Macrophages from Patients with Cirrhotic Ascites Showed Function Alteration of Host Defense Receptor

Abstract

Background: Patients with cirrhotic ascites (PCA) are susceptible to spontaneous bacterial peritonitis (SBP) which has increased morbidity and mortality. Since some host defense aspects of peritoneal macrophages (PMv) from PCA are altered this study examined factors related to receptor-mediated phagocytosis. Methods: Twelve PCA were studied. PMɸ were isolated from ascitic fluid (AF) samples removed from these patients. Uptake of mannose receptor (MR)-specific ligand, fluorescein isothiocyanate-mannosylated-bovine serum albumin (FITC-man-BSA), by patients' PMɸ and controls, a human monocytic cell line, was measured pre-and post-IL-4 treatment. Phagocytosis of FITC-labeled yeast particles by patients' PMɸ was measured pre-and post-IL-4 treatment. Fluorescence values were obtained using a spectrofuorometer. MRC1 gene was analyzed in blood samples from PCA and controls, healthy donors, using standard polymerase chain reaction (PCR) technique. Results: Past SBP episode(s) were reported in 58.3% of patients. Mean AF volume analyzed per patient was 1.3L. PMɸ ratio in cell yield was 53.73% (SD 18.1). Mean uptake absorbance of patients' PMv was 0.0841 (SD 0.077) compared to 0.338 (SD 0.34) of controls, P = 0.023. Following IL-4 treatment absorbance increased to 0.297 (SD 0.28) in patients' PMv (P = 0.018 on paired sample t-test), and to 0.532 (SD 0.398 in controls (P = 0.053 on independent sample t-test). Mean phagocytosis absorbance of patients' PMv was 0.1250 (SD 0.032) before IL-4 treatment compared to 0.2300 (SD 0.104) after (P = 0.026). PCR analysis for MRC1 gene was negative in all PCA samples compared to positive results in all controls. Conclusion: Since decreased phagocytosis and MR uptake were enhanced post-IL-4 treatment MR downregulation pre-treatment is plausible. Negative PCR results for MRC1 might suggest an anomaly, but this awaits further ellucidation. These altered host defense findings are relevant to infection pathophysiology, and their relevance to SBP susceptibility in PCA is worth verifying. ( J CLIN EXP HEPATOL 2014;4:279-286)

Vagal Regulation of Group 3 Innate Lymphoid Cells and the Immunoresolvent PCTR1 Controls Infection Resolution

“…bacteria) these cells produce a host of inflammatory signals including cytokines and lipid mediators that lead to vascular leakage and leukocyte recruitment (Hellmann et al, 2015). In addition, these cells also actively participate in clearance of invading pathogens and alteration in their phenotype impairs their ability to clear bacteria and leads to a dysregulated inflammatory response in experimental systems (Dahdah et al, 2014) and humans (Ahmed et al, 2014). In the present study we found that administration of PCTR1 to vagotomised mice 16h prior to challenge at a dose as low as 75ng/mouse restored the macrophage phenotype as well as phagocytic function.…”