Biomphalaria glabrata is an intermediate snail host for the human blood fluke Schistosoma mansoni. To survive in B. glabrata, S. mansoni must suppress the snail's haemocyte-mediated defence response; the molecular mechanisms by which this is achieved remain largely unknown. We report here that S. mansoni excretory-secretory products (ESPs) attenuate phosphorylation of extracellular signal-regulated kinase (ERK) in haemocytes from a B. glabrata strain susceptible to S. mansoni. Whole S. mansoni sporocysts also impair ERK signalling in these cells. In striking contrast, ERK signalling in haemocytes from a B. glabrata strain refractory to schistosome infection is unaffected by ESPs or sporocysts. Effects of ESPs on ERK are similar in the presence or absence of snail plasma, thus ESPs seem to affect haemocytes directly. These findings reveal novel schistosome interference mechanisms; as ERK regulates various haemocyte defence reactions, we propose that disruption of ERK signalling in haemocytes facilitates S. mansoni survival within susceptible B. glabrata.
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http://dx.doi.org/10.1016/j.dci.2008.05.014 | DOI Listing |
Cell Mol Life Sci
December 2024
Department of Internal Medicine and Gastroenterology, Internistisches Klinikum München Süd, Am Isarkanal 36, Munich, Germany.
Bacterial infections are prevalent and the major cause of morbidity and mortality in cirrhosis. Activation of human Kupffer cells (HKCs) from livers is essential for human innate immunity. Cytosolic phospholipase A2 (cPLA2) plays a crucial role in the control and balance of innate immune and inflammatory reactions.
View Article and Find Full Text PDFEndocrine
December 2024
Department of Endocrinology, Sher-i- Kashmir Institute of Medical Sciences, Srinagar, India.
Background: Polycystic ovary syndrome (PCOS) represents a multifaceted endocrine, reproductive, and metabolic disorder characterized by hyperandrogenism and hyperinsulinemia-induced insulin resistance (IR). Recent studies reported that the etiology of PCOS is likely correlated with genes involved in steriodogenesis, IR and glucose metabolism. Among the candidate genes in insulin signaling pathways, RAB5B, a small GTPase involved in vesicle trafficking, significantly impacts cellular pathways in ovarian follicular cells, leading to clinical and endocrine changes among women with PCOS.
View Article and Find Full Text PDFJ Adv Res
December 2024
Hebei Key Laboratory of Natural Products Activity Components and Function, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei 066004, China. Electronic address:
Introduction: Colonic fibrosis is a long-term complication of inflammatory bowel disease (IBD), often leading to functional impairment, intestinal obstruction, and surgery. Adiponectin (APN) is an adipokine derived from adipocytes that plays a pleiotropic role in fibrosis regulation, depending on tissue and cell type specific or disease context, but its role in colonic fibrosis remains unclear.
Objective: To explore the role and involved mechanism of APN in chronic colitis-associated colonic fibrosis.
Bioorg Chem
December 2024
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, People's Republic of China. Electronic address:
To explore potential anti-inflammatory lead compounds, ten new physalin steroids, including three neophysalins (1, 4, and 9) and seven physalins (2, 3, 5-8, and 10), along with eleven known analogs, were isolated from an ethanol extract of the calyx of Physalis alkekengi. The new structures were rigorously determined through comprehensive HRESIMS, 1D/2D-NMR, and X-ray diffraction analysis. Among these compounds, 1 was identified as a new 1,10-seco-neophysalin, and 2 was identified as a new 11,15-cyclo-9,10-seco-physalin characterized by an aromatic A-ring.
View Article and Find Full Text PDFAnticancer Drugs
August 2024
Department of Thoracic Surgery, Peking University Cancer Hospital Inner Mongolia Hospital.
This study aims to demonstrate the effect of toadflax (bufalin) on erlotinib resistance in nonsmall cell lung cancer (NSCLC) by inhibiting the fibroblast growth factor receptor (FGFR). The microfluidic mobility transferase and caliper mobility-shift assays were employed to detect the FGFR inhibition by bufalin and the binding reversibility. Further, the inhibitory effects of bufalin were determined in HCC827 and HCC827/ER cells in vitro, investigating relative FGFR overexpression by quantitative reverse transcriptase-PCR (RT-qPCR) and FGFR downstream proteins, that is, FGFR substrate 2 (FRS2), extracellular signal-regulated kinase (ERK), and S6 by western blot analysis.
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