In Vitro Synthesis of Interferon-γ, Interleukin-4, Transforming Growth Factor-β and Interleukin-1β by Peripheral Blood Mononuclear Cells from Tuberculosis Patients: Relationship with the Severity of Pulmonary Involvement

1999 ◽  
Vol 49 (2) ◽  
pp. 210 ◽  
Author(s):  
D. DLUGOVITZKY
Keyword(s):  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Pulmonary Involvement ◽  
Interferon Γ ◽  
Interleukin 4 ◽  
Peripheral Blood Mononuclear ◽  
In Vitro Synthesis ◽  
Tuberculosis Patients

scholarly journals Consumption of Galactooligosaccharides together with Probiotics Stimulates the In Vitro Peripheral Blood Mononuclear Cell Proliferation and IFNγ Production in Healthy Men

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Reetta Holma ◽  
Riina A. Kekkonen ◽  
Katja Hatakka ◽  
Tuija Poussa ◽  
Outi Vaarala ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Lactobacillus Rhamnosus ◽  
Interferon Γ ◽  
Transforming Growth Factor Β1 ◽  
Interleukin 4 ◽  
Peripheral Blood Mononuclear ◽  
Healthy Men

Probiotics and prebiotics modify the intestinal environment and could have immunomodulatory effects. The proliferation of spontaneous and phytohemagglutinin-stimulated peripheral blood mononuclear cells (PBMCs) and their production of interleukin-4, interleukin-5, transforming growth factor-β1, and interferon-γ (IFNγ) were determined in eighteen men at the baseline and during a 2-week period of probiotics (mixture of Lactobacillus rhamnosus GG, Lactobacillus rhamnosus LC705, Propionibacterium freudenreichii ssp. shermanii JS, and Bifidobacterium breve Bb99) and galactooligosaccharides (GOSs) (3.8 g/day). The spontaneous and stimulated proliferation of PBMC increased from the baseline during probiotics+GOS (P<0.001). The secretion of IFNγ, but not other cytokines, by stimulated PBMC increased during the same period (P<0.05). In conclusion, the consumption of this probiotic mixture including GOS appears to increase the capacity of PBMC to proliferate and release IFNγ selectively in healthy men.

scholarly journals Spontaneous secretion of interferon γ and interleukin 4 by human intraepithelial and lamina propria gut lymphocytes

Gut ◽  
1998 ◽  
Vol 42 (5) ◽  
pp. 643-649 ◽  
Author(s):  
M Carol ◽  
A Lambrechts ◽  
A Van Gossum ◽  
M Libin ◽  
M Goldman ◽  
...  
Keyword(s):  
Lamina Propria ◽  
Intestinal Mucosa ◽  
Mononuclear Cells ◽  
Critical Role ◽  
Gastrointestinal Diseases ◽  
Interferon Γ ◽  
Interleukin 4 ◽  
Peripheral Blood Mononuclear ◽  
Ifn Γ

Background—Cytokines secreted by intestinal T lymphocytes probably play a critical role in regulation of the gut associated immune responses.Aims—To quantify interferon γ (IFN-γ) and interleukin 4 (IL-4) secreting cells (SC) among human intraepithelial (IEL) and lamina propria (LPL) lymphocytes from the duodenum and right colon in non-pathological situations and in the absence of in vitro stimulation.Patients—Duodenal and right colonic biopsy specimens were obtained from patients with no inflammation of the intestinal mucosa.Methods—Intraepithelial and lamina propria cell suspensions were assayed for numbers of cells spontaneously secreting IFN-γ and IL-4 by a two site reverse enzyme linked immunospot technique (ELISPOT).Results—The relatively high proportion of duodenal lymphocytes spontaneously secreting IFN-γ (IEL 3.6%; LPL 1.9%) and IL-4 (IEL 1.3%; LPL 0.7%) contrasted with the very low numbers of spontaneously IFN-γ SC and the absence of spontaneously IL-4 SC among peripheral blood mononuclear cells. In the basal state, both IFN-γ and IL-4 were mainly produced by CD4+ cells. Within the colon, only 0.2% of IEL and LPL secreted IFN-γ in the basal state, and 0.1% secreted IL-4.Conclusions—Compared with peripheral lymphocytes substantial proportions of intestinal epithelial and lamina propria lymphocytes spontaneously secrete IFN-γ and/or IL-4. These cytokines are probably involved in the normal homoeostasis of the human intestinal mucosa. Disturbances in their secretion could play a role in the pathogenesis of gastrointestinal diseases.

scholarly journals Endothelial Cells Require STAT3 for Protection against Endotoxin-induced Inf lammation

2003 ◽  
Vol 198 (10) ◽  
pp. 1517-1525 ◽  
Author(s):  
Arihiro Kano ◽  
Michael J. Wolfgang ◽  
Qian Gao ◽  
Joerg Jacoby ◽  
Gui-Xuan Chai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Transforming Growth Factor ◽  
Endotoxic Shock ◽  
Transforming Growth Factor Β ◽  
Organ Damage ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Protective Function ◽  
Lps Challenge

Endothelial cells (ECs) are believed to be an important component in the protection from lipopolysaccharide (LPS)-induced endotoxic shock. However, the cellular and molecular mechanism is not well defined. Here, we report that signal transducer and activator of transcription (STAT) 3 is an essential regulator of the antiinflammatory function of ECs in systemic immunity. Because STAT3 deficiency results in early embryonic lethality, we have generated mice with a conditional STAT3 deletion in endothelium (STAT3E−/−). STAT3E−/− mice are healthy and fertile, and isolated ECs initiate normal tube formation in vitro. Conditional endothelial but not organ-specific (i.e., hepatocyte or cardiomyocyte) STAT3 knockout mice show an increased susceptibility to lethality after LPS challenge. The LPS response in STAT3E−/− mice shows exaggerated inflammation and leukocyte infiltration in multiple organs combined with elevated activity of serum alanine aminotransferase and aspartate aminotransferase, indicating organ damage. Concomitantly, proinflammatory cytokines are produced at an exaggerated level and for a prolonged period. This defect cannot be explained by lack of antiinflammatory cytokines, such as interleukin 10 and transforming growth factor β. Instead, we have shown that a soluble activity derived from endothelia and dependent on STAT3 is critical for suppression of interferon γ. These data define STAT3 signaling within endothelia as a critical antiinflammatory mediator and provide new insight to the protective function of ECs in inflammation.

scholarly journals Minor H Antigen HA-1–specific Regulator and Effector CD8+ T Cells, and HA-1 Microchimerism, in Allograft Tolerance

2004 ◽  
Vol 199 (7) ◽  
pp. 1017-1023 ◽  
Author(s):  
Junchao Cai ◽  
Junglim Lee ◽  
Ewa Jankowska-Gan ◽  
Richard Derks ◽  
Jos Pool ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Renal Allograft ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Cytotoxic T Lymphocyte ◽  
Severe Combined Immunodeficiency ◽  
Interferon Γ ◽  
T Cell Subsets ◽  
Delayed Type Hypersensitivity ◽  
Peripheral Blood Mononuclear

The role of the hematopoietic lineage-restricted minor histocompatibility (H) antigen HA-1 in renal allograft tolerance was explored. We obtained peripheral blood samples from three recipients of histocompatibility leukocyte antigen (HLA)–matched, HA-1–mismatched renal transplants, one of which had discontinued immunosuppression &gt;30 yr ago while sustaining normal kidney function. Peripheral blood mononuclear cells (PBMCs) were injected into the footpads of severe combined immunodeficiency mice to measure human delayed type hypersensitivity (DTH) responses. All three patients manifested regulated DTH responses to HA-1H peptide. By differential tetramer staining intensities, we observed two distinct minor H antigen HA-1–specific CD8+ T cell subsets. The one that stained dimly had the characteristics of a T regulatory (TR) cell and produced interleukin (IL) 10 and/or transforming growth factor (TGF) β. These HA-1–specific TR cells coexisted with bright tetramer-binding CD8+ T effector (TE) cells. The CD8+ TE cells mediated HA-1–specific DTH and produced interferon-γ. Suppression of these TE functions by TR cells was TGFβ, IL-10, and cytotoxic T lymphocyte–associated antigen 4 dependent. In addition, HA-1 microchimerism was detected in two recipients, primarily in the dendritic cell fraction of the PBMCs. This is the first demonstration of coexisting CD8+ memory TR and TE cells, both specific for the same HA-1 antigen, in the context of renal allograft tolerance.

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