Castleman’s disease is a lymphoproliferative disorder characterized by atypical hyperplasia of the lymph nodes and systemic symptoms; can also affect the skin and the blood is important.
This condition is categorized by the level of engagement (unicentric or multicentric) and lymph node pathology observed (hyaline-vascular, plasma cell or mixed cellularity). Pathogenesis also has a role in the classification and treatment of multicentric Castleman’s disease; This variant can either be associated with the presence of human herpesvirus-8 (HHV-8) infection or associated with POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes) syndrome, or idiopathic.
The main cytokines that are responsible for causing idiopathic multicentric Castleman disease (IMCD) is interleukin-6 (IL-6). Therefore, treatment with agents that bind to IL-6 (as siltuximab) or blocking IL-6 receptor (such as tocilizumab) have been used. We report a woman with IMCD were successfully treated with siltuximab; and his skin manifestations of systemic disease (lung and lymph nodes) improved within three months. However, nine months after the start siltuximab, he developed a cough worsened and new infiltrates in the right lung on positron emission tomography / computed tomography (PET / CT) scans; no other constitutional symptoms such as fever, night sweats and fatigue. Diagnosis including Castleman disease recurrence, lung neoplasm and infection.
Symptoms of pulmonary infiltrates on scanning resolved after treatment with systemic levofloxacin, showed that he had a fever pneumonia antibiotic sensitive. We found her therapy siltuximab blocked fever and constitutional symptoms associated IL-6 which is usually the hallmark of pneumonia. Therefore, patients who received the drug as siltuximab and tocilizumab that blocks IL-6 pathway and damage the acute phase inflammatory response may fail for real constitutional symptoms such as fever when infected.
Afebrile Pneumonia in a Patient With Multicentric Castleman Disease on Siltuximab: Infection Without Fever on Anti-Interleukin-6 Therapy
Anti-infective drugs furazolidone inhibits NF-kB signaling and induces apoptosis of cancer cells small cell lung
Targeting the nuclear factor kappa B (NF-kB) signaling pathway has been a promising strategy for the development of new antitumor drugs. In this paper, we found that anti-infective drug furazolidone (FZD) could significantly inhibit NF-kB-driven luciferase activity, and real FZD could inhibit both the constitutive and tumor necrosis factor-α (TNF) -triggered phosphorylation of NF kB p65 cancer small cell lung (SCLC). Further research revealed that FZD inhibitor inhibits the expression of kappa B kinase β (IKKβ) in SCLC cells.
In addition, we found that the FZD has significant antitumor activity in SCLC cells. Real FZD can suppress cell viability SCLC cells dose dependence, and FZD could significantly induce cleavage of poly ADP-ribose polymerase (PARP) and Caspase3, biomarkers of apoptosis, in SCLC cells. Flow cytometry was also revealed that the FZD induced apoptosis in SCLC cells.
Finally, we also found that overexpression of constitutively activated IKKβ can significantly eliminate the FZD-induced inhibition of cell growth in SCLC cells, which further confirms that the FZD shown anticancer activity of SCLC via regulate NF-kB signaling pathway
Description: The IL-17 family is comprised of at least six proinflammatory cytokines that share a conserved cysteine-knot structure but diverge at the N-terminus. IL-17 family members are glycoproteins secreted as dimers that induce local cytokine production and recruit granulocytes to sites of inflammation. IL-17 is induced by IL-15 and IL-23, mainly in activated CD4+ T cells distinct from Th1 or Th2 cells. IL-17F is the most homologous to IL-17, but is induced only by IL-23 in activated monocytes. IL-17B binds the IL-17B receptor, but not the IL-17 receptor; it is most homologous with IL-17D, which is expressed by resting CD4+ T cells and CD19+ B cells. IL-17E is mainly produced by Th2 cells and recruits eosinophils to lung tissue. IL-17C has a very restricted expression pattern but has been detected in adult prostate and fetal kidney libraries.
Description: Human IL-17 RA/IL-17 R Recombinant Protein expressed in Baculovirus with hIgG-His-tag. Sequence domain: 33-320aa. Application(s): SDS-PAGE. Endotoxin: < 1 EU per 1ug of protein (determined by LAL method).
Description: Cytokines are small, soluble proteins with pleiotropic effects on a variety of cell types. Cytokines have a regulatory function over the immune system and mediate aspects of inflammatory response. They exert their biological effects through the binding of membrane-bound receptors which, in turn, initiate signal transduction cascades and elicit physiological changes in their target cell. Interleukin-17 (IL-17) and its cognate receptor, IL-17R, are an example of such a cytokine receptor pair. Originally identified as a rodent cDNA termed CTLA8, IL-17 is capable of inducing the secretion of IL-6 and IL-8 and augmenting the expression of ICAM-1 in human fibroblast cultures. The IL-17 protein exhibits a striking degree of homology with the HSV13 protein which mimics its function. The IL-17 receptor is a type I transmembrane protein 864 amino acids in length, that is highly expressed in spleen and kidney.
Description: IL-17 binds to IL-17 receptors (IL-17 R), which share no homology with any known family of receptors. While the expression of IL-17 is restricted to activated T cells, IL-17 R mRNA exhibits a broad tissue distribution, and has been detected in virtually all cells and tissues tested. The amino acid sequence of human IL-17 R is 69% identical to mouse IL-17 R.
Description: Interleukin-17A Human Recombinant produced in E.Coli is a homodimeric, non-glycosylated polypeptide chain containing a total of 264 amino acids (2 chains of 132 aa) and having a molecular mass of 31kDa. ;The IL-17 is purified by proprietary chromatographic techniques.
Description: The originally described IL-17 protein, now known as IL-17A, is a homodimer of two 136 amino acid chains, secreted by activated T-cells that act on stromal cells to induce production of proinflammatory and hematopoietic bioactive molecules. Today, IL-17 represents a family of structurally-related cytokines that share a highly conserved C-terminal region but differ from one another in their N-terminal regions and in their distinct biological roles. The six known members of this family, IL-17A through IL-17F, are secreted as homodimers. IL-17A exhibits cross-species bioactivity between human and murine cells. Recombinant human IL-17A is a 31.3 kDa disulfide-linked homodimer of two 137 amino acid polypeptide chains.
Description: Human Interleukin-17A (IL-17A) is encoded by the IL17A gene located on the chromosome 6 and belongs to the IL-17 family that contains IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL-17F. They have a similar protein structure, with four highly conserved cysteine residues critical to their 3-dimensional shape, but no sequence similarity to any other known cytokines. Interleukin 17 is a T cell-expressed pleiotropic cytokine that exhibits a high degree of homology to a protein encoded by the ORF13 gene of herpesvirus Saimiri. Mature IL-17 containing one potential N-linked glycosylation site. Both recombinant and natural IL-17 have been shown to exist as disulfide linked homodimers. At the amino acid level, IL-17 exhibits 63 % amino acid identity with mouse IL-17. High levels of human IL-17 were induced from primary peripheral blood CD4+ T cells upon stimulation and they can induce stromal cells to produce proinflammatory and hematopoietic cytokines.
Description: The IL-17 family is comprised of at least six proinflammatory cytokines that share a conserved cysteine-knot structure but diverge at the N-terminus. IL-17 family members are glycoproteins secreted as dimers that induce local cytokine production and recruit granulocytes to sites of inflammation. IL-17 is induced by IL-15 and IL-23, mainly in activated CD4+ T cells distinct from Th1 or Th2 cells. IL-17F is the most homologous to IL-17, but is induced only by IL-23 in activated monocytes. IL-17B binds the IL-17B receptor, but not the IL-17 receptor; it is most homologous with IL-17D, which is expressed by resting CD4+ T cells and CD19+ B cells. IL-17E is mainly produced by Th2 cells and recruits eosinophils to lung tissue. IL-17C has a very restricted expression pattern but has been detected in adult prostate and fetal kidney libraries.
Description: The IL-17 family is comprised of at least six proinflammatory cytokines that share a conserved cysteine-knot structure but diverge at the N-terminus. IL-17 family members are glycoproteins secreted as dimers that induce local cytokine production and recruit granulocytes to sites of inflammation. IL-17 is induced by IL-15 and IL-23, mainly in activated CD4+ T cells distinct from Th1 or Th2 cells. IL-17F is the most homologous to IL-17, but is induced only by IL-23 in activated monocytes. IL-17B binds the IL-17B receptor, but not the IL-17 receptor; it is most homologous with IL-17D, which is expressed by resting CD4+ T cells and CD19+ B cells. IL-17E is mainly produced by Th2 cells and recruits eosinophils to lung tissue. IL-17C has a very restricted expression pattern but has been detected in adult prostate and fetal kidney libraries.
Description: Quantitative sandwich ELISA for measuring Human IL-17 in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Description: Quantitative sandwich ELISA for measuring Human IL-17 in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
Description: Quantitative sandwich ELISA for measuring Human IL-17 in samples from cell culture supernatants, serum, whole blood, plasma and other biological fluids.
In total, 210 patients were enrolled, with 19 different patterns (groups of pharmacological alone or in combination) of the prescribed treatment. Most patients begin their treatment with conventional synthetic (cs) DMARD alone or in combination with a glucocorticosteroid.
Chris
