The chemotactic activity for granulocytes produced by virally infected fibroblasts is identical to monocyte‐derived interleukin 8

Damme, Jo Van; Decock, Benny; Conings, René; Lenaerts, Jean‐Pierre; Opdenakker, Ghislain; Billiau, Alfons

doi:10.1002/eji.1830190706

Cited by 130 publications

(62 citation statements)

References 43 publications

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“…The discrepancies to previous reports (23)(24)(25)(26) may be explained by the easy inducibility of the IL-8 gene. Even adherence (29) or detachment (30) of cells represent sufficient stimuli for IL-8 production.…”

Section: Discussioncontrasting

confidence: 78%

Selective induction of monocyte and not neutrophil-attracting chemokines after influenza A virus infection.

Sprenger

Meyer

Kaufmann

et al. 1996

The Journal of Experimental Medicine

121

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SummaryIt is characteristic for virus infections that monocytes/macrophages and lymphocytes infiltrate infected tissue while neutrophils are absent. To understand the mechanisms selectively attracting mononuclear cells in viral diseases, we examined in an influenza A virus model the expression and regulation of chemokines as candidate molecules responsible for the immigration of leukocytes into inflamed tissue. After influenza A virus infection of human monocytes, a rapid expression of the mononuclear cell attracting CC-chemokine genes MIP-1 , MCP-1, and RANTES occurred which was followed by the release ofchemokine proteins. In striking contrast to CC-chemokines, the expression of the prototype neutrophil CXC-chemoattractants IL-8 and GRO-oe was completely suppressed after influenza A infection. The release of other neutrophil chemotactic factors was excluded by nficrochemotaxis assays. These results suggest that the virus-specific induction of mononuclear cell-attracting chemokines accounts for the preferential influx ofmononuclear leukocytes into virus-infected tissue.A hallmark of tissue inflammation is the recruitment, immigration and activation of leukocytes. Gradients of chemotactic factors direct transendothelial migration and movement through the extracellular matrix (1). Most viral diseases are characterized by the development of a specific infiltration consisting predominantly of mononuclear leukocytes while neutrophils are absent as long as no complicating bacterial superinfection occurs. Previous reports show that exposure of monocytes or macrophages to virus results in the release of various proinflammatory cytokines (2-5). Along this line, we demonstrated that an infection of monocytes with influenza A or coxsackie B3 virus induced TNF-o~, IL-1, and IL-6 production (6-9). However, the induction of these proinflammatory cytokines cannot explain the development of characteristic mononuclear leukocyte infiltrations in virally infected tissue.In virus infections, little attention has been focused on the chemokine family and a systematic analysis is still missing. Chemokines are potent chemoattractant cytokines (10, 11) and have to be considered as the main candidate molecules responsible for the selective recruitment of distinct leukocyte populations. Members of the CC-chemokine subfamily, such as MIP-lcl 1 (macrophage inflammatory protein-lc~), MCP-1 (monocyte chemotactic protein-I), and RANTES (regulated upon activation, normal T cell expressed and secreted) preferentially attract monocytes and lymphocytes (12). The CXC-chemokines which contain an ELR-motifpreceding the first cysteine, such as IL-8 (interleukin-8) or GRO-ci (melanoma growth stimulatory activity) are major neutrophil chemoattractants (13).As a first step to study the mechanisms responsible for the generation of a typical virus-induced tissue infiltration consisting predominantly of mononuclear cells, we employed influenza A virus to infect human monocytes. Here we report the selective induction of mononuclear cell attracting chemokine...

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Section: Discussioncontrasting

confidence: 78%

Selective induction of monocyte and not neutrophil-attracting chemokines after influenza A virus infection.

Sprenger

Meyer

Kaufmann

et al. 1996

The Journal of Experimental Medicine

121

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“…46,47 IL-8 is produced by numerous cells including fibroblasts, endothelial cells, lymphocytes, neutrophils, and macrophages. 22,[48][49][50][51][52] In the present study, the levels of IL-8 expression and cardiomyocyte apoptosis peaked at the same stage (stage II), but the cardiomyocytes that underwent apoptosis showed no IL-8 expression. Furthermore, the number of CD68-positive macrophages peaked at the later stage of MI (stage III) and showed no IL-8 expression.…”

Section: Discussionmentioning

confidence: 72%

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

et al. 2006

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To clarify the role of myocardial apoptosis associated with the expression of proinflammatory cytokines in human myocardial infarction (MI), we have analyzed the expression of apoptosis positive for single-stranded DNA (ss-DNA) antibody, tumor necrosis factor (TNF)-a, and interleukin (IL)-8 in 147 samples of infarcted myocardial tissue from 65 patients. ss-DNA-positive apoptotic nuclei were found mainly in cardiomyocytes in the border zones and granulation tissue cells in the infarct foci. The ss-DNA index (SI) of cardiomyocytes (average 0.13%) peaked at stage II (established myocardial necrosis), the value being significantly higher than at stages III (macrophage infiltration), IV (granulation formation), and V (scar formation) (Po0.05), whereas the SI of granulation tissue (average 0.08%) at stages III, IV, and V showed no significant differences between the three stages. These results suggest that cardiomyocyte apoptosis in the border zone is responsible for cellular loss in the acute stage of MI, whereas granulation tissue apoptosis may not be involved in the process of ventricular remodeling. TNF-a was expressed in cardiomyocytes in the border zones of infarct foci, but no significant positive correlation was found between SI and TNF-a index in cardiomyocytes (r ¼ 0.08, P ¼ 0.37), suggesting that TNF-a does not serve as a direct trigger of cardiomyocyte apoptosis in vivo. The number of IL-8-positive cells peaked at stage II, and IL-8-myeloperoxidase-double-positive neutrophils were frequently detected, indicating that infiltrating neutrophils are the predominant source of IL-8 in the infarcted myocardium. These results suggest that, in human MI, TNF-a produced by cardiomyocytes does not play a critical role in their apoptosis, and that IL-8 produced by neutrophils is responsible for the subsequent accumulation and activation of neutrophils, thus increasing the degree of myocardial damage.

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“…MT1-MMP is also known to participate in wound healing and is expressed by monocytes. IL-8, GRO-␣, and GRO-␥ belong to the subgroup of CXC chemokine family members that contain the ELR motif near the N terminus, which is essential for neutrophil chemotactic activity (34). MT1-MMP processing of IL-8 removes the first five residues, which is more active than the untruncated form.…”

Section: Discussionmentioning

confidence: 99%

Membrane protease proteomics: Isotope-coded affinity tag MS identification of undescribed MT1–matrix metalloproteinase substrates

Tam

Morrison

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

268

228

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By proteolytic modification of low abundant signaling proteins and membrane receptors, proteases exert potent posttranslational control over cell behavior at the postsecretion level. Hence, substrate discovery is indispensable for understanding the biological role of proteases in vivo. Indeed, matrix metalloproteinases (MMPs), long associated with extracellular matrix degradation, are increasingly recognized as important processing enzymes of bioactive molecules. MS is now the primary proteomic technique for detecting, identifying, and quantitating proteins in cells or tissues. Here we used isotopecoded affinity tag labeling and multidimensional liquid chromatography inline with tandem MS to identify MDA-MB-231 breast carcinoma cell proteins shed from the cell surface or the pericellular matrix and extracellular proteins that were degraded or processed after transfection with human membrane type 1-MMP (MT1-MMP). Potential substrates were identified as those having altered protein levels compared with the E240A inactive MT1-MMP mutant or vector transfectants. New substrates were biochemically confirmed by matrix-assisted laser desorption ionization-time-of-flight MS and Edman sequencing of cleavage fragments after incubation with recombinant soluble MT1-MMP in vitro. We report many previously uncharacterized substrates of MT1-MMP, including the neutrophil chemokine IL-8, secretory leukocyte protease inhibitor, pro-tumor necrosis factor ␣, death receptor-6, and connective tissue growth factor, indicating that MT1-MMP is an important signaling protease in addition to its traditionally ascribed roles in pericellular matrix remodeling. Moreover, the high-throughput and quantitative nature of isotope-coded affinity tag labeling combined with tandem MS sequencing is a previously undescribed degradomic screen for protease substrate discovery that should be generally adaptable to other classes of protease for exploring proteolytic function in complex and dynamic biological contexts.I n all living organisms, proteases exert high-order posttranslational control over a diverse range of cellular functions. Altered protease expression and substrate proteolysis are pivotal elements in the pathogenesis of many diseases (1) with 53 hereditary genetic diseases of proteolysis recognized (2). Indeed, proteases represent Ϸ10% of current drug targets (3). Elucidating the substrate repertoire of a protease is critical to understanding its biological role, but given the large number of proteases (Ͼ553) present in the human genome (2), this is a daunting task. Innovative approaches using combinatorial or positional scanning libraries of fluorogenic (4) and inhibitory peptides (5) and oriented (6) and phage display (7) peptide libraries can determine consensus protease cleavage sequences. However, bioinformatic identification of proteins containing these sequences followed by biochemical and in vivo validation of proteolytic susceptibility has led to the identification of relatively few biologically relevant new substrates. This is not s...

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The chemotactic activity for granulocytes produced by virally infected fibroblasts is identical to monocyte‐derived interleukin 8

Cited by 130 publications

References 43 publications

Selective induction of monocyte and not neutrophil-attracting chemokines after influenza A virus infection.

Selective induction of monocyte and not neutrophil-attracting chemokines after influenza A virus infection.

Myocardial apoptosis associated with the expression of proinflammatory cytokines during the course of myocardial infarction

Membrane protease proteomics: Isotope-coded affinity tag MS identification of undescribed MT1–matrix metalloproteinase substrates

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