Functional aspects of the interaction between interleukin-8 and sulfated glycosaminoglycans

Pichert, Annelie; Schlorke, Denise; Franz, Sandra; Arnhold, J

doi:10.4161/biom.21316

Cited by 42 publications

(34 citation statements)

References 75 publications

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“…To more closely examine the apparent propensity for human leukocytes to migrate specifically to a sub-Matrigel (“subepithelial”) location in the corneal facsimile model, we double stained HAdV-D37-infected and mock-infected facsimiles for CXCL8 and heparan sulfate. The latter is a prominent component of corneal epithelial basement membranes (Torricelli et al 2013), a constituent of Matrigel (Benton et al 2011), and was shown previously to bind CXCL8 (Webb et al 1993; Middleton et al 1997; Pichert et al 2012). By confocal microscopy, CXCL8 was expressed in HAdV-D37-infected but not in mock-infected facsimiles (Fig.…”

Section: Resultsmentioning

confidence: 99%

Novel model of innate immunity in corneal infection

Rajaiya

Zhou

Barequet

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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The cornea functions as the major refractive interface for vision and protects the internal eye from insult. Current understanding of innate immune responses to corneal infection derives from a synthesis of in vitro and in vivo analyses. However, monolayer cell cultures and mouse models do not accurately duplicate all aspects of innate immunity in human patients. Here, we describe a three-dimensional culture system that incorporates human cells and extracellular matrix to more completely simulate the human cornea for studies of infection. Human corneal stromal fibroblasts were mixed with type I collagen in 3-μm pore size transwell inserts, and overlayed with Matrigel to simulate a human corneal stroma and epithelial basement membrane. These were then infected with a cornea-tropic adenovirus, and exposed on their inferior side to leukocytes derived from human peripheral blood. Subsequent analyses were performed with histology, confocal microscopy, ELISA, and fluorescence-activated cell sorting (FACS). CXCL8, a neutrophil chemokine shown previously as the first cytokine induced in infection of human corneal cells, increased upon adenovirus infection of facsimiles in a dose-responsive fashion. Myeloperoxidase-positive cells infiltrated infected corneal facsimiles in a sub-Matrigel location, possibly due to CXCL8 colocalization with heparan sulfate, a Matrigel constituent. Cellular infiltration was significantly inhibited by treatment with chemical inhibitors of p38 MAPK and Src kinase, both constituents of a signaling cascade previously suggested to regulate inflammation after adenovirus infection. FACS analysis determined that both virus and corneal fibroblasts were necessary for the induction of leukocyte migration into the facsimiles. The corneal facsimile, literally a cornea in a test tube, permits mechanistic studies on human tissue in a highly tractable system.

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Section: Resultsmentioning

confidence: 99%

Novel model of innate immunity in corneal infection

Rajaiya

Zhou

Barequet

et al. 2015

In Vitro Cell.Dev.Biol.-Animal

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“…IL-8 is a multifunctional proinflammatory chemokine produced mainly through activation of TLR signaling [68,69]. Upon virus infection, IL-8 recruits immune cells, such as macrophages, neutrophils, and dendritic cells, to the site of infection, inducing phagocytosis, apoptosis, and cell death [70,71]. HEV infection in Huh7 cells significantly upregulated the IL-8 promoter activity, and a HEVencoded ORF1 was subsequently shown to heighten IL-8 expression ( Fig.…”

Section: Hev-mediated Irf Activationmentioning

confidence: 99%

Host Innate Immunity against Hepatitis E Virus and Viral Evasion Mechanisms

Kang

Myoung

2017

Journal of Microbiology and Biotechnology

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Hepatitis E virus (HEV) infections cause epidemic or sporadic acute hepatitis, which are mostly self-limiting. However, viral infection in immunocompromised patients and pregnant women may result in serious consequences, such as chronic hepatitis and liver damage, mortality of the latter of which reaches up to 20-30%. Type I interferon (IFN)-induced antiviral immunity is known to be the first-line defense against virus infection. Upon HEV infection in the cell, the virus genome is recognized by pathogen recognition receptors, leading to rapid activation of intracellular signaling cascades. Expression of type I IFN triggers induction of a barrage of IFN-stimulated genes, helping the cells cope with viral infection. Interestingly, some of the HEV-encoded genes seem to be involved in disrupting signaling cascades for antiviral immune responses, and thus crippling cytokine/chemokine production. Antagonistic mechanisms of type I IFN responses by HEV have only recently begun to emerge, and in this review, we summarize known HEV evasion strategies and compare them with those of other hepatitis viruses.

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“…The interaction of IL-8 with these GAGs is critical for the chemotractant capability of IL-8. Mutant IL-8 lacking the C-terminal GAG binding domain does not recruit neutrophils to the same extent as WT IL-8 [57]. Taken together, the results of these studies suggest that the interaction of cytokines and chemokines with the ECM is critical for migration of inflammatory cells to the site of tissue damage, permitting both the clearance of infection and the propagation of the inflammatory response.…”

Section: The Ecmmentioning

confidence: 99%

Transitional Remodeling of the Hepatic Extracellular Matrix in Alcohol-Induced Liver Injury

Poole

Arteel

2016

BioMed Research International

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Alcohol consumption is a common custom worldwide, and the toxic effects of alcohol on several target organs are well understood. The liver is the primary site of alcohol metabolism and is therefore the major target of alcohol toxicity. Alcoholic liver disease is a spectrum of disease states, ranging from simple steatosis (fat accumulation), to inflammation, and eventually to fibrosis and cirrhosis if untreated. The fibrotic stage of ALD is primarily characterized by robust accumulation of extracellular matrix (ECM) proteins (collagens) which ultimately impairs the function of the organ. The role of the ECM in early stages of ALD is poorly understood, but recent research has demonstrated that a number of changes in the hepatic ECM in prefibrotic ALD not only are present, but may also contribute to disease progression. The purpose of this review is to summarize the established and proposed changes to the hepatic extracellular matrix (ECM) that may contribute to earlier stages of ALD development and to discuss potential mechanisms by which these changes may mediate the progression of the disease.

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Functional aspects of the interaction between interleukin-8 and sulfated glycosaminoglycans

Cited by 42 publications

References 75 publications

Novel model of innate immunity in corneal infection

Novel model of innate immunity in corneal infection

Host Innate Immunity against Hepatitis E Virus and Viral Evasion Mechanisms

Transitional Remodeling of the Hepatic Extracellular Matrix in Alcohol-Induced Liver Injury

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