Cytokine levels in the sera of patients with idiopathic pulmonary fibrosis

Tsoutsou, Pelagia G.; Gourgoulianis, Konstantinos; Petinaki, Efthymia; Germenis, Anastasios E.; Tsoutsou, Anthousa; Mpaka, Maria; Efremidou, Smaragda; Molyvdas, Pashalis-Adam

doi:10.1016/j.rmed.2005.06.016

Cited by 64 publications

(42 citation statements)

References 33 publications

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“…The Ni and MALP-2-mediated synergistic induction of CXCL8 in HLF is also reminiscent of our previous observations with IL-6 (7). This is of particular concern in regards to pulmonary health given the correlation of elevated CXCL8 and IL-6 production with numerous respiratory disorders, including asthma (12,27) and pulmonary fibrosis (13,28).…”

Section: Discussionmentioning

confidence: 99%

“…In order to gain a better understanding of how Ni may influence microbial-driven inflammation in the lung, the current study focuses on changes in CXCL8 and CXCL10 expression in HLF after mixed exposures to Ni and MALP-2. Although any number of chemokines may be modulated during mixed exposures of chemical and microbial stimuli, CXCL8 and CXCL10 were chosen because both of these chemokines can be up-regulated during inflammation (12)(13)(14), yet display differential properties that can affect the development of respiratory disorders (e.g., fibrosis). Also included in the study is CCL2, another proinflammatory chemokine shown previously to be up-regulated after exposure to M. fermentans and MALP-2 (5, 15).…”

mentioning

confidence: 99%

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Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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Particulate matter air pollution (PM) has been linked with chronic respiratory diseases. Real-life exposures are likely to involve a mixture of chemical and microbial stimuli, yet little attention has been paid to the potential interactions between PM components (e.g., Ni) and microbial agents on the development of inflammatory-like conditions in the lung. Using the Toll-like receptor (TLR)-2 agonist MALP-2 as a lipopeptide relevant to microbial colonization, we hypothesized that nickel sensitizes human lung fibroblasts (HLF) for microbial-driven chemokine release through modulation of TLR signaling pathways. NiSO 4 (200 mM) synergistically enhanced CXCL8, yet antagonized CXCL10 mRNA expression and protein release from HLF in response to MALP-2. RT 2 -PCR pathway-focused array results indicated that NiSO 4 exposure did not alter the expression of TLRs or their downstream signaling mediators, yet significantly increased the expression of cyclooxygenase 2 (COX-2). Moreover, when NiSO 4 was given in combination with MALP-2, there was an amplified induction of COX-2 mRNA and protein along with its metabolic product, PGE2, in HLF. The COX-2 inhibitor, NS-398, attenuated NiSO 4 and MALP-2-induced PGE2 and CXCL8 release and partially reversed the NiSO 4 -dependent inhibition of MALP-2-induced CXCL10 release from HLF. These data indicate that NiSO 4 alters the pattern of TLR-2-dependent chemokine release from HLF via a COX-2-mediated pathway. The quantitative and qualitative effects of NiSO 4 on microbial-driven chemokine release from HLF shed new light on how PM-derived metals can exacerbate respiratory diseases.Keywords: COX-2; nickel; inflammation; chemokines; fibroblasts Particulate matter air pollution (PM) is a contributing risk factor for many adverse health effects, including respiratory diseases (1). Real-life scenarios are likely to involve exposures not only to chemical stresses such as PM, but microbial stimuli as well. While much attention has been paid to microbial-driven inflammation in the lung, limited information is available regarding the potential interactions between PM exposures and microbial stress on respiratory function. There are reports, however, of increased numbers of hospitalizations for respiratory disorders including infections on days of increased levels of PM (2). In support of these epidemiologic findings, several rodent models have shown PM exposure can increase susceptibility to infectious bacteria such as Listeria monocytogenes and Streptococcus pneumoniae (3, 4).Recent evidence suggests that colonization with species originally considered commensal and not causing overt disease (e.g., Mycoplasma fermentans) also has the potential to interact with other stimuli and/or alter biological responses in infected host cells (5, 6). For example, we have previously shown that exposure of human lung fibroblast cells (HLF) to M. fermentans synergistically enhances the release of IL-6 by PM in the form of residual oil fly ash (ROFA) compared to either stimulus alone (7). It is well recognized t...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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“…An increased production of IL-10 by alveolar macrophages has been demonstrated in interstitial lung disease (Martinez et al 1997). The levels of IL-2, -8, -10, and -12 are higher in sera of patients with IPF compared with those of controls (Tsoutsou et al 2006). The bronchoalveolar lavage fluid of sarcoidosis patients contains a higher level of IL-10 compared with that of control patients (Barbarin et al 2003), possibly due to increased release from alveolar macrophages (Oltmanns et al 2003).…”

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confidence: 99%

Expression of the Immunomodulator IL-10 in Type I Pneumocytes of the Rat: Alterations of IL-10 Expression in Radiation-induced Lung Damage

Haase

Klawitter

Geyer

et al. 2007

J Histochem Cytochem.

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Fibrosing alveolitis is a disease with inflammatory, proliferative, and fibrotic components. In different models, it has been shown that the cytokine interleukin-10 (IL-10) plays a conflicting role in inflammation-associated fibrotic processes, inasmuch as it is an antiinflammatory cytokine but also a TH2 cytokine with inherent pro-fibrotic effects. IL-10 is produced primarily by inflammatory cells. In this report, we show in a rat model of radiation-induced fibrosing alveolitis that IL-10 is also produced by type I alveolar epithelial cells in both normal and fibrotic lungs. The total amount of IL-10 in the lung is increased after irradiation, but type I pneumoyctes contain less IL-10. The R3/1 permanent type I pneumocyte cell line also contains IL-10, which is reduced after irradiation. Whereas in the normal lung, the entire alveolar surface is covered by IL-10—producing pneumocytes, this continuity is interrupted in fibrotic lungs, because type I pneumocytes lack full differentiation and thus full spreading over the alveolar surface. The exposure of the IL-10—negative epithelial basal membrane may allow for an easier attachment of inflammatory cells such as alveolar macrophages. These cells have the potential to act in a pro-inflammatory way by tumor necrosis factor α and also in a pro-fibrotic way by activating TH2 cytokines.

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“…87 These data are bolstered by a more recent investigation of the serum levels of several cytokines in IPF patients that found cytokines IL-2, IL-8, IL-10, and IL-12 to be significantly elevated, with IL-8 specifically negatively correlating with PFTs. 88 While studying a broader ILD population, and including only a small sample of IPF patients, a study by Vasakova et al similarly discovered a negative correlation between IL-8 BALF levels and lung function testing. 89 Finally, in a study by Richards et al referred to elsewhere in this review, …”

Section: Interleukin-8mentioning

confidence: 99%

Idiopathic pulmonary fibrosis biomarkers: clinical utility and a way of understanding disease pathogenesis

Flynn¹,

Baker²,

Kass

2015

CBF

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Idiopathic pulmonary fibrosis (IPF) is a typically fatal disease that remains incompletely understood despite intense study and the arrival of drugs that may alter the natural history of the disease. Rendering an accurate diagnosis and predicting prognosis remain challenging problems to clinicians. One potential solution to these clinical problems is the identification of IPF biomarkers, easily measured factors that can be employed to predict clinical behavior. Candidate biomarkers have been identified by research in the laboratory on potential culprit cells or genes that may contribute to the pathogenesis of IPF. In this review, we present the current data on a number of well-studied IPF biomarker candidates and their potential role in the pathogenesis of disease. We also establish a framework for evaluating utility of incorporating these IPF biomarkers into clinical practice.

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Cytokine levels in the sera of patients with idiopathic pulmonary fibrosis

Abstract: IL-2, IL-8, IL-10 and IL-12 (p40) were found to be elevated in the sera of patients with IPF. IFN-gamma was found to be decreased in the sera of patients with IPF.

Cited by 64 publications

References 33 publications

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Expression of the Immunomodulator IL-10 in Type I Pneumocytes of the Rat: Alterations of IL-10 Expression in Radiation-induced Lung Damage

Idiopathic pulmonary fibrosis biomarkers: clinical utility and a way of understanding disease pathogenesis

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