Search results for "inflammation"

2014

Type I interferon (IFN-α/β) represents the key element of the antiviral defense mechanisms against most viruses, however, rotaviruses that infect the gut epithelium, display little sensitivity to type I IFN. Here, we report that the intestinal epithelium is a unique cell compartment in the organism that does not depend on type I IFN in antiviral defenses. Type I IFN was unable to induce antiviral gene expression in intestinal epithelial cells (IEC) that correlated well with low epithelial expression of both chains of the IFN-α/β receptor complex. In stark contrast, IECs strongly responded to IFN-λ on baseline, upon IFN treatment and virus challenge. Commensal microflora was found to establi…

Genetic Variation Determines Mast Cell Functions in Experimental Asthma

2011

Abstract Mast cell-deficient mice are a key for investigating the function of mast cells in health and disease. Allergic airway disease induced as a Th2-type immune response in mice is employed as a model to unravel the mechanisms underlying inception and progression of human allergic asthma. Previous work done in mast cell-deficient mouse strains that otherwise typically mount Th1-dominated immune responses revealed contradictory results as to whether mast cells contribute to the development of airway hyperresponsiveness and airway inflammation. However, a major contribution of mast cells was shown using adjuvant-free protocols to achieve sensitization. The identification of a traceable ge…

Correction: Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan.

2018

[This corrects the article DOI: 10.1371/journal.pone.0163841.].

Predominant role of NF-kappa B p65 in the pathogenesis of chronic intestinal inflammation.

1998

NF-kappa B is a key transcription factor of lymphocytes and macrophages with important regulatory functions in the immune system and inflammatory processes. These functions are at least partially based on its ability to regulate the promoters of a variety of genes whose products, such as cytokines, adhesion molecules and acute phase proteins, are critical for inflammatory processes. In the present study, we describe a method to treat established intestinal inflammation by local or systemic application of antisense phosphorothioate oligonucleotides targeting the translation start site of the p65 subunit of NF-kappa B. Specific downregulation of p65 by administration of antisense phosphorothi…

HSP90 and HSP70: Implication in Inflammation Processes and Therapeutic Approaches for Myeloproliferative Neoplasms.

2015

Myeloproliferative neoplasms (MPN) are clonal stem cell disorders that lead to the excessive production of one or more blood cell lineages. It has been reported that, in most MPN, inflammatory cytokines are frequently increased, indicating that inflammation plays a crucial role in these disorders. Heat shock proteins (HSP) are induced in response to many stressful conditions from heat shock to hypoxia and inflammation. Besides their chaperone and cytoprotective functions, HSPs are key players during inflammation, hence the term “chaperokine.” Through their chaperone activity, HSP90, a stabilizer of many oncogenes (e.g., JAK2), and HSP70, a powerful antiapoptotic chaperone, tightly regulate …

Disulfide stress and its targets in acute pancreatitis

2014

Under physiological conditions, the balance between ROS production and removal properly maintains the intracellular redox-sensitive signaling as well as the appropriate status of protein thiols and disulfides. However, inflammation among other factors can modify this balance causing a rapid increase in intracellular ROS levels and hence thiol oxidation, eventually leading to oxidative stress. In the case of acute pancreatitis, both redox signaling and oxidative stress seem to contribute to the progression of the severe form of the disease. In this review we will focus on the reversible oxidation of protein cysteines during the course of acute pancreatitis. We describe disulfide stress in an…

Expression of cell adhesion molecules in inflammatory myopathies.

1995

We examined the expression of cell adhesion molecules in 25 cases of inflammatory myopathies. Inflammatory myopathies showed upregulation of adhesion molecules. ICAM-1 was strongly expressed on endothelial cells as well as on fibroblasts and infiltrating leukocytes while the expression of VCAM-1, similar in its distribution, was much weaker. A few muscle fibers in polymyositis revealed sarcolemmal labeling for ICAM-1. ELAM-1 showed only weak expression on vessels. The inflammatory cellular infiltrates contained varying amounts of cells bearing the VCAM-1 ligand VLA-4 and the ELAM-1 ligand SLeX as well as large amounts of cells expressing LFA-1 alpha and beta, ligands of ICAM-1.

Mast cells are crucial for early inflammation, migration of Langerhans cells, and CTL responses following topical application of TLR7 ligand in mice.

2007

Abstract Until recently, IgE-activated mast cells have been regarded merely as effector cells of adaptive immune responses, involved in allergic reactions and mucosal immunity to parasites. Herein, we report that murine dermal mast cells, activated by local administration of a cream containing the synthetic TLR7 ligand imiquimod, are essential to initiate an early inflammatory reaction. The mast-cell–derived cytokines TNF-α and IL-1β play an important role in this process. Furthermore, TLR7-activated mast cells are also able to promote the emigration of Langerhans cells, which partly depends on the expression of mast-cell–derived IL-1β. We have previously shown that TLR7 ligation enhances t…

Reciprocal IFN-gamma and TGF-beta responses regulate the occurrence of mucosal inflammation.

1997

The above new findings concerning the immunological mechanisms governing mucosa, immune responses and oral tolerance in TCR-transgenic mice, as well as those operative in mice with experimental colitis, greatly expand our understanding of the processes that normally control mucosal inflammation and possibly other types of inflammation as well (Fig. 1). They indicate that, in the nondiseased mouse, ingested proteins evoke a Th1-cell (IFN-gamma) response in the mucosal follicles that is quickly counter-regulated by induction of T-cell anergy/deletion, if this Th1-cell response is inhibited (experimentally by anti-IL-12), TGF beta-producing cells appear, and these are capable of active immune …

A central role for Notch in effector CD8(+) T cell differentiation.

2014

Activated CD8(+) T cells choose between terminal effector cell (TEC) or memory precursor cell (MPC) fates. We found that the signaling receptor Notch controls this 'choice'. Notch promoted the differentiation of immediately protective TECs and was correspondingly required for the clearance of acute infection with influenza virus. Notch activated a major portion of the TEC-specific gene-expression program and suppressed the MPC-specific program. Expression of Notch was induced on naive CD8(+) T cells by inflammatory mediators and interleukin 2 (IL-2) via pathways dependent on the metabolic checkpoint kinase mTOR and the transcription factor T-bet. These pathways were subsequently amplified d…