Leucocyte response and anti-inflammatory cytokines in community acquired pneumonia

Kolling, U K; Hansen, F; Braun, J.; Rink, Lothar; Katus, Hugo A.; Dalhoff, K

doi:10.1136/thorax.56.2.121

Cited by 48 publications

(39 citation statements)

References 23 publications

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“…No acute phase response was observed for IL-5, IL-12, IFN-c, MCP and MIP. Our results are comparable with former findings in human and experimental pneumococcal pneumonia, in which the inflammatory response is characterised by an extended pro-inflammatory response resulting in high levels of IL-6 and IL-1RA [2,10,13,21,[35][36][37]. In this study, cytokines and chemokines were only measured in serum.…”

Section: Community-acquired Pneumonia H Endeman Et Alsupporting

confidence: 79%

“…The human immune response to CAP varies between the different causative microorganisms and severities of disease. An important early component of the host response is the release of cytokines produced by inflammatory cells [2,3]. In experimental settings, the appearance of cytokines depends on the time after induction of endotoxaemia.…”

mentioning

confidence: 99%

“…The role of each specific cytokine in the inflammatory response to CAP is still a subject of ongoing research. In general, tumour necrosis factor (TNF)-a and interleukin (IL)-6 are considered essential pro-inflammatory proteins and IL-10 is considered the most important cytokine with anti-inflammatory properties [2,[4][5][6][7]. These three cytokines are reported to play an important role in the susceptibility to experimental pneumonia caused by different pathogens [8][9][10].…”

mentioning

confidence: 99%

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Systemic cytokine response in patients with community-acquired pneumonia

Endeman¹,

Meijvis²,

Rijkers³

et al. 2010

European Respiratory Journal

105

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The role of individual cytokines and polymorphisms in pneumonia has been described, but the relationship between different cytokines and polymorphisms in relation to causative microorganisms, antibiotics, corticosteroids and clinical course has not. This study questions the relationship between cytokines, polymorphisms and clinical characteristics of pneumonia.Patients diagnosed with pneumonia were included in the study. Serum cytokine levels were measured during hospital stay, genotyping was performed, causative microorganisms were identified and patients were monitored throughout the hospital stay.In 201 patients with pneumonia interleukin (IL)-1 receptor antagonist (IL-1RA), IL-6, IL-8 and IL-10 acted as acute phase proteins. After admission, the levels of these cytokines decreased rapidly. Single nucleotide polymorphisms did not influence cytokine production and were not associated with clinical outcome. Cytokine serum levels were significantly higher in patients with pneumococcal pneumonia. The decrease in levels of cytokines was independently influenced by the start of corticosteroid therapy.IL-1RA, IL-6, IL-8 and IL-10 are acute phase proteins, independent of genotype. Their levels are influenced by the nature of the causative microorganism and the start of corticosteroids therapy.

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Section: Community-acquired Pneumonia H Endeman Et Alsupporting

confidence: 79%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Systemic cytokine response in patients with community-acquired pneumonia

Endeman¹,

Meijvis²,

Rijkers³

et al. 2010

European Respiratory Journal

105

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“…7 17 18 Leucopenia was also associated with an almost fourfold higher risk of any or early treatment failure. In a recent study Kolling et al 19 found that leucocytes had a beneficial effect in CAP, not only due to their antimicrobial activity but also because they are able to modulate the pro-inflammatory cytokine response.…”

Section: Discussionmentioning

confidence: 99%

Risk factors of treatment failure in community acquired pneumonia: implications for disease outcome

Menéndez

Torres²,

Zalacaín³

et al. 2004

Thorax

275

235

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“…Therefore, it appears likely that, under inflammatory conditions in the lung, increased levels of several shedding products are found in the alveolar fluid. In fact, this has been described for CX3CL1, JAM-A, CXCL16, TNF, TNFR, TGF-␣, IL6R, and syndecans in human sputum samples (20,89,123,153,198) or murine alveolar lavage fluid (32,33,148).…”

Section: Adam17mentioning

confidence: 99%

ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets

Dreymueller

Uhlig

Ludwig

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

117

107

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-Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and, as recent research has shown, are the pivotal shedding enzymes mediating acute lung inflammation in a cell-specific manner. ADAM17 promotes endothelial and epithelial permeability, transendothelial leukocyte migration, and inflammatory mediator production by smooth muscle and epithelial cells. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. ADAM10 also promotes allergic asthma by driving B cell responses. Additionally, ADAM10 acts as a receptor for Staphylococcus aureus (S. aureus) ␣-toxin and is crucial for bacterial virulence. ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development. Pharmacological inhibitors that allow us to locally or systemically target and differentiate ADAM-family members in the lung suppress acute and asthmatic inflammatory responses and S. aureus virulence. These promising results encourage further research to develop therapeutic strategies based on selected ADAMs. These studies need also to address the role of the ADAMs in repair and regeneration in the lung to identify further therapeutic opportunities and possible side effects. metalloproteinase; shedding; inflammation; edema; asthma ACUTE OR CHRONIC INFLAMMATION in the lung can lead to a fatal loss of lung functions. Acute inflammation resulting from infection, aspiration of gastric juice, or overventilation during intensive care is initially characterized by enhanced inflammatory mediator production, edema formation, and recruitment of innate immune cells with the risk of lung damage. Asthma, chronic obstructive pulmonary disease (COPD), and lung fibrosis are fatal chronic diseases that are driven by persistent inflammation with a lack of resolution and impaired tissue regeneration. Targeting the immune response is the underlying principle of many treatment strategies against these diseases (reviewed in Ref. 7).The cytokines, growth factors, receptors, and adhesion molecules that drive the inflammatory process are all under intensive scrutiny. Many of these molecules undergo functional modulation by limited proteolysis, bringing the participating proteases into the focus of attention. Among these proteases is a class of metalloproteinases that subdivides into the matrix metalloproteinases (MMP) and the families of a disintegrin and metalloproteinases (ADAM) and ADAM with trombospondin motif. MMPs have already been intensively investigated with resp...

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Leucocyte response and anti-inflammatory cytokines in community acquired pneumonia

Cited by 48 publications

References 23 publications

Systemic cytokine response in patients with community-acquired pneumonia

Systemic cytokine response in patients with community-acquired pneumonia

Risk factors of treatment failure in community acquired pneumonia: implications for disease outcome

ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets

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