Thiol regulation of the production of TNF-α, IL-6 and IL-8 by human alveolar macrophages

Gosset, Philippe; Wallaert, B.; Tonnel, A. B.; Fourneau, Christophe

doi:10.1034/j.1399-3003.1999.14a17.x

Cited by 100 publications

(61 citation statements)

References 35 publications

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“…Accordingly, the present authors decided to stimulate AM immediately after sorting and to quantify the concentration of the different inflammatory mediators both early (4 h) and late (24 h). Fifthly, the concentration of LPS used and the time points chosen were similar to those of previous studies [10,41,42]. However, different results in LTB 4 and/or ROI release may have been found if different LPS concentrations and/or different time points had been used [17,41].…”

Section: Discussionmentioning

confidence: 49%

Decreased macrophage release of TGF- and TIMP-1 in chronic obstructive pulmonary disease

Pons¹

2005

European Respiratory Journal

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The present study tested the hypothesis that alveolar macrophages (AM) from patients with chronic obstructive pulmonary disease (COPD) release more pro-inflammatory and/ or less anti-inflammatory mediators than those from smokers with normal lung function and neversmokers.AM were sorted by flow cytometry from bronchoalveolar lavage fluid in 13 patients with COPD (mean¡SEM 67¡2 yrs, forced expiratory volume in one second (FEV1) 61¡4% reference), 16 smokers with normal lung function (55¡2 yrs, FEV1 97¡4% reference) and seven never-smokers (67¡7 yrs, FEV1 94¡4% reference). After sorting, AM were cultured (with and without lipopolysaccharide stimulation) after 4 h and 24 h, and the concentrations of leukotriene B 4 (LTB 4 ), transforming growth factor (TGF)-b 1 and tissue inhibitor of metalloproteinase (TIMP)-1 were quantified in the supernatant by ELISA. The production of reactive oxygen intermediates (ROI) in freshly isolated AM was determined by flow cytometry.LTB 4 secretion and ROI production were not different between groups. In contrast, AM from COPD patients released significantly less TGF-b 1 and TIMP-1 than those from smokers with normal lung function and nonsmokers.In conclusion, these observations are compatible with reduced anti-inflammatory and antielastolytic capacity in chronic obstructive pulmonary disease, which is likely to contribute to the pathogenesis of the disease.

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Section: Discussionmentioning

confidence: 49%

Decreased macrophage release of TGF- and TIMP-1 in chronic obstructive pulmonary disease

Pons¹

2005

European Respiratory Journal

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“…Many previous studies have indicated that the intracellular GSH level modifies cytokine production in monocytes and macrophages [11,22]. As shown in Table 2, co-administration resulted in a Th1-dominant pattern compared with the control and single-administration groups, and this was found to become a Th2-dominant pattern by 24 hr.…”

Section: Discussionmentioning

confidence: 73%

Enhancement of Antigen-Specific Immunoglobulin G Production in Mice by Co-Administration of L-Cystine and L-Theanine

et al. 2007

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ABSTRACT. Supplementation with both cystine and glutamic acid increases the synthesis of glutathione (GSH), which has a marked effect on immune cell function, as compared with supplementation with either amino acid alone in human macrophages in vitro. As dietary glutamic acid is metabolized during intestinal transport, oral administration of L-theanine (γ-glutamylethylamide), which is metabolized to glutamic acid mainly in the liver, may act as a glutamic acid donor in vivo. The present study was performed to investigate the effects of oral administration of L-cystine and/or L-theanine on GSH levels and immune responses. Co-administration of L-cystine (200 mg/kg) and L-theanine (80 mg/kg) for 11 days before immunization significantly increased the levels of total GSH in the liver 6 hr after immunization as compared with the levels in control mice. To examine the effects of administration of L-cystine and/or L-theanine on the balance of T helper (Th) 1/Th2 cell responses, the serum ratios of the Th1 cytokine, interferon (IFN)-γ, and the Th2 cytokine, interleukin (IL)-10, were investigated. At 24 hr after immunization, co-administration significantly increased the IL-10/IFN-γ ratio compared with the ratios of the control and single-administration mice. Furthermore, co-administration before primary immunization significantly enhanced serum antigen-specific IgG levels. Taken together, these findings suggest that co-administration of L-cystine and L-theanine enhances antigen-specific IgG production partly through augmentation of GSH levels and Th2-mediated responses.

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“…It should also be noted that the association between GSH and cytokine response has biological plausibility. GSH is part of the thiol regulation pathway within all human (9,12,13). Depleting immune cells of GSH modulates their ability to produce cytokines to a variety of foreign antigens (9,12,13).…”

mentioning

confidence: 99%

“…GSH is part of the thiol regulation pathway within all human (9,12,13). Depleting immune cells of GSH modulates their ability to produce cytokines to a variety of foreign antigens (9,12,13). Our finding that human GSH depletion is associated with decreased cytokine release from PBMCs in response to V. vulnificus may be a first step in understanding the human cellular mechanisms behind susceptibility to this bacterium.…”

mentioning

confidence: 99%

Inflammatory Cytokine Response to Vibrio vulnificus Elicited by Peripheral Blood Mononuclear Cells from Chronic Alcohol Users Is Associated with Biomarkers of Cellular Oxidative Stress

et al. 2003

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Vibrio vulnificus is the leading cause of death in the United States associated with the consumption of raw seafood, particularly oysters. In epidemiological studies, primary septicemia and inflammation-mediated septic shock caused by V. vulnificus is strongly associated with liver disease, often in the context of chronic alcohol abuse. The present study was undertaken to determine whether clinical biomarkers of liver function or cellular oxidative stress are associated with peripheral blood mononuclear cell inflammatory cytokine responses to V. vulnificus. Levels of interleukin-1␤ (IL-1␤), IL-6, IL-8, and tumor necrosis factor alpha elicited in response to V. vulnificus and measured in cell supernatants were not associated with the liver biomarkers aspartate aminotransferase (AST) or alanine aminotransferase (ALT) or the AST/ALT ratio. Vibrio vulnificus is a gram-negative bacterium found commonly in marine and estuarine environments. In the United States, it predominates in the warm waters of the Gulf and Atlantic Coasts (25, 27, 28). Despite not being a notifiable disease, each year there are 20 to 50 reported cases of V. vulnificus primary septicemia in the United States, occurring most often following the consumption of naturally contaminated raw oysters (2, 14). V. vulnificus also has the ability to cause gastroenteritis, which is generally self-limiting, and wound infections in otherwise healthy individuals (17, 32). Primary septicemia is seen almost exclusively in people with an underlying condition affecting their immune system. In epidemiological studies, primary septicemia caused by V. vulnificus is most often associated with preexisting liver disease, although other conditions, such as diabetes mellitus, hemochromatosis, immunodeficiency, or malignancy, may also increase susceptibility to this organism (2,14,17,24,41). The impairment of iron metabolism and resultant iron overload associated with many of these conditions is thought to support increased V. vulnificus growth and reduced immune clearance (1, 15, 16). Primary septicemia caused by V. vulnificus appears to follow a classical septic shock pathway, including an overwhelming inflammatory cytokine response followed by multiorgan failure and death. Presently, there is no effective treatment for V. vulnificus once someone has developed primary septicemia, and death usually ensues. It should be noted that V. vulnificus has many similarities with other gram-negative, encapsulated, opportunistic bacterial pathogens and likely exploits similar host susceptibility pathways that could be targeted for intervention.To date, the majority of V. vulnificus studies have focused on the bacterial factors involved in disease (41). Therefore, while much is now known about some of the bacterial factors involved in the disease process, little is understood about host cellular factors leading to susceptibility. It has been previously shown that V. vulnificus has the ability to elicit inflammationassociated cytokines from primary human cells in vitro and from animals...

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Thiol regulation of the production of TNF-α, IL-6 and IL-8 by human alveolar macrophages

Cited by 100 publications

References 35 publications

Decreased macrophage release of TGF- and TIMP-1 in chronic obstructive pulmonary disease

Decreased macrophage release of TGF- and TIMP-1 in chronic obstructive pulmonary disease

Enhancement of Antigen-Specific Immunoglobulin G Production in Mice by Co-Administration of L-Cystine and L-Theanine

Inflammatory Cytokine Response to Vibrio vulnificus Elicited by Peripheral Blood Mononuclear Cells from Chronic Alcohol Users Is Associated with Biomarkers of Cellular Oxidative Stress

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