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brucellosis/プロリン

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Hypothalamic proline-rich polypeptide is an oxidative burst regulator.

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The AGAPEPAEPAQPGVY proline-rich polypeptide (PRP) was isolated from neurosecretory granules of the bovine neurohypophysis; it is produced by N. supraopticus and N. paraventricularis. PRP possesses immune-modulating activity, preventing the death of Gram-negative bacteria-infected mice. Here we show
Brucella melitensis bacteria cause persistent, intracellular infections in small ruminants as well as in humans, leading to significant morbidity and economic loss worldwide. The majority of experiments on the transcriptional responses of Brucella to conditions inside the host have been performed

Clinical features and functional significance of the P369S/R408Q variant in pyrin, the familial Mediterranean fever protein.

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OBJECTIVE Familial Mediterranean fever (FMF) is caused by mutations in MEFV, which encodes pyrin. The nature of substitutions P369S and R408Q in exon 3 remains unclear. Exon 3 encoding pyrin's B-box domain is necessary for interactions with proline serine threonine phosphatase interacting protein 1

Familial Mediterranean fever patients with hidradenitis suppurativa.

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BACKGROUND Hidradenitis suppurativa (HS) has recently been described as a component of two autoinflammatory syndromes: PASH (pyoderma gangrenosum, acne, and HS) and PAPASH (pyoderma gangrenosum, acne, pyogenic arthritis, and HS). These associations together with others such as inflammatory bowel

Pyrin binds the PSTPIP1/CD2BP1 protein, defining familial Mediterranean fever and PAPA syndrome as disorders in the same pathway.

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Pyrin, the familial Mediterranean fever protein, is found in association with the cytoskeleton in myeloid/monocytic cells and modulates IL-1beta processing, NF-kappaB activation, and apoptosis. These effects are mediated in part through cognate interactions with the adaptor protein ASC, which shares

Prevalence of proline racemase/ hydroxyproline epimerase gene in human brucella isolates in Iran.

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Background: Human brucellosis is a zoonotic disease caused by Brucella melitensis, Brucella abortus, and Brucella suis. Brucella causes a chronic disease, which subverts the immune defense system of their hosts. In this study, the prevalence of an important Brucella virulence determinant, prpA,

Pyrin-PSTPIP1 colocalises at the leading edge during cell migration.

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A set of mutations in the MEditerranean FeVer (MEFV) gene causes familial Mediterranean fever (FMF), the most common auto-inflammatory disease. The gene encodes a protein named pyrin, which appears to play an important role in inflammatory pathways. Furthermore, pyrin, which is expressed in

Antigenic properties of peptidic mimics for epitopes of the lipopolysaccharide from Brucella.

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The lipopolysaccharide (LPS) is up to now the only identified major virulence determinant of Brucella. This bacterium is responsible for brucellosis in animals and for Malta fever in humans. Several monoclonal antibodies (mAbs) directed against various LPS epitopes have been characterized. Two mAbs,

A common pathway in periodic fever syndromes.

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Familial Mediterranean fever (FMF) is an autosomal recessive disease due to mutations in pyrin, which normally inhibits pro-interleukin-1beta (IL-1beta) cytokine processing to the active form. A novel role for pyrin has been proposed by Shoham et al., who studied patients with an autosomal dominant

Multivalent Fusion DNA Vaccine against Brucella abortus.

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As an alternative brucellosis prevention method, we evaluated the immunogenicity induced by new multivalent DNA vaccines in BALB/c mice. We constructed the vaccines by fusion of BAB1_0273 and/or BAB1_0278 open reading frames (ORFs) from genomic island 3 (GI-3) and the Brucella abortus 2308 sodC gene
Salmonella is an intracellular pathogen with a cellular infection mechanism similar to that of Brucella, making it a suitable choice for use in an anti-Brucella immune boost system. This study explores the efficacy of a Salmonella Typhimurium delivery-based combination vaccine for four heterologous

Autoinflammatory gene mutations in Behçet's disease.

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BACKGROUND Behçet's disease (BD) shares clinical features with well-recognised autoinflammatory disorders. In addition, mutations in genes for familial Mediterranean fever and tumour necrosis factor receptor-associated periodic syndrome have been reported to have increased in patients with

The Relationship between NALP3 and Autoinflammatory Syndromes.

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The nucleotide-binding domain, leucine-rich repeat/pyrin domain-containing-3 (NALP3) inflammasome, which is required for synthesis of interleukin-1β, has been implicated in the pathogenesis of several autoinflammatory syndromes. This review of the literature summarizes the interconnectedness of

A B lymphocyte mitogen is a Brucella abortus virulence factor required for persistent infection.

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Microbial pathogens with the ability to establish chronic infections have evolved strategies to actively modulate the host immune response. Brucellosis is a disease caused by a Gram-negative intracellular pathogen that if not treated during the initial phase of the infection becomes chronic as the

Brucella alters the immune response in a prpA-dependent manner.

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Brucellosis, a disease caused by the gram-negative bacterium Brucella spp., is a widespread zoonosis that inflicts important animal and human health problems, especially in developing countries. One of the hallmarks of Brucella infection is its capacity to establish a chronic infection,
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