Search results for "Pathogenesis"

The Streptococcal Exotoxin Streptolysin O Activates Mast Cells To Produce Tumor Necrosis Factor Alpha by p38 Mitogen-Activated Protein Kinase- and Pr…

2003

ABSTRACTStreptolysin O (SLO), a major virulence factor of pyogenic streptococci, binds to cholesterol in the membranes of eukaryotic cells and oligomerizes to form large transmembrane pores. While high toxin doses are rapidly cytocidal, low doses are tolerated because a limited number of lesions can be resealed. Here, we report that at sublethal doses, SLO activates primary murine bone marrow-derived mast cells to degranulate and to rapidly induce or enhance the production of several cytokine mRNAs, including tumor necrosis factor alpha (TNF-α). Mast cell-derived TNF-α plays an important protective role in murine models of acute inflammation, and the production of this cytokine was analyzed…

Complement Component 3 expressed by the endometrial ectopic tissue is involved in the endometriotic lesion formation through mast cell activation

2020

AbstractThe pathophysiology of endometriosis (EM) is an excellent example of immune dysfunction, reminiscent of tumor microenvironment as well. Here, we report that an interplay between C3 and mast cells (MCs) is involved in the pathogenesis of ectopic EM. C3 is at the epicenter of the regulatory feed forward loop, amplifying the inflammatory microenvironment, in which the MCs are protagonists. Thus, C3 can be considered a marker of EM and its local synthesis can promote the engraftment of the endometriotic cysts. We generated a murine model of EM via injection of minced uterine tissue from a donor mouse, into the peritoneum of the recipient mice. The wild type mice showed greater amount of…

The Terminal Complement Complex (TCC) in the Plasma of Patients with Type 1 Diabetes Mellitus. Relationship with Albumin Excretion Rate

1991

Increased TCC levels were found to be present in the plasma of patients with type 1 diabetes associated with the presence of anti-heparan sulfate antibodies and increased urinary excretion of albumin. The authors suggest a role of terminal complement activation in the pathogenesis of diabetic nephropathy.

Urinary MicroRNA Profiling Predicts the Development of Microalbuminuria in Patients with Type 1 Diabetes

2015

Microalbuminuria provides the earliest clinical marker of diabetic nephropathy among patients with Type 1 diabetes, yet it lacks sensitivity and specificity for early histological manifestations of disease. In recent years microRNAs have emerged as potential mediators in the pathogenesis of diabetes complications, suggesting a possible role in the diagnosis of early stage disease. We used quantiative polymerase chain reaction (qPCR) to evaluate the expression profile of 723 unique microRNAs in the normoalbuminuric urine of patients who did not develop nephropathy (n = 10) relative to patients who subsequently developed microalbuminuria (n = 17). Eighteen microRNAs were strongly associated w…

Factor VIII and Antithrombin III in Atherosclerosis Obliterans of the Lower Limbs

1984

In the multifactorial pathogenesis of atherosclerosis (the W.H.O. gives a list of about forty risk factors) recent acquisitions have allowed to determine in part the role carried out by the term “haemocoagulative disorders” (90) showing the possible connections between haematic components of haemocoagulation and vascular wall that up to now have been only hypothesised.

Paenibacillus larvae Chitin-Degrading Protein PlCBP49 Is a Key Virulence Factor in American Foulbrood of Honey Bees

2014

Paenibacillus larvae, the etiological agent of the globally occurring epizootic American Foulbrood (AFB) of honey bees, causes intestinal infections in honey bee larvae which develop into systemic infections inevitably leading to larval death. Massive brood mortality might eventually lead to collapse of the entire colony. Molecular mechanisms of host-microbe interactions in this system and of differences in virulence between P. larvae genotypes are poorly understood. Recently, it was demonstrated that the degradation of the peritrophic matrix lining the midgut epithelium is a key step in pathogenesis of P. larvae infections. Here, we present the isolation and identification of PlCBP49, a mo…

Replication of hepatitis C virus

2000

The evolution of collective infectious units in viruses

2019

Viruses frequently spread among cells or hosts in groups, with multiple viral genomes inside the same infectious unit. These collective infectious units can consist of multiple viral genomes inside the same virion, or multiple virions inside a larger structure such as a vesicle. Collective infectious units deliver multiple viral genomes to the same cell simultaneously, which can have important implications for viral pathogenesis, antiviral resistance, and social evolution. However, little is known about why some viruses transmit in collective infectious units, whereas others do not. We used a simple evolutionary approach to model the potential costs and benefits of transmitting in a collect…

The Efficacy of Antigen Processing Is Critical for Protection against Cytomegalovirus Disease in the Presence of Viral Immune Evasion Proteins▿

2009

ABSTRACT Cytomegaloviruses (CMVs) code for immunoevasins, glycoproteins that are specifically dedicated to interfere with the presentation of antigenic peptides to CD8 T cells. Nonetheless, the biological outcome is not an immune evasion of the virus, since CD8 T cells can control CMV infection even when immunoevasins are expressed. Here, we compare the processing of a protective and a nonprotective epitope derived from the same viral protein, the antiapoptotic protein M45 in the murine model. The data provide evidence to conclude that protection against CMVs critically depends on antigenic peptides generated in an amount sufficient to exhaust the inhibitory capacity of immunoevasins.

OP0204 Autophagy and Unfolded Protein Response: A Fine Balance that can Influence the Pathogenesis of Ankylosing Spondylitis and Inflammatory Bowel D…

2015

Background We have shown an increase in the unfolded protein response (UPR) with decreased ERAP1 or ERAP2 function in an in vitro system. Similarly UPR has been demonstrated to correlate with onset of disease in the HLA-B27 rat model. UPR has been difficult to demonstrate in the gut of AS patients but autophagy is upregulated. ERAP2 is associated with both AS and inflammatory bowel disease (IBD). Objectives Here we explore the moderating effect of autophagy on UPR. Specifically we study the impact of suppressing autophagy on UPR. Methods Lamina Propria Mononuclear cells (LPMC) were isolated from terminal ileal biopsies of 10 AS patients. Autophagy was suppressed with 2 agents anisomycin and…