scholarly journals Identification of the Molecular Basis of Nanocurcumin-Induced Telocyte Preservation within the Colon of Ulcerative Colitis Rat Model

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Eetmad A. Arafat ◽  
Rehab Elsayed Marzouk ◽  
Sally Abdallah Mostafa ◽  
Walaa H. E. Hamed
Keyword(s):  
Gene Expression ◽  
Ulcerative Colitis ◽  
Rat Model ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Distinct Type ◽  
Colonic Tissue ◽  
Significant Elevation ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background. Telocytes (TCs) are a distinct type of interstitial cells that play a vital role in the pathogenesis of ulcerative colitis and colonic tissue hemostasis. The aim of this study was to examine the effect of nanocurcumin (NC) on the morphometric and immunohistochemical characterization of TCs in the ulcerative colitis (UC) rat model. Methods. Forty rats were randomly divided into control, NC, UC, and UC+NC groups. At the end of the experiment, the colon was dissected and prepared for histopathological and immunohistochemical assessment. Tissue homogenates were prepared for real-time PCR assessment of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta (TGF-β) gene expression. Our results revealed extensive mucosal damage with inflammatory cell infiltration, significant reduction of CD34, and vimentin immunostained TCs in the colon of the UC group with significant elevation of expression of IL-6, TNF-α, and TGF-β. The UC+NC-treated group revealed significant elevation of TC count compared to the UC group besides, a significant reduction of the three gene expression. Conclusion. NC successfully targeted the colonic tissue, improved the mucosal lesion, preserve TCs distribution, and count through its anti-inflammatory and fibrinolytic properties.

Effect of intestinal colonisation by two Lactobacillus strains on the immune response of gnotobiotic mice

2014 ◽  
Vol 5 (4) ◽  
pp. 409-419 ◽  
Author(s):  
R.S. Steinberg ◽  
M. Lima ◽  
N.L. Gomes de Oliveira ◽  
A. Miyoshi ◽  
J.R. Nicoli ◽  
...  
Keyword(s):  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Quantitative Polymerase Chain Reaction ◽  
Necrosis Factor Alpha ◽  
Interleukin 5 ◽  
Germ Free ◽  
Intestinal Colonisation ◽  
Tnf Α ◽  
Tgf Β1 ◽  
Intragastric Gavage

The effect of intestinal colonisation on the immune system was investigated in germ-free mice monoassociated with Lactobacillus strains isolated from calf faeces. Single doses of Lactobacillus acidophilus L36 or Lactobacillus salivarius L38 were administered to germ-free mice by intragastric gavage. Ten days later, the mice were euthanised. Gene expression levels of interleukin 5 (IL-5), IL-6, IL-10, IL-12b, IL-17a, gamma interferon (IFN-γ), transforming growth factor beta 1 (TGF-β1), and tumour necrosis factor alpha (TNF-α) were quantified in segments of the small and large intestines by real time quantitative polymerase chain reaction. All the mice were colonised rapidly after Lactobacillus administration with intestinal counts ranging from 6.53 to 8.26 log cfu/g. L. acidophilus L36 administration increased the expression of cytokines involved with the Th2 (IL-5, IL-6 and TGF-β1) and Th17 (IL-17a, TNF-α and IL-6) inflammatory response, whereas L. salivarius L38 appeared to stimulate a pattern of less diversified cytokines in the intestine. Intragastric gavage of L. acidophilus L36 and L. salivarius L38 induced similar levels of colonisation in the digestive tracts of germ-free mice but stimulated different immune responses in the intestinal mucosa. The different immunomodulation patterns might facilitate the potential use of these lactobacilli as probiotics to treat distinct pathological conditions, for example protection against Citrobacter rodentium infection by stimulating IL-17 production.

scholarly journals Altered Cytokine Production and Impaired Antimycobacterial Immunity in Protein-Malnourished Guinea Pigs

1998 ◽  
Vol 66 (8) ◽  
pp. 3562-3568 ◽  
Author(s):  
Guixiang Dai ◽  
David N. McMurray
Keyword(s):  
Transforming Growth Factor Beta ◽  
Guinea Pigs ◽  
Transforming Growth Factor ◽  
Serum Levels ◽  
Peritoneal Macrophages ◽  
Protein Malnutrition ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cd4 Lymphocytes

ABSTRACT Protein malnutrition leads to multiple detrimental alterations of host immune responses to mycobacterial infection. In this study, we demonstrated that splenocytes from low-protein (LP) guinea pigs vaccinated 6 weeks previously with attenuated Mycobacterium tuberculosis H37Ra failed to control the accumulation of virulentM. tuberculosis H37Rv in cocultured autologous peritoneal macrophages, despite the fact that they were able to control the accumulation of virulent tubercle bacilli in cocultured syngeneic peritoneal macrophages from normally nourished guinea pigs as successfully as did those from high-protein (HP) counterparts. Vaccine-induced growth control of virulent M. tuberculosisH37Rv in these cocultures appeared to be mediated by CD4 lymphocytes but not CD8 cells. Tuberculin (purified protein derivative [PPD])-induced lymphoproliferation was markedly impaired in vaccinated LP guinea pigs, and the depletion of CD4 lymphocytes significantly decreased lymphocyte proliferation whereas CD8 cell depletion did not. Protein malnutrition also impaired the abilities of cells from vaccinated LP guinea pigs to produce cytokines, including interferon, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β), in response to PPD, despite the demonstration of higher serum levels of TNF-α and TGF-β after an intravenous injection of PPD into LP guinea pigs. In contrast, peritoneal macrophages from protein-malnourished guinea pigs produced a higher level of TGF-β 4 days after infection in vitro with M. tuberculosis H37Rv than did those from protein adequate controls. These results suggest that dietary protein malnutrition impairs vaccine-induced resistance to M. tuberculosis, in part, by altering the cytokine profile to favor macrophage deactivation.

Abstract P100: Gene Targeting of Npr1 Reveals Its Repressive Role in Cardiac Hypertrophy and Proinflammatory Cytokine Gene Expression

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Kailash N Pandey ◽  
Elangovan Vellaichamy
Keyword(s):  
Gene Expression ◽  
Guanylyl Cyclase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cytokine Gene Expression ◽  
Heart Weight ◽  
Cytokine Gene ◽  
Wild Type ◽  
Necrosis Factor Alpha ◽  
Natriuretic Peptide Receptor A

The objective of the present study was to examine whether genetically determined differences in the Npr1 gene (coding for guanylyl cyclase/natriuretic peptide receptor-A; GC-A/NPRA) affect the expression of cardiac pro-inflammatory cytokines and nuclear factor kappa-B (NF-kB) levels in Npr1 gene-targeted mice. The Npr1 gene-disrupted null mutant ( Npr1 −/− ; 0-copy) mice had 32-38 mmHg higher systolic blood pressure (SBP) and 60% greater heart weight to body weight (HW:BW) ratio, however, Npr1 gene-duplicated mice ( Npr1 ++/++ ; 4-copy) exhibited 10-15 mmHg lower SBP with no change in the HW:BW ratio compared with wild-type ( Npr1 +/+ ; 2-copy) mice. Significant up-regulation of interleukin-6 (IL-6; 2-fold tumor necrosis factor-alpha), TNF-α; 4-fold), and transforming growth factor-beta (TGF-β1; 4-fold), along with increases in NF-κB and activating protein-1 (AP-1) binding activities (170% and 130%, p < 0.01, respectively), were increased in the Npr1 −/− mice hearts. Conversely, a significant decrease in cytokine gene expression and NF-κB and AP-1 binding activities were found in gene-duplicated mice hearts compared with wild-type mice. The ventricular guanylyl cyclase (GC) activity and cGMP levels were reduced by almost 10-fold and 5-fold, respectively, in Npr1 -/- mice. However, GC activity and cGMP levels were increased, respectively, by almost 9-fold and 6-fold, respectively, in gene-duplicated mice. The present results provide direct evidence that duplication of Npr1 gene in mice represses the inflammatory cytokine gene expression via inhibition NF-κB- and AP-1-mediated signaling mechanisms, and is associated with cardiac protection.

Assessing the relationship of respiratory muscle strength and cytokine status in patients with community-acquired pneumonia

2021 ◽  
Vol 31 (3) ◽  
pp. 311-319
Author(s):  
A. A. Dei ◽  
B. I. Geltser ◽  
M. V. Antonyuk ◽  
T. A. Gvozdenko ◽  
E. P. Kalinina ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Respiratory Muscle ◽  
Transforming Growth Factor ◽  
Community Acquired Pneumonia ◽  
Necrosis Factor Alpha ◽  
The Third ◽  
Endogenous Intoxication ◽  
Tnf Α ◽  
Relationship Of

Aim. Assessment of the role of cytokine-mediated changes in the development of respiratory muscle (RM) dysfunction in patients with community-acquired pneumonia (СAP). Methods. 84 men aged 18 – 26 years with a median of age 19.5 [18.4; 22.8]. Mild to moderate CAP (MCAP) was diagnosed in 62 (73.8%) patients and severe (SCAP) in 22 (26.2%). The expiratory (MEP, MRPDout) and inspiratory (MIP, MRPDin. SNIP) strength indices of RM were recorded on a MicrоRPM apparatus (CareFusion, UK). The severity of endogenous intoxication was verified using the following indices: hematologic (HII), leukocyte (LII), and nuclear. Serum concentrations of interleukins-2, -8, -10, basic fibroblast growth factor, transforming growth factor-beta, tumor necrosis factor-alpha (TNF-α), and a soluble receptor for TNF-α. Data processing was performed by cluster and correlation analysis methods. Results. Three clusters of patients with CAP were identified by the characteristic combinations of indicators of RM strength, endogenous intoxication, and cytokine status. The first cluster had MCAP, the second – both MCAP and SCAP, the third – SCAP. In the first cluster, dysfunction of expiratory RM prevailed, and in the second and third – dysfunction of inspiratory RM. In the midst of CAP, significant negative correlations of RM strength indicators with LII, HII, TNF-α, IL-10, IL-8, and IL-2 levels were recorded. The endogenous intoxication indices reached control values in all patients during recovery. The first cluster showed a decrease in the level of analyzed cytokines against isolated dysfunction of expiratory RM. The second cluster showed a tendency toward restoration of TNF-α and IL-8 levels, and only their SNIP index was normal. The third cluster showed minimal medians of RM strength against the continuing imbalance in the profile of pro- and anti-inflammatory cytokines during recovery. Conclusion. RM dysfunction in CAP is associated with cytokine-mediated dysfunction. The degree of cytokine involvement in this process depends on the severity of endogenous intoxication and the volume of alveolar inflammation.

scholarly journals Citocinas e proteínas de fase aguda do soro como marcadores de regressão da resposta inflamatória ao tratamento da tuberculose pulmonar

2008 ◽  
Vol 34 (11) ◽  
pp. 942-949 ◽  
Author(s):  
Eliana Peresi ◽  
Sônia Maria Usó Ruiz Silva ◽  
Sueli Aparecida Calvi ◽  
Jussara Marcondes-Machado
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Growth Factor Beta ◽  
Necrosis Factor

OBJETIVO: Analisar o padrão de citocinas pró- e antiinflamatórias e da resposta de fase aguda (RFA) como marcadores de resposta ao tratamento da tuberculose pulmonar. MÉTODOS: Determinação dos níveis de interferon-gama (IFN-γ), tumor necrosis factor-alpha (TNF-α, fator de necrose tumoral-alfa), interleucina-10 (IL-10) e transforming growth factor-beta (TGF-β, fator transformador de crescimento-beta), pelo método ELISA, em sobrenadante de cultura de células mononucleares do sangue periférico e monócitos, assim como dos níveis de proteínas totais, albumina, globulinas, alfa-1-glicoproteína ácida (AGA), proteína C reativa (PCR) e velocidade de hemossedimentação (VHS) em 28 doentes com tuberculose pulmonar, em três tempos: antes (T0), aos três meses (T3) e aos seis meses (T6) de tratamento, em relação aos controles saudáveis, em um único tempo. RESULTADOS: Os pacientes apresentaram valores maiores de citocinas e RFA que os controles em T0, com diminuição em T3 e diminuição (TNF-α, IL-10, TGF-β, AGA e VHS) ou normalização (IFN-γ e PCR) em T6. CONCLUSÕES: PCR, AGA e VHS são possíveis marcadores para auxiliar no diagnóstico de tuberculose pulmonar e na indicação de tratamento de indivíduos com baciloscopia negativa; PCR (T0 > T3 > T6 = referência) pode também ser marcador de resposta ao tratamento. Antes do tratamento, o perfil Th0 (IFN-γ, IL-10, TNF-α e TGF-β), indutor de e protetor contra inflamação, prevaleceu nos pacientes; em T6, prevaleceu o perfil Th2 (IL-10, TNF-α e TGF-β), protetor contra efeito nocivo pró-inflamatório do TNF-α ainda presente. O comportamento do IFN-γ (T0 > T3 > T6 = controle) sugere sua utilização como marcador de resposta ao tratamento.

scholarly journals A distinct pattern of cytokine gene expression by human CD83+ blood dendritic cells

Blood ◽  
1995 ◽  
Vol 86 (9) ◽  
pp. 3295-3301 ◽  
Author(s):  
LJ Zhou ◽  
TF Tedder
Keyword(s):  
Gene Expression ◽  
Dendritic Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Distinct Pattern ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Tgf Beta ◽  
Necrosis Factor Alpha ◽  
Gm Csf

Dendritic cells are the most potent antigen-presenting cells of the immune system. Although dendritic cells are likely to secrete selective cytokines that facilitate antigen presentation, the difficulty in isolating pure dendritic cells in sufficient numbers has made assessment of this function imprecise. In this study, pure populations of CD83+ human blood dendritic cells were isolated by previously established enrichment procedures and subsequent cell sorting. Cytokine gene expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR) amplification of mRNA. Resting CD83+ dendritic cells expressed interleukin-6 (IL-6), IL-8, IL-10, tumor necrosis factor- alpha (TNF-alpha), and transforming growth factor-beta 1 (TGF-beta 1) mRNA, while activation of cells with phorbol myristate acetate induced IL-1 alpha and beta, IL-9, TNF-beta, interferon-gamma, granulocyte- macrophage colony-stimulating factor (GM-CSF), M-CSF, and G-CSF mRNA expression. Resting CD83+ cells also expressed the Rantes, MCP-1, MIP-1 alpha, and MIP-1 beta chemokines, with 1–309 expression induced upon activation. Resting and activated CD83+ dendritic cells also expressed receptors for IL-2 (CD25), TGF-beta 1 and -beta 3, and GM-CSF as determined by indirect immunofluorescence staining. These results indicate that dendritic cells have the ability to produce a variety of soluble factors which are likely to contribute substantially to the potent allostimulatory activity of these cells.

Effects of SMAD7 Overexpression on Peritoneal Inflammation in a Rat Peritoneal Dialysis Model

2007 ◽  
Vol 27 (5) ◽  
pp. 580-588 ◽  
Author(s):  
Jing Nie ◽  
Wenke Hao ◽  
Xianrui Dou ◽  
Xin Wang ◽  
Ning Luo ◽  
...  
Keyword(s):  
Body Weight ◽  
Peritoneal Dialysis ◽  
Gene Transfer ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Necrosis Factor Alpha ◽  
Smad Signaling ◽  
Peritoneal Inflammation ◽  
Tnf Α

Objective Transforming growth factor-beta (TGF-β) has been shown to play a role in peritoneal complications due to long-term peritoneal dialysis (PD). In this study, we examined the effects of the TGF-β signaling pathway on peritoneal inflammation associated with PD in rats by over-expressing Smad7, an inhibitor of TGF-β/Smad signaling. Methods Peritoneal inflammation was induced in male Sprague-Dawley rats by intraperitoneal injections of 4.25% glucose dialysate (100 mg/kg body weight) daily for 4 weeks, with the addition of lipopolysaccharides (0.6 mg/kg body weight) on days 8, 10, 12, 22, 24, and 26. Peritoneal Smad7 gene transfer was achieved using an ultrasound microbubble mediated, doxycycline regulated, Smad7-expressing plasmid on day 0 and day 14 after initiation of PD. An empty vector was used as control. All rats were sacrificed after 4 weeks of PD. Peritoneal inflammatory response, including infiltration of total leukocytes (OX-1 positive) and macrophages (ED-1 positive) and expression of interleukin (IL)-1β) and tumor necrosis factor-alpha (TNF-α), was examined by immunofluorescence and RT-PCR. Results After PD, peritoneal inflammation developed in control animals, as demonstrated by an increase in the number of OX-1-positive and ED-1-positive cells and upregulation of IL-1β and TNF-α mRNA and protein expression. In contrast, in animals treated with Smad7 gene transfer, IL-1β and TNF-α expression and OX-1-positive and ED-1-positive cell infiltration were significantly inhibited. Furthermore, prevention of peritoneal inflammation by overexpression of Smad7 was associated with inhibition of phosphorylation of Smad2/3, a downstream of the TGF-β signaling pathway, as well as TGF-β1 expression. Conclusion Overexpression of Smad7 suppresses peritoneal inflammation induced by high glucose and lipopolysaccharides. The ability of Smad7 gene transfer to inhibit peritoneal inflammation indicates that targeting TGF-β/Smad signaling may represent a new therapeutic strategy for the treatment of peritoneal complications associated with PD.

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