scholarly journals Chlamydia pneumoniae Influence on Cytokine Production in Steroid-Resistant and Steroid-Sensitive Asthmatics

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 112
Author(s):  
Dóra Paróczai ◽  
Tímea Mosolygó ◽  
Dávid Kókai ◽  
Valéria Endrész ◽  
Dezső P. Virok ◽  
...  
Keyword(s):  
Chlamydia Pneumoniae ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Inhaled Corticosteroids ◽  
Asthma Management ◽  
Peripheral Blood Mononuclear ◽  
Steroid Resistant ◽  
Asthmatic Patients ◽  
Tnf Α ◽  
Steroid Sensitive

Medications for asthma management consisting of inhaled corticosteroids act by controlling symptoms. However, some patients do not respond to steroid treatment due to immunological factors at the cytokine level. Chlamydia pneumoniae (C. pneumoniae) infection is strongly implicated in asthma pathogenesis, causing altered immune responses. We investigated the association of C. pneumoniae serostatus with the production of certain cytokines by peripheral blood mononuclear cells (PBMCs) of steroid-resistant and -sensitive asthmatic patients. Our most important findings are the following: In the case of C. pneumoniae seropositive patients we detected pronounced spontaneous interleukin (IL)-10 secretion and, in the case of steroid-resistant patients, IL-10 secretion was at a significantly higher level as compared with in-sensitive patients (p < 0.01). Furthermore, steroid-resistant seropositive patients produced a significantly higher level of IL-10 spontaneously and under antigen stimulation as compared with steroid-resistant seronegative individuals (p < 0.05). Concerning spontaneous TNF-α secretion by C. pneumoniae seropositive asthmatics, we observed that steroid-resistant patients produced significantly more of this cytokine than steroid-sensitive patients. In the steroid-resistant patients’ sera, a remarkably high MMP-9 concentration was associated with C. pneumoniae seronegativity. Our study revealed that the differences in the cytokine production in steroid-sensitive and -resistant asthmatic patients can be influenced by their C. pneumoniae serostatus.

The Effect of Acupuncture on Proinflammatory Cytokine Production in Patients with Chronic Headache: A Preliminary Report

2003 ◽  
Vol 31 (06) ◽  
pp. 945-954 ◽  
Author(s):  
Hyun-Ja Jeong ◽  
Seung-Heon Hong ◽  
Yong-Che Nam ◽  
Hee-Sook Yang ◽  
Yeoung-Su Lyu ◽  
...  
Keyword(s):  
Chronic Headache ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Acupuncture Treatment ◽  
Clinical Signs ◽  
Inhibitory Effect ◽  
Acute Stage ◽  
Control Group ◽  
Peripheral Blood Mononuclear ◽  
Tnf Α

Acupuncture has been widely used as a treatment for various conditions like headache and stroke, especially in Asian countries such as Korea and China. But few scientific investigations have been carried out. The aim of the present study is to investigate the effect of acupuncture on the production of inflammatory cytokines in patients with chronic headache (CH). Patients with CH were treated with acupuncture during the acute stage. Clinical signs of CH disappeared markedly after three months of treatment with acupuncture. Peripheral blood mononuclear cells obtained from a normal group and those from the patients with CH, before and after treatment with acupuncture, were cultured for 24 hours in the presence or absence of lipopolysaccharide (LPS). The amount of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) in LPS culture supernatant was significantly increased in the patients with CH compared to the healthy control group (p < 0.05). But those cytokines came down toward the levels of the healthy group (p < 0.05) after treatment with acupuncture, although the levels still remained elevated. Plasma cytokine levels were analyzed to evaluate any change due to acupuncture treatment. There was little difference in the levels of IL-1β or IL-6 due to the treatment with acupuncture in the patients with CH, but significantly reduced plasma levels of TNF-α were observed. These data suggest that acupuncture treatment has an inhibitory effect on pro-inflammatory cytokine production in patients with CH.

Chlamydia pneumoniae enhances the Th2 profile of stimulated peripheral blood mononuclear cells from asthmatic patients

2016 ◽  
Vol 77 (5) ◽  
pp. 382-388 ◽  
Author(s):  
Tamar A. Smith-Norowitz ◽  
Kobkul Chotikanatis ◽  
David P. Erstein ◽  
Jason Perlman ◽  
Yitzchok M. Norowitz ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Chlamydia Pneumoniae ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Asthmatic Patients ◽  
Blood Mononuclear Cells

Endotoxin acts synergistically with C. difficile toxin B to increase IL-1 β production: A potential role for the intestinal biome in modifying the severity of C. difficile colitis

2021 ◽  
Author(s):  
P Htwe ◽  
H H Aung ◽  
B Kywe ◽  
P T Niang ◽  
T S Oo ◽  
...  
Keyword(s):  
Potential Role ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Intestinal Microbiome ◽  
Peripheral Blood Mononuclear ◽  
Toxin B ◽  
E Coli ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Stool Samples

Abstract. Background Inflammation is a crucial driver of host damage in patients with C. difficile colitis. We examined the potential for the intestinal microbiome to modify inflammation in patients with C. difficile colitis via the effects of gut-derived endotoxin on cytokine production. Methods Endotoxin from E. coli and P. aeruginosa as well as stool-derived endotoxin was tested for their ability to enhance IL-1β and TNFα- production by toxin B-stimulated peripheral blood mononuclear cells. Inflammasome and TLR-4 blocking studies were done to discern the importance of these pathways, while metagenomic studies were done to characterize predominant organisms from stool samples. Results Endotoxin significantly enhanced the ability of C. difficile toxin B to promote IL-1β production but not TNF- α. The magnitude of this effect varied by endotoxin type and was dependent on combined inflammasome and TLR-4 activation. Stool-derived endotoxin exhibited a similar synergistic effect on IL-1 β production with less synergy observed for stools that contained a high proportion of gamma-proteobacteria. Conclusions The ability of endotoxin to enhance IL-1 β production highlights a manner by which the microbiome can modify inflammation and severity of C. difficile disease. This information may be useful in devising new therapies for severe C. difficile colitis.

Psychological Stress and Cytokine Production in Multiple Sclerosis

2011 ◽  
Vol 15 (2) ◽  
pp. 226-233 ◽  
Author(s):  
Matthew Sorenson ◽  
Linda Janusek ◽  
Herbert Mathews
Keyword(s):  
Multiple Sclerosis ◽  
Psychological Stress ◽  
Perceived Stress ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Mood Disturbance ◽  
Peripheral Blood Mononuclear ◽  
Disease Symptoms ◽  
Tnf Α

Objective:Psychological variables such as perceived stress appear to play a role in symptom onset or disease exacerbation in multiple sclerosis (MS). The authors sought to determine if perceived stress is indeed associated with the expression of pro-inflammatory cytokines and disease symptoms in individuals with MS. To do so, the authors examined the relationships among disease symptomatology, perceived stress, and cytokine production from peripheral blood mononuclear cells in 42 outpatients with MS and 36 normative controls.Method:The authors drew peripheral blood from all subjects prior to the completion of a series of psychological instruments. The authors measured stress using the Perceived Stress scale and negative mood with the Profile of Mood States. Disease symptoms were measured using the Multiple Sclerosis Symptom Checklist. Cytokine production was induced separately by lipopolysaccharide and a combination of phytohemagglutinin and phorbol-12-myristate-13-acetate.Results:In MS subjects, the induced production of interleukin (IL)-6 and IL-10 positively correlated with psychological stress, mood disturbance, and disease symptomatology. In contrast, psychological stress in control subjects significantly correlated with level of tumor necrosis factor-alpha (TNF-α), and mood disturbance correlated with levels of TNF-α and interferon-gamma. As well, compared to controls, MS subjects exhibited a significant fourfold increase in the production of IL-12.Conclusion:There is, in those with MS, a pattern of IL-6 and IL-10 production that correlates significantly with perceived stress and disease symptomatology.

"Tien-Hsien Liquid" Can Modulate Antigen-Stimulated Cytokine Production by T-Cells Isolated from Patients with Recurrent Aphthous Ulcerations

2005 ◽  
Vol 33 (04) ◽  
pp. 559-571 ◽  
Author(s):  
Andy Sun ◽  
Jean-San Chia ◽  
Won-Bo Wang ◽  
Chun-Pin Chiang
Keyword(s):  
T Cells ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Interferon Γ ◽  
Enzyme Linked Immunosorbent Assay ◽  
Peripheral Blood Mononuclear ◽  
Tnf Α ◽  
Ifn Γ ◽  
Factor Α ◽  
Necrosis Factor

Recurrent aphthous ulcerations (RAU) represent a common oral mucosal disease with altered humoral and cellular immunities. Tien-Hsien liquid (THL) is an extract of Chinese medicinal herbs with immunomodulating effects. Our previous study found that THL can modulate the antigen-stimulated proliferative response of peripheral blood mononuclear cells and T-cells isolated from RAU patients. In this study, we further tested whether THL can modulate the antigen-stimulated cytokine production by T-cells isolated from RAU patients. To achieve this goal, T-cells isolated from 19 RAU patients were incubated with phytohemagglutinin (PHA), glutaraldehyde-inactivated tetanus toxoid (TT), glucosyltransferase D (GtfD), or antigens of Streptococcus mutans in the presence or absence of THL. The levels of interleukin (IL)-2, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), IL-6, or IL-10 in the supernatants of T-cell cultures were measured by cytokine enzyme-linked immunosorbent assay (ELISA) kits. We found that THL significantly increased the PHA- or TT-stimulated TNF-α, IL-6, and IL-10 production by T-cells isolated from RAU patients. However, THL could also significantly decrease the TT-stimulated IL-2 production, the GtfD-stimulated IL-2, TNF-α, IL-6 and IL-10 production, and the S. mutans-stimulated IFN-γ, TNF-α, and IL-10 production by T-cells isolated from RAU patients. These results indicate that THL can modulate the antigen-stimulated cytokine production by T-cells isolated from RAU patients. Because RAU is probably a Thl-mediated disease with elevated levels of IL-2, IFN-γ, TNF-α and IL-6 in either the patient's sera or oral lesions and these increased levels of cytokines can be reduced by THL, we suggest that THL may be a potential immunoceutical agent for treatment of RAU.

scholarly journals Measurement of Cytokine Secretion, Intracellular Protein Expression, and mRNA in Resting and Stimulated Peripheral Blood Mononuclear Cells

2000 ◽  
Vol 7 (6) ◽  
pp. 920-924 ◽  
Author(s):  
Kathleen E. Sullivan ◽  
Joie Cutilli ◽  
Lisa M. Piliero ◽  
Darlene Ghavimi-Alagha ◽  
Stuart E. Starr ◽  
...  
Keyword(s):  
Phorbol Myristate Acetate ◽  
Mononuclear Cells ◽  
Cytokine Production ◽  
Gamma Interferon ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Myristate Acetate ◽  
Peripheral Blood Mononuclear ◽  
Valuable Adjunct ◽  
Tnf Α

ABSTRACT Quantitation of cytokine production is a valuable adjunct to standard immunologic assays in defining several pathologic processes. Nevertheless, there is little agreement about which tissues should be assayed, which type of assay should be performed, and which stimulation protocol should be used. As these types of assays enter the clinical arena, there is need for standardization. There is also a need to maximize the amount of information which may be derived from a single sample. We compared secreted interleukin 4 (IL-4), IL-2, IL-6, tumor necrosis factor alpha (TNF-α), and gamma interferon proteins as measured by enzyme-linked immunosorbent assay with intracellular cytokine production (IL-2 and gamma interferon) as detected by flow cytometry and quantitative competitive PCR for IL-2, IL-4, TNF-α, and gamma interferon mRNA and cDNA. Results from unstimulated cells and cells stimulated with phorbol myristate acetate, phytohemagglutinin, and phorbol myristate acetate plus phytohemagglutin were compared. All three methodologies detected significant stimulation of cytokine production. The combination of phytohemagglutinin and phorbol myristate acetate was overall the most-potent stimulus.

scholarly journals Chlamydia pneumoniae-induced tumour necrosis factor alpha responses are lower in children with asthma compared with non-asthma

2018 ◽  
Vol 5 (1) ◽  
pp. e000239 ◽  
Author(s):  
Tamar Anne Smith-Norowitz ◽  
Kobkul Chotikanatis ◽  
Diana Weaver ◽  
Jared Ditkowsky ◽  
Yitzchok Meir Norowitz ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Chlamydia Pneumoniae ◽  
Mononuclear Cells ◽  
Tumour Necrosis Factor Alpha ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

IntroductionChlamydia pneumoniae respiratory tract infection has been implicated in the pathogenesis of reactive airway disease and asthma. Innate cytokine responses that are protective of infection with intracellular pathogens may be impaired in patients with asthma. Tumour necrosis factor alpha (TNF-α) is a cytokine related to functions of monocytes and may inhibit C. pneumoniae infection. We investigated TNF-α responses in C. pneumoniae-infected peripheral blood mononuclear cells (PBMCs) in patients with asthma and non-asthma, and whether ciprofloxacin, azithromycin or doxycycline affects TNF-α responses.MethodsPBMC (1.5×106) from paediatric patients with asthma (n=19) and non-asthmatic controls (n=6) were infected or mock infected for 1 hour with or without C. pneumoniae AR-39 at a multiplicity of infection=0.1, and cultured+ciprofloxacin, azithromycin or doxycycline (0.1 ug/mL) for 48 hours. TNF-α levels were measured in supernatants by ELISA.ResultsWhen PBMC from patients with asthma were infected with C. pneumoniae, levels of TNF-α were significantly lower than in subjects without asthma (48 hours) (5.5±5.6, 38.4±53.7; p=0.0113). However, baseline responses (no infection with C. pneumoniae) were similar in asthma and non-asthma (1.0±1.7, 1.1±1.2; p=0.89). When PBMC frompatiens with asthma were infected with C. pneumoniae+ciprofloxacin, azithromycin or doxycycline, TNF-α levels increased (25%–45%); this affect was not observed in PBMC from patients without asthma.ConclusionsWe identified differences in the quantity of TNF-α produced by C. pneumoniae-infected PBMC in asthma compared with non-asthma.

Patients with multiple sclerosis resisted to glucocorticoid therapy: abnormal expression of heat-shock protein 90 in glucocorticoid receptor complex

2008 ◽  
Vol 14 (7) ◽  
pp. 919-926 ◽  
Author(s):  
M Matysiak ◽  
B Makosa ◽  
A Walczak ◽  
K Selmaj
Keyword(s):  
Multiple Sclerosis ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mononuclear Cells ◽  
Heat Shock Protein 90 ◽  
Peripheral Blood Mononuclear ◽  
Steroid Resistant ◽  
Blood Mononuclear Cells ◽  
Steroid Sensitive ◽  
Cytoplasmic Complex

Objective The majority of patients with multiple sclerosis (MS) respond favorably to glucocorticoids (GS) for their relapse treatment (steroid-sensitive multiple sclerosis). Unfortunately, a small subset of patients with multiple-sclerosis fails to adequately respond even to high dose of GS (steroid-resistant multiple sclerosis). Mechanism of GS therapeutic unresponsiveness is not resolved. Methods Transcripts for glucocorticoid receptor (GR) was assessed in peripheral blood mononuclear cells by real-time polymerase chain reaction in patients with steroid-sensitive and steroid-resistant multiple sclerosis. GR expression was assessed by Western blotting. The amount of heat-shock protein 90 (hsp90) in GR cytoplasmic complex was assessed by immunoprecipitation. Hsp90 was shown to stabilize the GR complex, to prevent its translocation to nucleus, and to inhibit GR transcription. Results Peripheral blood mononuclear cells of steroid-resistant multiple sclerosis transcripts for all three isoforms of GR, α, β, and γ, were reduced by about two-folds compared with patients with steroid-sensitive multiple sclerosis. We have not found an increase in the β and γ transcripts of GR, which might serve as a dominant negative mutants, over GR α in steroid-resistant multiple sclerosis. The amount of hsp90 in the GR complex in cytoplasm was significantly higher in steroid-resistant multiple sclerosis compared with steroid-sensitive multiple sclerosis. Conclusions Molecular mechanism of GS unresponsiveness in some patients with multiple sclerosis might be related to increased presence of hsp90 in the GR cytoplasmic complex, leading to the inhibition of GR translocation to nucleus and reduction in its transcription.

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