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Anita K Mcelroy - One of the best experts on this subject based on the ideXlab platform.
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rift valley fever virus inhibits a pro inflammatory Response in experimentally infected human monocyte derived macrophages and a pro inflammatory Cytokine Response may be associated with patient survival during natural infection
Virology, 2012Co-Authors: Anita K Mcelroy, Stuart T NicholAbstract:Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon Response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune Response via expression of various Cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune Response via decreased expression of IFN-α2, IFN-β and TNF-α. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory Cytokine Response and patient survival.
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rift valley fever virus inhibits a pro inflammatory Response in experimentally infected human monocyte derived macrophages and a pro inflammatory Cytokine Response may be associated with patient survival during natural infection
Virology, 2012Co-Authors: Anita K Mcelroy, Stuart T NicholAbstract:Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon Response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune Response via expression of various Cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune Response via decreased expression of IFN-α2, IFN-β and TNF-α. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory Cytokine Response and patient survival.
Annie Wongberinger - One of the best experts on this subject based on the ideXlab platform.
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early platelet dynamics during staphylococcus aureus bacteremia is associated with dysregulated Cytokine Response and predictive of microbial persistence and mortality
Social Science Research Network, 2021Co-Authors: Rachid Douglaslouis, Brian V Lee, Emi Minejima, Mimi Lou, Juliane Bubeck Wardenburg, Annie WongberingerAbstract:Background Platelets play key roles in host immune Response during sepsis. Microbial persistence and early dysregulated Cytokine Response predict poor outcomes in patients with Staphylococcus aureus bacteremia (SAB). Our objective was to determine the relationship between early platelet trends and Cytokine Response, microbial persistence and 30-day mortality in patients with SAB. Methods A two-center observational study was conducted in hospitalized patients with monomicrobial SAB. Electronic medical records were reviewed for pertinent demographic, laboratory, and clinical information. Eligible subjects were grouped by platelet count at onset and Day 4 of SAB: normal platelet (NP, > 150 x 109/L) and thrombocytopenia (TC, < 150 x 109/L). The groups were compared for clinical characteristics and outcomes. Results 812 patients met inclusion criteria. The median age was 59 years with MRSA accounting for 34% of SAB. The most common comorbidities were hypertension followed by diabetes then renal disease. Thrombocytopenia (TC) occurred in 29% of patients at SAB onset: 15% (n = 120) were mild and 14% (n = 114) were moderate-to-severe (MS). Compared to patients with normal platelet (NP) at SAB onset (n = 578), higher proportion of patients with TC had alcohol use disorder (p = 0.015), active malignancy (p = 0.002), liver disease (p < 0.001), in addition to requiring intensive care unit (ICU) level of care during hospital stay (p < 0.001). TC patients had a longer duration of bacteremia (3 days vs 2 days; p = 0.008) and higher risk for 30-day mortality (18% vs 6%; p < 0.001) overall compared to those with NP. Changes in platelet count from SAB onset to Day 4 differed significantly between those with persistent (PB) versus resolving bacteremia (RB). Notably, patients who had NP at SAB onset but developed new onset of TC by Day 4 had a higher risk for 30-day mortality compared to those who maintained NP at Day 4 (20% vs 4%; p < 0.001). Those with recovery of their platelet count from TC to NP by Day 4 (n = 20) had their SAB shortened by one day (2 days vs 3 days; p = 0.413) and trended toward lower risk for 30-day mortality (5% vs 22%; p = 0.068) compared to those with sustained TC by Day 4 (n = 88). Conclusion Our results suggest that platelet dynamics during early course of SAB are associated with dysregulated Cytokine Response and predictive of 30-day mortality. Future studies should be conducted to assess the impact of utilizing platelet count within the first four days of S. aureus bacteremia to guide clinical interventions and to further investigate S. aureus virulence factors that impair recovery of platelet count in patients with thrombocytopenia.
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a dysregulated balance of proinflammatory and anti inflammatory host Cytokine Response early during therapy predicts persistence and mortality in staphylococcus aureus bacteremia
Critical Care Medicine, 2015Co-Authors: Emi Minejima, Mimi Lou, Joyce Bensman, Rosemary C She, Wendy J Mack, Martin Tuan Tran, Jason Yamaki, Paul Nieberg, Annie WongberingerAbstract:OBJECTIVES The contribution of individual immune Response to Staphylococcus aureus bacteremia on outcome has not been well studied. The objective was to relate the host Cytokine Response to outcome of Staphylococcus aureus bacteremia. DESIGN Prospective observational study. SETTING Three U.S. university-affiliated medical centers. PATIENTS Adult patients infected with Staphylococcus aureus bacteremia hospitalized between July 2012 and August 2014. INTERVENTIONS Blood specimens were obtained at Staphylococcus aureus bacteremia onset and 72 hours after therapy initiation. Levels of tissue necrosis factor, interleukin-6, interleukin-8, interleukin-17A, and interleukin-10 were measured by enzyme-linked immunosorbent assay at each time point and compared between those with persistent bacteremia (≥ 4 d) and resolving bacteremia. Primary outcome was persistent bacteremia after 4 days of effective therapy. Secondary outcomes were 30-day mortality and 30-day recurrence. MEASUREMENTS AND MAIN RESULTS A total of 196 patients were included (mean age, 59 yr); of them, 33% had methicillin-resistant Staphylococcus aureus bacteremia. Forty-seven percent of the methicillin-resistant Staphylococcus aureus strains were staphylococcal cassette chromosome mec IV. Persistent bacteremia occurred in 24% of patients (47/196); they were more likely to die than resolving bacteremia group (28% vs 5%; p < 0.001). Compared with resolving bacteremia group, persistent bacteremia patients had higher initial median levels of tissue necrosis factor (44.73 vs 21.68 pg/mL; p < 0.001), interleukin-8 (124.76 vs 47.48 pg/mL; p = 0.028), and interleukin-10 (104.31 vs 29.72 pg/mL; p < 0.001). Despite 72 hours of treatment, levels remained higher for the persistent bacteremia group than for the resolving bacteremia group (tissue necrosis factor: 26.95 vs 18.38 pg/mL, p = 0.02; interleukin-8: 70.75 vs 27.86 pg/mL, p = 0.002; interleukin-6: 67.50 vs 21.81 pg/mL, p = 0.005; and interleukin-10: 30.98 vs 12.60 pg/mL, p < 0.001). Interleukin-17A levels were similar between groups at both time points. After controlling for confounding variables by multivariate analysis, interleukin-10/tissue necrosis factor ratio at 72 hours most significantly predicted persistence (odds ratio, 2.98; 95% CI, 1.39-6.39; p = 0.005) and mortality (odds ratio, 9.87; 95% CI, 2.64-36.91; p < 0.001) at values more than 1.00 and more than 2.56, respectively. CONCLUSIONS Sustained elevation of interleukin-10/tissue necrosis factor ratio at 72 hours suggests a dysregulated immune Response and may be used to guide management to improve outcomes.
Chin Chang Cheng - One of the best experts on this subject based on the ideXlab platform.
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less systemic Cytokine Response in patients following microendoscopic versus open lumbar discectomy
Journal of Orthopaedic Research, 2005Co-Authors: Tsung Jen Huang, Robert Wenwei Hsu, Chin Chang ChengAbstract:Abstract The magnitude of the tissue damage from surgery impacts the trauma Response. This Response is proportional to the severity of surgical stress. Systemic Cytokines are recognized as markers of postoperative tissue trauma. Microendoscopic discectomy (MED) recently has become popular for treating lumbar disc herniations, and is associated with favorable clinical outcomes compared with open discectomy (OD). This study postulates that MED is a less traumatic procedure, and therefore has a lower surgical stress Response compared to OD. In this study, a quantitative comparison of the overall effects of surgical trauma resulting from MED and OD was performed through analyzing patient systemic Cytokines Response. From April, 2002 to June, 2003, 22 consecutive patients who had symptomatic lumbar disc herniations were prospectively randomized to undergo either intracanalicular MED (N = 10) or OD (N = 12). In this study, the Vertebroscope System (Zeppelin, Pullach, Germany) was used to perform the endoscopic discectomy procedure in all MED patients. Serum levels of tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6), and Interleukin-8 (IL-8) were measured before surgery and at 1, 2, 4, 8 and 24 h after surgery using an enzyme-linked immunosorbent assay. Serum C-reactive protein (CRP) was measured at the same time interval. The results showed the MED patients had shorter postoperative hospital stay (mean, 3.57 ± 0.98 vs. 5.92 ± 2.39 days, p = 0.025) and less intraoperative blood loss (mean, 87.5 ± 69.4 vs. 190 ± 115 ml, p = 0.042). The operating length, including the set-up time, was longer in the MED group (mean, 109 ± 35.9 vs. 72.1 ± 17.8 min, p = 0.01). The mean size of skin incision made for the MED patients was 1.86 ± 0.13 cm (range 1.7–2.0 cm); and 6.3 ± 0.98 cm for the OD patients (range 5.5–8 cm), p = 0.001. The patients’ pain severity of the involved limbs on 10-point Visual Analog Scale before operation in MED group was 7.5 ± 0.3 (range 6–9) and 8 ± 0.2 (range 7–9) in OD group, p = 0.17; and after surgery, 1.5 ± 0.2 (range 1–2) in MED group and 1.4 ± 0.1 (range 1–3) in OD group, p = 0.91. CRP levels peaked at 24 h in both groups, and OD patients displayed a significantly greater postoperative rise in serum CRP (mean, 27.78 ± 15.02 vs. 13.84 ± 6.25 mg/l, p = 0.026). Concentrations of TNF-α, IL-1β, and IL-8 were detected only sporadically. Serum IL-6 increased less significantly following MED than after OD. In the MED group, IL-6 level peaked 8 h after surgery, with the Response statistically less than in the open group (mean, 6.27 ± 5.96 vs. 17.18 ± 11.60 pg/ml, p = 0.025). A statistically significant correlation was identified between IL-6 and CRP values (r = 0.79). Using the modified MacNab criteria, the clinical outcomes were 90% satisfactory (9/10) in MED patients and 91.6% satisfactory (11/12) in OD patients at a mean 18.9 months (range 10–25) follow-up. Based on the current data, surgical trauma, as reflected by systemic IL-6 and CRP Response, was significantly less following MED than following OD. The difference in the systemic Cytokine Response may support that the MED procedure is less traumatic. Moreover, our MED patients had achieved satisfactory clinical outcomes as the OD patients at a mean 18.9 months follow-up after surgery.
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less systemic Cytokine Response in patients following microendoscopic versus open lumbar discectomy
Journal of Orthopaedic Research, 2005Co-Authors: Tsung Jen Huang, Robert Wenwei Hsu, Chin Chang ChengAbstract:The magnitude of the tissue damage from surgery impacts the trauma Response. This Response is proportional to the severity of surgical stress. Systemic Cytokines are recognized as markers of postoperative tissue trauma. Microendoscopic discectomy (MED) recently has become popular for treating lumbar disc herniations, and is associated with favorable clinical outcomes compared with open discectomy (OD). This study postulates that MED is a less traumatic procedure, and therefore has a lower surgical stress Response compared to OD. In this study, a quantitative comparison of the overall effects of surgical trauma resulting from MED and OD was performed through analyzing patient systemic Cytokines Response. From April, 2002 to June, 2003, 22 consecutive patients who had symptomatic lumbar disc herniations were prospectively randomized to undergo either intracanalicular MED (N=10) or OD (N=12). In this study, the Vertebroscope System (Zeppelin, Pullach, Germany) was used to perform the endoscopic discectomy procedure in all MED patients. Serum levels of tumor necrosis factor-alpha (TNF-alpha), Interleukin-1beta (IL-1beta), Interleukin-6 (IL-6), and Interleukin-8 (IL-8) were measured before surgery and at 1, 2, 4, 8 and 24h after surgery using an enzyme-linked immunosorbent assay. Serum C-reactive protein (CRP) was measured at the same time interval. The results showed the MED patients had shorter postoperative hospital stay (mean, 3.57+/-0.98 vs. 5.92+/-2.39 days, p=0.025) and less intraoperative blood loss (mean, 87.5+/-69.4 vs. 190+/-115 ml, p=0.042). The operating length, including the set-up time, was longer in the MED group (mean, 109+/-35.9 vs. 72.1+/-17.8 min, p=0.01). The mean size of skin incision made for the MED patients was 1.86+/-0.13 cm (range 1.7-2.0 cm); and 6.3+/-0.98 cm for the OD patients (range 5.5-8 cm), p=0.001. The patients' pain severity of the involved limbs on 10-point Visual Analog Scale before operation in MED group was 7.5+/-0.3 (range 6-9) and 8+/-0.2 (range 7-9) in OD group, p=0.17; and after surgery, 1.5+/-0.2 (range 1-2) in MED group and 1.4+/-0.1 (range 1-3) in OD group, p=0.91. CRP levels peaked at 24h in both groups, and OD patients displayed a significantly greater postoperative rise in serum CRP (mean, 27.78+/-15.02 vs. 13.84+/-6.25mg/l, p=0.026). Concentrations of TNF-alpha, IL-1beta, and IL-8 were detected only sporadically. Serum IL-6 increased less significantly following MED than after OD. In the MED group, IL-6 level peaked 8h after surgery, with the Response statistically less than in the open group (mean, 6.27+/-5.96 vs. 17.18+/-11.60 pg/ml, p=0.025). A statistically significant correlation was identified between IL-6 and CRP values (r=0.79). Using the modified MacNab criteria, the clinical outcomes were 90% satisfactory (9/10) in MED patients and 91.6% satisfactory (11/12) in OD patients at a mean 18.9 months (range 10-25) follow-up. Based on the current data, surgical trauma, as reflected by systemic IL-6 and CRP Response, was significantly less following MED than following OD. The difference in the systemic Cytokine Response may support that the MED procedure is less traumatic. Moreover, our MED patients had achieved satisfactory clinical outcomes as the OD patients at a mean 18.9 months follow-up after surgery.
Stuart T Nichol - One of the best experts on this subject based on the ideXlab platform.
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rift valley fever virus inhibits a pro inflammatory Response in experimentally infected human monocyte derived macrophages and a pro inflammatory Cytokine Response may be associated with patient survival during natural infection
Virology, 2012Co-Authors: Anita K Mcelroy, Stuart T NicholAbstract:Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon Response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune Response via expression of various Cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune Response via decreased expression of IFN-α2, IFN-β and TNF-α. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory Cytokine Response and patient survival.
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rift valley fever virus inhibits a pro inflammatory Response in experimentally infected human monocyte derived macrophages and a pro inflammatory Cytokine Response may be associated with patient survival during natural infection
Virology, 2012Co-Authors: Anita K Mcelroy, Stuart T NicholAbstract:Rift Valley fever virus (RVFV) causes significant morbidity and mortality in humans and livestock throughout Africa and the Middle East. The clinical disease ranges from mild febrile illness, to hepatitis, retinitis, encephalitis and fatal hemorrhagic fever. RVFV NSs protein has previously been shown to interfere in vitro with the interferon Response, and RVFV lacking the NSs protein is attenuated in several animal models. Monocytes and macrophages are key players in the innate immune Response via expression of various Cytokines and chemokines. Here we demonstrate that wild-type RVFV infection of human monocyte-derived macrophages leads to a productive infection and inhibition of the innate immune Response via decreased expression of IFN-α2, IFN-β and TNF-α. Using a recombinant virus lacking the NSs protein, we show that this effect is mediated by the viral NSs protein. Finally, analysis of RVF patient samples demonstrated an association between a pro-inflammatory Cytokine Response and patient survival.
Betty A Wuhsieh - One of the best experts on this subject based on the ideXlab platform.
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nlrx1 facilitates histoplasma capsulatum induced lc3 associated phagocytosis for Cytokine production in macrophages
Frontiers in Immunology, 2018Co-Authors: Juinhua Huang, Chuyu Liu, Wenyu Chen, Tzuhsuan Chang, Hungwei Kan, Sungtsang Hsieh, Jenny P Y Ting, Betty A WuhsiehAbstract:LC3-associated phagocytosis (LAP) is an emerging non-canonical autophagy process that bridges signaling from pattern-recognition receptors (PRRs) to autophagic machinery. LAP formation results in incorporation of lipidated LC3 into phagosomal membrane (termed LAPosome). Increasing evidence reveals that LAP functions as an innate defense mechanism against fungal pathogens. However, the molecular mechanism involved and the consequence of LAP in regulating anti-fungal immune Response remain largely unexplored. Here we show that Histoplasma capsulatum is taken into LAPosome upon phagocytosis by macrophages. Interaction of H. capsulatum with Dectin-1 activates Syk and triggers subsequent NADPH oxidase-mediated reactive oxygen species (ROS) Response that is involved in LAP induction. Inhibiting LAP induction by silencing LC3α/β or treatment with ROS inhibitor impairs the activation of MAPKs-AP-1 pathway, thereby reduces macrophage proinflammatory Cytokine Response to H. capsulatum. Additionally, we unravel the importance of NLRX1 in fungus-induced LAP. NLRX1 facilitates LAP by interacting with TUFM which associates with autophagic proteins ATG5-ATG12 for LAPosome formation. Macrophages from Nlrx1 -/- mice or TUFM-silenced cells exhibit reduced LAP induction and LAP-mediated MAPKs-AP-1 activation for Cytokine Response to H. capsulatum. Furthermore, inhibiting ROS production in Nlrx1 -/- macrophages almost completely abolishes H. capsulatum-induced LC3 conversion, indicating that both Dectin-1/Syk/ROS-dependent pathway and NLRX1-TUFM complex-dependent pathway collaboratively contribute to LAP induction. Our findings reveal new pathways underlying LAP induction by H. capsulatum for macrophage Cytokine Response.
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distinct roles of complement receptor 3 dectin 1 and sialic acids in murine macrophage interaction with histoplasma yeast
Journal of Leukocyte Biology, 2010Co-Authors: Jrshiuan Lin, Juinhua Huang, Liyin Hung, Betty A WuhsiehAbstract:The yeast cells of dimorphic fungal pathogen Histoplasma reside primarily within the macrophages of an infected host; the interaction between the yeast and macrophage has a profound impact on host defense against the fungus. We used blocking antibodies and saccharides to identify the receptors that participate in the phagocytosis of and the Cytokine Response to Histoplasma. The phagocytosis and Cytokine Response results show that sialic acids on the macrophages were involved in the interaction between macrophages and Histoplasma. CR3, although not the only receptor involved, was responsible for phagocytosis and Cytokine Response. It is unclear which receptors other than CR3 are responsible for phagocytosis, but we did rule out the participation of TLR2, TLR4, MR, DC-SIGN/SIGNR1, FcgammaR, VLA-5, and Dectin-1. Even though Dectin-1 did not participate in phagocytosis, it collaborated with CR3 in the Cytokine Response to Histoplasma, suggesting that in the presence of phagocytic receptors, Histoplasma triggers Cytokine signals through Dectin-1. Moreover, macrophage phagocytosis of and Cytokine Response to Histoplasma are Syk kinase-dependent. Our study delineated the distinct roles of CR3, Dectin-1, and sialic acids in the interaction with Histoplasma and suggested that multiple receptor use might be important to host defense against Histoplasma.
