to human rhinovirus 16 (HRV16). Indeed, we have found p38 MAPK activation in human alveolar macrophages within 15 min of exposure to HRV16, and this activation lasts up to 1 h. The targets of p38 MAPK activation include transcriptional activators of the MCP-1 promoter. The transcription factor ATF-2, a p38 MAPK substrate, is phosphorylated 45 min after HRV16 exposure. Furthermore, IκBα, the inhibitor of the transcription factor NF-κB, is degraded. Prevention of HRV16 binding was effective in blocking p38 MAPK activation, ATF-2 phosphorylation, and MCP-1 release. This is the first report of a relationship between HRV16 exposure, MCP-1 release and monocytic-lineage cells suggesting that MCP-1 plays a role in establishing the inflammatory microenvironment initiated in the human airway upon exposure to rhinovirus.

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Circadian variation of sputum inflammatory cells in mild asthma

Cited by 67 publications

References 35 publications

A circadian based inflammatory response – implications for respiratory disease and treatment

A circadian based inflammatory response – implications for respiratory disease and treatment

Night-time symptoms: a forgotten dimension of COPD

The Role of p38 MAPK in Rhinovirus-Induced Monocyte Chemoattractant Protein-1 Production by Monocytic-Lineage Cells

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