scholarly journals CD23 Mediates Antimycobacterial Activity of Human Macrophages

2009 ◽  
Vol 77 (12) ◽  
pp. 5537-5542 ◽  
Author(s):  
M. Djavad Mossalayi ◽  
Ioannis Vouldoukis ◽  
Maria Mamani-Matsuda ◽  
Tina Kauss ◽  
Jean Guillon ◽  
...  
Keyword(s):  
Antimicrobial Activity ◽  
Human Monocyte ◽  
Antimycobacterial Activity ◽  
Mycobacterial Infection ◽  
Interleukin 10 ◽  
Functional Surface ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Tnf Α ◽  
Human Immune

ABSTRACT Engagement of surface receptors contributes to the antimicrobial activity of human immune cells. We show here that infection of human monocyte-derived macrophages (MDM) with live Mycobacterium avium induced the expression of CD23 on their membrane. Subsequent cross-linking of surface CD23 by appropriate ligands induced a dose-dependent antibacterial activity of MDM and the elimination of most infected cells. The stimulation of inducible nitric oxide synthase-dependent generation of NO from MDM after CD23 activation played a major role during their anti-M. avium activity. CD23 activation also induced tumor necrosis factor alpha (TNF-α) production from MDM. Mycobacteria reduction was partially inhibited by the addition of neutralizing anti-TNF-α antibody to cell cultures without affecting NO levels, which suggested the role of this cytokine for optimal antimicrobial activity. Finally, interleukin-10, a Th2 cytokine known to downregulate CD23 pathway, is shown to decrease NO generation and mycobacteria elimination by macrophages. Therefore, (i) infection with M. avium promotes functional surface CD23 expression on human macrophages and (ii) subsequent signaling of this molecule contributes to the antimicrobial activity of these cells through an NO- and TNF-α-dependent pathway. This study reveals a new human immune response mechanism to counter mycobacterial infection involving CD23 and its related ligands.

scholarly journals Major Outer Membrane Protein Omp25 of Brucella suis Is Involved in Inhibition of Tumor Necrosis Factor Alpha Production during Infection of Human Macrophages

2001 ◽  
Vol 69 (8) ◽  
pp. 4823-4830 ◽  
Author(s):  
Véronique Jubier-Maurin ◽  
Rose-Anne Boigegrain ◽  
Axel Cloeckaert ◽  
Antoine Gross ◽  
Maria-Teresa Alvarez-Martinez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Macrophage Infection ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Tnf Α ◽  
Brucella Suis ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Brucella spp. can establish themselves and cause disease in humans and animals. The mechanisms by whichBrucella spp. evade the antibacterial defenses of their host, however, remain largely unknown. We have previously reported that live brucellae failed to induce tumor necrosis factor alpha (TNF-α) production upon human macrophage infection. This inhibition is associated with a nonidentified protein that is released into culture medium. Outer membrane proteins (OMPs) of gram-negative bacteria have been shown to modulate macrophage functions, including cytokine production. Thus, we have analyzed the effects of two major OMPs (Omp25 and Omp31) of Brucella suis 1330 (wild-type [WT] B. suis) on TNF-α production. For this purpose, omp25and omp31 null mutants of B. suis(Δomp25 B. suis and Δomp31 B. suis, respectively) were constructed and analyzed for the ability to activate human macrophages to secrete TNF-α. We showed that, in contrast to WTB. suis or Δomp31 B. suis, Δomp25 B. suis induced TNF-α production when phagocytosed by human macrophages. The complementation of Δomp25 B. suis with WT omp25 (Δomp25-omp25 B. suis mutant) significantly reversed this effect: Δomp25-omp25 B. suis-infected macrophages secreted significantly less TNF-α than did macrophages infected with the Δomp25 B. suismutant. Furthermore, pretreatment of WT B. suis with an anti-Omp25 monoclonal antibody directed against an epitope exposed at the surface of the bacteria resulted in substancial TNF-α production during macrophage infection. These observations demonstrated that Omp25 of B. suis is involved in the negative regulation of TNF-α production upon infection of human macrophages.

scholarly journals A Defect in Interleukin-10 Leads to Enhanced Malarial Disease in Plasmodium chabaudi chabaudi Infection in Mice

1999 ◽  
Vol 67 (9) ◽  
pp. 4435-4442 ◽  
Author(s):  
Ching Li ◽  
Inés Corraliza ◽  
Jean Langhorne
Keyword(s):  
Body Weight ◽  
Knockout Mice ◽  
Interleukin 10 ◽  
Plasmodium Chabaudi ◽  
Double Knockout ◽  
Direct Stimulation ◽  
Necrosis Factor Alpha ◽  
Glucose Levels ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT Infection of interleukin-10 (IL-10)-nonexpressing (IL-10−/−) mice with Plasmodium chabaudi chabaudi (AS) leads to exacerbated pathology in female mice and death in a proportion of them. Hypoglycemia, hypothermia, and loss in body weight were significantly greater in female IL-10−/−mice than in male knockout mice and all wild-type (WT) mice during the acute phase of infection. At this time, both female and male IL-10−/− mice produced more gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and IL-12p40 mRNA than their respective WT counterparts. Inactivation of IFN-γ in IL-10−/− mice by the injection of anti-IFN-γ antibodies or by the generation of IL-10−/− IFN-γ receptor−/− double-knockout mice resulted in reduced mortality but did not affect body weight, temperature, or blood glucose levels. The data suggest that IFN-γ-independent pathways may be responsible for these pathological features of P. chabaudimalaria and may be due to direct stimulation of TNF-α by the parasite. Since male and female knockout mice both produce more inflammatory cytokines than their WT counterparts, it is likely that the mortality seen in females is due to the nature or magnitude of the response to these cytokines rather than the amount of IFN-γ or TNF-α produced.

scholarly journals High Coping Self-Efficacy Associated With Lower Sweat Inflammatory Cytokines in Adults: A Pilot Study

2019 ◽  
Vol 22 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Melissa Hladek ◽  
Jessica Gill ◽  
Chen Lai ◽  
Kate Lorig ◽  
Sarah Szanton
Keyword(s):  
Chronic Disease ◽  
Pilot Study ◽  
Self Efficacy ◽  
Emotional Regulation ◽  
Longitudinal Research ◽  
Interleukin 10 ◽  
Cross Sectional Study ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Tnf Α

Introduction/Background: Chronic diseases, like diabetes and heart disease, are considered inflammatory conditions with elevated levels of the proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) and the anti-inflammatory cytokine interleukin-10 (IL-10). Disease progression is not consistent from person to person. Psychosocial factors are hypothesized to play a modifying role. Self-efficacy, the confidence in one’s ability to perform well in a specific life domain or at a specific task, is associated with better health outcomes. Coping self-efficacy is confidence in one’s ability to handle life’s problems through emotional regulation, problem-solving, and social support. Little is known about associations between coping self-efficacy and inflammation. Aim: The purpose of this pilot study was to examine associations between coping self-efficacy and IL-6, IL-10, and TNF-α levels. Method: This was a cross-sectional study conducted over two visits. Sociodemographic variables, chronic disease count, body mass index (BMI), and coping self-efficacy were collected. Inflammatory markers were collected via sweat using the sweat patch, a noninvasive collection device. Results: Higher TNF-α and IL-10 levels were significantly associated with low coping self-efficacy (β = −.03, p = .028; β = −.017, p = .007, respectively) after adjustment for age, sex, race, BMI, and chronic disease count. IL-6 trended toward significance after adjustment as well (β = −.22, p = .054). Conclusions: This pilot study showed that high coping self-efficacy was associated with lower IL-6, IL-10, and TNF-α levels, indicating a potential buffering effect of high coping self-efficacy. Further longitudinal research with larger sample sizes is needed.

scholarly journals Infection of Human Dendritic Cells with a Mycobacterium tuberculosis sigE Mutant Stimulates Production of High Levels of Interleukin-10 but Low Levels of CXCL10: Impact on the T-Cell Response

2006 ◽  
Vol 74 (6) ◽  
pp. 3296-3304 ◽  
Author(s):  
Elena Giacomini ◽  
Ambar Sotolongo ◽  
Elisabetta Iona ◽  
Martina Severa ◽  
Maria Elena Remoli ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Mycobacterium Tuberculosis ◽  
Human Monocyte ◽  
Interleukin 10 ◽  
T Cell Response ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Effector Cells ◽  
Human Dendritic Cells

ABSTRACT The Mycobacterium tuberculosis genome encodes 13 sigma factors. We have previously shown that mutations in some of these transcriptional activators render M. tuberculosis sensitive to various environmental stresses and can attenuate the virulence phenotype. In this work, we focused on extracytoplasmic factor σE and studied the effects induced by the deletion of its structural gene (sigE) in the infection of human monocyte-derived dendritic cells (MDDC). We found that the wild-type M. tuberculosis strain (H37Rv), the sigE mutant (ST28), and the complemented strain (ST29) were able to infect dendritic cells (DC) to similar extents, although at 4 days postinfection a reduced ability to grow inside MDDC was observed for the sigE mutant ST28. After mycobacterium capture, the majority of MDDC underwent full maturation and expressed both inflammatory cytokines, such as tumor necrosis factor alpha, and the regulatory cytokines interleukin-12 (IL-12), IL-18, and beta interferon (IFN-β). Conversely, a higher level of production of IL-10 was observed in ST28-infected MDDC compared to H37Rv- or ST29-infected cell results. However, in spite of the presence of IL-10, supernatants from ST28-infected DC induced IFN-γ production by T cells similarly to those from H37Rv-infected DC culture. On the other hand, IL-10 impaired CXCL10 production in sigE mutant-infected DC and, indeed, its neutralization restored CXCL10 secretion. In line with these results, supernatants from ST28-infected cells showed a decreased capability to recruit CXCR3+ CD4+ T cells compared to those obtained from H37Rv-infected DC culture. Thus, our findings suggest that the sigE mutant-induced secretion of IL-10 inhibits CXCL10 expression and, in turn, the recruitment of activated-effector cells involved in the formation of granulomas.

scholarly journals Toll-Like Receptor 2 Recognition of the Microsporidia Encephalitozoon spp. Induces Nuclear Translocation of NF-κB and Subsequent Inflammatory Responses

2008 ◽  
Vol 76 (10) ◽  
pp. 4737-4744 ◽  
Author(s):  
Jeffrey Fischer ◽  
Colby Suire ◽  
Hollie Hale-Donze
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Responses ◽  
Host Recognition ◽  
Direct Role ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Encephalitozoon Intestinalis ◽  
Intracellular Parasites ◽  
Tnf Α ◽  
Interfering Rna

ABSTRACT Microsporidia are obligate intracellular parasites that are ubiquitous in nature and have been recognized as causing an important emerging disease among immunocompromised individuals. Limited knowledge exists about the immune response against these organisms, and virtually nothing is known about the receptors involved in host recognition. Toll-like receptors (TLR) are pattern recognition receptors that bind to specific molecules found on pathogens and signal a variety of inflammatory responses. In this study, we show that both Encephalitozoon cuniculi and Encephalitozoon intestinalis are preferentially recognized by TLR2 and not by TLR4 in primary human macrophages. This is the first demonstration of host receptor recognition of any microsporidian species. TLR2 ligation is known to activate NF-κB, resulting in inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukin-8 (IL-8). We found that the infection of primary human macrophages leads to the nuclear translocation of NF-κB in as early as 1 h and the subsequent production of TNF-α and IL-8. To verify the direct role of TLR2 parasite recognition in the production of these cytokines, the receptor was knocked down in primary human macrophages using small interfering RNA. This knockdown resulted in decreases in both the nuclear translocation of NF-κB and the levels of TNF-α and IL-8 after challenge with spores. Taken together, these experiments directly link the initial inflammatory response induced by Encephalitozoon spp. to TLR2 stimulation in human macrophages.

Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

Biologia ◽  
2007 ◽  
Vol 62 (3) ◽  
Author(s):  
Albena Alexandrova ◽  
Elena Bandžuchová ◽  
Anton Kebis ◽  
Marián Kukan ◽  
Daniel Kuba
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Matrix Metalloproteinase ◽  
Oxidative Dna Damage ◽  
Interleukin 10 ◽  
Matrix Metalloproteinase 2 ◽  
Necrosis Factor Alpha ◽  
Tissue Samples ◽  
Tnf Α ◽  
Rat Livers

AbstractCopper is known to induce oxidative stress in a number of models. It was shown that many pathophysiological events were associated with oxidative stress. Further, oxidative stress can increase gene expression of cytokines and of metalloproteinases. We previously found that copper toxic effects in isolated perfused rat livers were associated with significant oxidative stress (as assessed by lipid peroxidation, protein oxidation and oxidative DNA damage, particularly at concentration of 0.03 mM of Cu2+ in the perfusate). Here we investigated gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10); matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in frozen liver tissue samples by the real-time PCR assay. Compared to controls, copper at concentration of 0.01 mM did not affect gene expression of TNF-α, IL-10, MMP-2 and MMP-9, whereas copper at concentration of 0.03 mM significantly decreased gene expression of all the four TNF-α, IL-10, MMP-2 and MMP-9 by 69%, 81%, 43%, and 62%, respectively. These results suggest that copper-induced oxidative stress in the isolated rat liver can lead to the suppression of gene expression. Because TNF-α and metalloproteinases are involved also in liver regeneration, the suppression of these genes by copper may be one of the mechanisms by which acute intoxication of animals and humans with copper may impair regenerative capability of the liver.

scholarly journals Intracellular and Extracellular Cytokine Production by Human Mixed Mononuclear Cells in Response to Group B Streptococci

2000 ◽  
Vol 68 (1) ◽  
pp. 320-327 ◽  
Author(s):  
Daniel J. Kwak ◽  
Nancy H. Augustine ◽  
Wellington G. Borges ◽  
Joanna L. Joyner ◽  
Wayne F. Green ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Brefeldin A ◽  
Severe Infection ◽  
Human Monocyte ◽  
Group B Streptococci ◽  
Necrosis Factor Alpha ◽  
Intracellular Cytokines ◽  
Tnf Α ◽  
Ifn Γ ◽  
Group B

ABSTRACT Group B streptococci (GBS) are a major cause of severe infection in newborns, pregnant females, and other immunocompromised hosts. Infection often includes septicemia, shock, pneumonia, and respiratory failure. In previous studies, we have reported that GBS induce marked production of tumor necrosis factor alpha (TNF-α) by human mononuclear cells. The present study was designed to measure the production of TNF-α as well as additional cytokines, including interleukin 1β (IL-1β), IL-6, IL-8, IL-12, and gamma interferon (IFN-γ) but also to determine from what cells and at what time point during incubation with GBS that these cytokines are produced. Mixed mononuclear cells were incubated with heat-killed GBS, media alone, or 1 μg of Escherichia coli lipopolysaccharide (LPS). Brefeldin A was added to each sample prior to staining, which prevented the export of cytokines by the Golgi apparatus. The cells were then stained with the appropriate conjugated antibodies and analyzed by using a flow cytometer. Results indicate that intracellular cytokines appear, in almost all cases, simultaneous to or before secreted proteins are detected. In contrast to the response to LPS, where TNF-α, IL-1β, IL-6, and IL-8 appear almost simultaneously, the human monocyte response to GBS results in the production of TNF-α but delayed appearance of IL-1β, IL-6, and IL-8. The lymphocyte response to GBS was also strikingly different from that to LPS in that both secreted IFN-γ and IL-12 was detected, while LPS failed to induce production of these critical cytokines. This suggests an important role for TNF-α, IFN-γ, and IL-12 in GBS pathogenesis and/or immunity.

scholarly journals Impacts of different intensities of exercise on inflammation and hypoxia markers in low altitude

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Fatih Baygutalp ◽  
Yusuf Buzdağlı ◽  
Murat Ozan ◽  
Mitat Koz ◽  
Nurcan Kılıç Baygutalp ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Maximal Oxygen Consumption ◽  
Interleukin 10 ◽  
Bicycle Ergometer ◽  
Exercise Session ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Rest Condition ◽  
Low Altitude ◽  
Hypoxia Markers

Abstract Background This study aims to determine and compare the effects of exercise modalities with different intensities on the secretion of key inflammation and hypoxia markers in amateur athletes. Methods Twenty-three athletes with a mean age of 20.1 years, living at low altitude (1850 m) participated in this study. The participants' maximal oxygen consumption values (VO2 max) were determined with an incremental cycle exercise test as 54.15 ± 6.14 mL kg min−1. Athletes performed four protocols: at rest, 50% VO2 max, 75% VO2 max and 100% VO2 max (until exhaustion) with one-week intervals. 50% VO2 max, 75% VO2 max sessions were performed continuously for 30 min on a bicycle ergometer and 100% VO2 max session was performed by cycling until exhaustion. Blood samples were obtained at rest and immediately after each exercise session. Serum tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), interleukin-10 (IL-10), and hypoxia inducible factor-1 alpha (HIF-1α) levels were measured. Results There were significant differences in serum TNF-α levels in 75% VO2 max and 100% VO2 max sessions (489.03 ± 368.37 and 472.70 ± 365.21 ng/L, respectively) compared to rest conditions (331.65 ± 293.52 ng/L). Serum CRP levels of 50% VO2 max and 75% VO2 max sessions (1.19 ± 0.50; 1.07 ± 0.52 mg/L) were significantly higher than the rest condition (0.74 ± 0.35 mg/L). There were significant differences in serum IL-10 levels of rest condition and 50% VO2 max; 50% VO2 max, and 100% VO2 max sessions (328.09 ± 128.87; 446.36 ± 142.84; 347.44 ± 135.69; 324.88 ± 168.06 pg/mL). Serum HIF-1α levels were significantly higher in 75% VO2 max session compared to rest (1.26 ± 0.16; 1.08 ± 0.19 ng/mL) (P < 0.05 for all comparisons). Conclusions Both inflammatory and anti-inflammatory pathway is induced on different exercise intensities. Exercise protocols performed until exhaustion may lead to activation of inflammatory pathways and hypoxia-induced damage.

scholarly journals Moderate Dose of Lipopolysaccharide Induces Tumor Necrosis Factor-alpha and Interleukin-6 Production by Human Monocyte-derived Macrophages

2021 ◽  
Vol 9 (A) ◽  
pp. 468-472
Author(s):  
Nuraiza Meutia ◽  
Lokot Donna Lubis ◽  
Eka Roina Megawati
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Tumor Necrosis Factor Alpha ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Human Monocyte ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

BACKGROUND: Macrophages have been widely used for in vitro studies. Despite different types and doses of stimulatory agents that have been tested, there is no consensus for the method. AIM: This study was aimed to determine a sufficient dose of lipopolysaccharide (LPS) to stimulate inflammatory response in macrophages. METHODS: Whole blood was collected from four donors after written informed consent. The monocytes were isolated from peripheral blood mononuclear cells and stimulated with macrophage colony-stimulating factor, LPS, and Interferon-gamma for 6 days until differentiated into macrophages. The production of Tumor necrosis factor-alpha (TNF-α) and Interleukin-6 (IL-6) were quantified after 24-h further stimulation with 100 ng/mL and 2 μg/mL of LPS. RESULTS: Both doses increased TNF-α _production compare to their controls, but not statistically different (p > 0.05). There were also no differences in IL-6 production between treatments, 56.55 ± 32.30 pg/mL and 70.96 ± 65.08 pg/mL, respectively. CONCLUSION: A dose of 100 ng/mL of LPS was sufficient to stimulate inflammatory response in human monocyte-derived macrophages. A 24-h duration of macrophage stimulation was sufficient to observed the production TNF-α.

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