scholarly journals High-dose intravenous immunoglobulins might modulate inflammation in COVID-19 patients

2021 ◽  
Vol 4 (9) ◽  
pp. e202001009
Author(s):  
María Luisa Rodríguez de la Concepción ◽  
Erola Ainsua-Enrich ◽  
Esteban Reynaga ◽  
Carlos Ávila-Nieto ◽  
Jose Ramón Santos ◽  
...  
Keyword(s):  
Immune Responses ◽  
Binding Protein ◽  
Intravenous Immunoglobulins ◽  
High Dose ◽  
Intestinal Damage ◽  
Fatty Acid Binding ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor ◽  
Lps Binding

The use of high-dose of intravenous immunoglobulins (IVIGs) as immunomodulators for the treatment of COVID-19–affected individuals has shown promising results. IVIG reduced inflammation in these patients, who progressively restored respiratory function. However, little is known about how they may modulate immune responses in COVID-19 individuals. Here, we have analyzed the levels of 41 inflammatory biomarkers in plasma samples obtained at day 0 (pretreatment initiation), 3, 7, and 14 from five hospitalized COVID-19 patients treated with a 5-d course of 400 mg/kg/d of IVIG. The plasmatic levels of several cytokines (Tumor Necrosis Factor, IL-10, IL-5, and IL-7), chemokines (macrophage inflammatory protein-1α), growth/tissue repairing factors (hepatic growth factor), complement activation (C5a), and intestinal damage such as Fatty acid–binding protein 2 and LPS-binding protein showed a progressive decreasing trend during the next 2 wk after treatment initiation. This trend was not observed in IVIG-untreated COVID-19 patients. Thus, the administration of high-dose IVIG to hospitalized COVID-19 patients may improve their clinical evolution by modulating their hyperinflammatory and immunosuppressive status.

scholarly journals Selective Early Production of CCL20, or Macrophage Inflammatory Protein 3α, by Human Mast Cells in Response to Pseudomonas aeruginosa

2003 ◽  
Vol 71 (1) ◽  
pp. 365-373 ◽  
Author(s):  
Tong-Jun Lin ◽  
Lauren H. Maher ◽  
Kaede Gomi ◽  
Jeffrey D. McCurdy ◽  
Rafael Garduno ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mast Cells ◽  
Immune Responses ◽  
Immunoglobulin E ◽  
Calcium Ionophore ◽  
Human Mast Cell ◽  
Gm Csf ◽  
Human Mast Cells ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

ABSTRACT Mast cells are important as sentinel cells in host defense against bacterial infection. Much of their effectiveness depends upon recruiting other immune cells; however, little is known about the mechanisms of this response. CCL20, also known as macrophage inflammatory protein-3α (MIP-3α), Exodus, and LARC, is a chemokine known to be a potent chemoattractant for immature dendritic cells and T cells. In this study, we examined the human mast cell production of both CCL20 and granulocyte-macrophage colony-stimulating factor (GM-CSF), a critical cytokine for innate immune responses in the lung, in response to Pseudomonas aeruginosa. Reverse transcription-PCR and Western blot analysis demonstrated that the human mast cells (HMC-1) express CCL20 mRNA and are able to produce a significant amount (32.4 ng/ml) of CCL20 protein following stimulation by calcium ionophore and phorbol myristate acetate. Importantly, P. aeruginosa potently stimulated CCL20 production in human cord blood-derived mast cells (CBMC), with production peaking at 6 h after stimulation. This time course of expression was distinct from that of GM-CSF, which peaked after 24 to 48 h. Significant CCL20 production did not occur following immunoglobulin E-mediated activation of CBMC under conditions which induced a substantial GM-CSF response. Interestingly, the CCL20 response of mast cells to P. aeruginosa was relatively resistant to inhibition by the corticosteroid dexamethasone, interleukin-10, or cyclosporine, while GM-CSF production was potently inhibited. However, P. aeruginosa-induced CCL20 production was blocked by the protein kinase C (PKC) inhibitor Ro 31-8220 and a PKC pseudosubstrate. These results support a role for human mast cells in the initiation of immune responses to P. aeruginosa infection.

scholarly journals Persistent Systemic Microbial Translocation, Inflammation, and Intestinal Damage During Clostridioides difficile Infection

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Alessandra Oliva ◽  
Lucia Aversano ◽  
Massimiliano De Angelis ◽  
Maria Teresa Mascellino ◽  
Maria Claudia Miele ◽  
...  
Keyword(s):  
Fecal Microbiota Transplantation ◽  
Cell Damage ◽  
Binding Protein ◽  
Fecal Microbiota ◽  
Microbial Translocation ◽  
Intestinal Cell ◽  
Intestinal Damage ◽  
Fatty Acid Binding ◽  
Clostridioides Difficile ◽  
Clostridioides Difficile Infection

Abstract Background Clostridioides difficile infection (CDI) might be complicated by the development of nosocomial bloodstream infection (n-BSI). Based on the hypothesis that alteration of the normal gut integrity is present during CDI, we evaluated markers of microbial translocation, inflammation, and intestinal damage in patients with CDI. Methods Patients with documented CDI were enrolled in the study. For each subject, plasma samples were collected at T0 and T1 (before and after CDI therapy, respectively), and the following markers were evaluated: lipopolysaccharide-binding protein (LPB), EndoCab IgM, interleukin-6, intestinal fatty acid binding protein (I-FABP). Samples from nonhospitalized healthy controls were also included. The study population was divided into BSI+/BSI- and fecal microbiota transplantation (FMT) +/FMT- groups, according to the development of n-BSI and the receipt of FMT, respectively. Results Overall, 45 subjects were included; 8 (17.7%) developed primary n-BSI. Markers of microbial translocation and intestinal damage significantly decreased between T0 and T1, however, without reaching values similar to controls (P < .0001). Compared with BSI-, a persistent high level of microbial translocation in the BSI+ group was observed. In the FMT+ group, markers of microbial translocation and inflammation at T1 tended to reach control values. Conclusions CDI is associated with high levels of microbial translocation, inflammation, and intestinal damage, which are still present at clinical resolution of CDI. The role of residual mucosal perturbation and persistence of intestinal cell damage in the development of n-BSI following CDI, as well as the possible effect of FMT in the restoration of mucosal integrity, should be further investigated.

scholarly journals Limited Role for Interleukin-18 in the Host Protection Response to Pulmonary Infection with Pseudomonas aeruginosa in Mice

2004 ◽  
Vol 72 (10) ◽  
pp. 6176-6180 ◽  
Author(s):  
Chikara Nakasone ◽  
Kazuyoshi Kawakami ◽  
Tomoaki Hoshino ◽  
Yusuke Kawase ◽  
Koichi Yokota ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Pulmonary Infection ◽  
Interleukin 18 ◽  
Necrosis Factor Alpha ◽  
Host Protection ◽  
Limited Role ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT We report that clearance of Pseudomonas aeruginosa, accumulation of neutrophils, and synthesis of tumor necrosis factor alpha and macrophage inflammatory protein 2 in the infected lung were not largely different in interleukin-18 (IL-18) knockout or transgenic mice compared with control mice. Our results suggest a limited role for IL-18 in the host defense against P. aeruginosa.

scholarly journals Prevention of gastrointestinal injury by using glutamine in cardiac surgery

2015 ◽  
Vol 18 (3) ◽  
pp. 19 ◽  
Author(s):  
S. M. Yefremov ◽  
V. A. Shmyrev ◽  
M. N. Deryagin ◽  
I. A. Kornilov ◽  
A. N. Shilova ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Intestinal Damage ◽  
Double Blind ◽  
Fatty Acid Binding ◽  
Double Blind Placebo ◽  
Intestinal Integrity ◽  
Acid Binding Protein

A pilot double-blind, placebo-controlled, randomized study The aim of this study was to evaluate the efficiency of perioperative administration of glutamine to preserve intestinal integrity in patients undergoing cardiac surgery. 24 patients scheduled for elective coronary artery bypass surgery under cardiopulmonary bypass were included in this prospective, randomized, double-blind placebo controlled pilot study. 12 patients were randomized to receive glutamine (20% solution of N(2)-L-alanyl-L-glutamine) 0.4 g/kg a day, while the remaining 12 patients received an equivalent placebo dose (0.9% solution of NaCl). Infusion of glutamine/placebo was started after the induction of anesthesia and was continued for 24 hours. The primary end-point was dynamics of plasma concentration of a specific marker of intestinal damage, intestinal fatty acid binding protein (I-FABP). The secondary end-points were liver fatty acid binding protein (L-FABP), alpha glutathione s-transferase (aGST), heat shock protein 70 (HSP 70). There were no between-group differences of all the studied biochemical parameters at any stage of the study. Plasma I-FABP levels (median [25-75 percentile]) were markedly elevated during CPB and remained the same postoperatively: 962 (577-2 067) and 883 (444-1 625) г/ml 5 min after un-clamping of aorta, 2203 (888-3 429) and 1 560 (506-2 657) г/ml <sup>2</sup> hours post-bypass, 897 (555-1 424) and 794 (505-951) г/ml 6 hours post-bypass in the GLN and control groups respectively. Perioperative administration of glutamine in dose of 0.4 g/kg a day does not appear to preserve intestinal integrity in low risk cardiac surgery patients.

scholarly journals Immunopathologic Alterations in Murine Models of Sepsis of Increasing Severity

1999 ◽  
Vol 67 (12) ◽  
pp. 6603-6610 ◽  
Author(s):  
Samuel Ebong ◽  
Douglas Call ◽  
Jean Nemzek ◽  
Gerald Bolgos ◽  
David Newcomb ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
Local Environment ◽  
Murine Models ◽  
Sham Treatment ◽  
Treatment Groups ◽  
Inflammatory Protein ◽  
Cytokine Levels ◽  
Physiologic Parameters ◽  
Macrophage Inflammatory Protein ◽  
Necrosis Factor

ABSTRACT We investigated inflammatory and physiologic parameters in sepsis models of increasing lethality induced by cecal ligation and puncture (CLP). Mice received imipenem for antibiotic therapy, and groups were sacrificed at 2, 4, 8, 12, 16, 20, and 24 h after CLP. The severity of sepsis increased with needle puncture size (lethality with 18-gauge puncture [18G], 100%; 21G, 50%; 25G, 5%; sham treatment, 0%). While the temperature (at 12 h) and the activity and diurnal rhythm (at day 4) of the 25G-treated CLP group recovered to normal, the 21G and 18G treatment groups exhibited severe hypothermia along with decreased activities. A direct correlation was also observed between the severity of sepsis and cytokine (interleukin 1β [IL-1β], tumor necrosis factor [TNF], IL-6, and IL-10) concentrations in both the peritoneum and the plasma. There were substantially higher cytokine levels in the more severe CLP models than in the sham-treated one. Peritoneal and plasma TNF levels were always less than 40 pg/ml in all models. None of the cytokines in the septic mice peaked within the first hour, which is in contrast to the results of most endotoxin models. Chemokine (KC and macrophage inflammatory protein 2) profiles also correlated with the severity of sepsis. Except for the chemokines, levels of inflammatory mediators were always higher at the site of inflammation (peritoneum) than in the circulation. Our study demonstrated that sepsis of increasing severity induced increased cytokine levels both within the local environment (peritoneum) and systemically (plasma), which in turn correlated with morbidity and mortality.

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