scholarly journals T-Bet Is Dependent on Stat-4 Inhibiting Acute Colitis but Not Stat-1 Using L4 Somatic Antigen of Heligmosomoides polygyrus

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Agustina Tri Endharti ◽  
Sofy Permana
Keyword(s):  
T Lymphocytes ◽  
Inflammatory Response ◽  
Rectal Administration ◽  
Somatic Antigen ◽  
Acute Colitis ◽  
Wasting Disease ◽  
Protective Mechanisms ◽  
Heligmosomoides Polygyrus ◽  
Optimal Production ◽  
Different Doses

Helminths may alter the immunoinflammatory reactions of colitis. Proteins derived from H. polygyrus have prospective therapy for colitis. The goal of this study was to interpret the protective mechanisms of L4 somatic antigen (LSA) from Heligmosomoides polygyrus against an inflammatory response to the pathogenesis of DNBS-induced colitis. Colitis was actuated in mice by rectal instillation of DNBS. The mice were randomly divided into five groups containing control, DNBS alone, and three groups, with different doses of LSA (50, 100, and 200 μg/mL), respectively. Mice initiated colitis by rectal administration of DNBS and after that were immunized with LSA for 14 days. Mice treated with LSA inhibited wasting disease compared with DNBS only group. The percentages of cells producing IFN-γ were reduced by LSA treatment. The level of T lymphocytes CD4+IFN-γ+ cells in the LPL was significantly diminished by LSA at both 100 and 200 μg/mL groups (p<0.05). The mRNA expression of T-bet was significantly declined in LSA immunized mice, but not RORγ-T mRNA, whereas GATA-3 expression tended to increase. The activation of STAT-4 significantly reduced LSA-treated mice but not STAT-1. It can be concluded that T-bet is required for optimal production of IFN-γ in colitis.

scholarly journals Cangrelor ameliorates CLP-induced pulmonary injury in sepsis by inhibiting GPR17

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Qiancheng Luo ◽  
Rui Liu ◽  
Kaili Qu ◽  
Guorong Liu ◽  
Min Hang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lavage Fluid ◽  
Surface Expression ◽  
Pulmonary Injury ◽  
Protective Mechanisms ◽  
Tnf Α ◽  
Anti Platelet Drug ◽  
G Protein Coupled ◽  
Very High ◽  
Masson Staining

Abstract Background Sepsis is a common complication of severe wound injury and infection, with a very high mortality rate. The P2Y12 receptor inhibitor, cangrelor, is an antagonist anti-platelet drug. Methods In our study, we investigated the protective mechanisms of cangrelor in CLP-induced pulmonary injury in sepsis, using C57BL/6 mouse models. Results TdT-mediated dUTP Nick-End Labeling (TUNEL) and Masson staining showed that apoptosis and fibrosis in lungs were alleviated by cangrelor treatment. Cangrelor significantly promoted surface expression of CD40L on platelets and inhibited CLP-induced neutrophils in Bronchoalveolar lavage fluid (BALF) (p < 0.001). We also found that cangrelor decreased the inflammatory response in the CLP mouse model and inhibited the expression of inflammatory cytokines, IL-1β (p  < 0.01), IL-6 (p < 0.05), and TNF-α (p < 0.001). Western blotting and RT-PCR showed that cangrelor inhibited the increased levels of G-protein-coupled receptor 17 (GPR17) induced by CLP (p < 0.001). Conclusion Our study indicated that cangrelor repressed the levels of GPR17, followed by a decrease in the inflammatory response and a rise of neutrophils in BALF, potentially reversing CLP-mediated pulmonary injury during sepsis.

Heligmosomoides polygyrus immunomodulatory factor (IMF), targets T-lymphocytes

1998 ◽  
Vol 20 (12) ◽  
pp. 601-611 ◽  
Author(s):  
TELFORD ◽  
WHEELER ◽  
PPLEBY ◽  
BOWEN ◽  
PRITCHARD
Keyword(s):  
T Lymphocytes ◽  
Heligmosomoides Polygyrus

scholarly journals Effects ofRhizophora mangleon Experimental Colitis Induced by TNBS in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Felipe Meira de Faria ◽  
Anderson Luiz-Ferreira ◽  
Eduardo Augusto Rabelo Socca ◽  
Ana Cristina Alves de Almeida ◽  
Ricardo José Dunder ◽  
...  
Keyword(s):  
Chemical Composition ◽  
Inflammatory Response ◽  
Ethyl Acetate ◽  
Immune Modulation ◽  
Experimental Colitis ◽  
Rectal Administration ◽  
Etoac Fraction ◽  
Phytochemical Studies ◽  
Cox 1

Male Unib-WH rats were pretreated for two weeks with butanolic (BuOH) and ethyl acetate (EtOAc) fractions. Colitis was induced by rectal administration of TNBS, the treatment continued, and animals were sacrificed on day 7 after the TNBS administration. Phytochemical studies were performed in order to provide the characterization of the tannins present in the bark ofR. mangle. Results showed that EtOAc fraction increased the levels of IL-10 (**P<0.01) and diminished the levels of TNF-α(***P<0.001) and IL-6 (**P<0.01). BuOH fraction reduced the MPO activity (**P<0.01) and levels of TBARS (***P<0.001); it also increased COX-1 expression, diminished the levels of TNF-α(***P<0.001), and increased the levels of IL-12 (***P<0.001). Besides, both treatments augmented the levels of GSH (*P<0.05), the activity of GSH-Px (**P<0.01for BuOH fraction and ***P<0.001for EtOAc fraction), and CAT (**P<0.01). In conclusion, both treatments ameliorated the injury induced by TNBS through different mechanisms, probably by their chemical composition which directed its activity into an antioxidant or anti-inflammatory response, leading to an immune modulation.

scholarly journals S1742 Rectal Administration of Tranilast Ameliorated Acute Colitis in Mice Through Increased Expression of Heme Oxygenase-1

2010 ◽  
Vol 138 (5) ◽  
pp. S-265
Author(s):  
Xiaomei Sun ◽  
Kenji Suzuki ◽  
Masaki Nagata ◽  
Hana Yamaguchi ◽  
Yusuke Kawauchi ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Rectal Administration ◽  
Heme Oxygenase 1 ◽  
Acute Colitis

scholarly journals Cangrelor ameliorates CLP-induced pulmonary injury in sepsis by inhibiting GPR17

2020 ◽  
Author(s):  
Qiancheng Luo ◽  
Rui Liu ◽  
Guorong Liu ◽  
Min Hang ◽  
Guo Chen ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Surface Expression ◽  
Pulmonary Injury ◽  
Protective Mechanisms ◽  
Tnf Α ◽  
G Protein Coupled ◽  
Very High ◽  
Masson Staining

Abstract BackgroundSepsis is a common complication of severe wound injury and infection, with a very high mortality rate. The P2Y12 receptor inhibitor, cangrelor, is an antagonist antiplatelet drug.MethodsIn our study, we investigated the protective mechanisms of cangrelor in CLP-induced pulmonary injury in sepsis, using mouse models.ResultsTdT-mediated dUTP Nick-End Labeling (TUNEL) and Masson staining showed that apoptosis and fibrosis in lungs were alleviated by cangrelor treatment. Cangrelor significantly promoted surface expression of CD40L on platelets and inhibited CLP-induced neutrophils in Bronchoalveolar lavage fluid (BALF). We also found that cangrelor decreased the inflammatory response in the CLP mouse model and inhibited the expression of inflammatory cytokines, IL-1β, IL-6, and TNF-α. Western blotting and RT-PCR showed that cangrelor inhibited the increased levels of G-protein-coupled receptor 17 ༈GPR17༉induced by CLP. Conclusion: Our study indicated that cangrelor repressed the levels of GPR17, followed by a decrease in the inflammatory response and a rise of neutrophils in BALF, potentially reversing CLP-mediated pulmonary injury during sepsis.

scholarly journals Cangrelor ameliorates CLP-induced pulmonary injury in sepsis by inhibiting GPR17

2020 ◽  
Author(s):  
Qiancheng Luo ◽  
Rui Liu ◽  
Guorong Liu ◽  
Min Hang ◽  
Guo Chen ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lavage Fluid ◽  
Surface Expression ◽  
Antiplatelet Drug ◽  
Pulmonary Injury ◽  
Protective Mechanisms ◽  
Tnf Α ◽  
G Protein Coupled ◽  
Very High ◽  
Masson Staining

Abstract Background: Sepsis is a common complication of severe wound injury and infection, with a very high mortality rate. The P2Y12 receptor inhibitor, cangrelor, is an antagonist antiplatelet drug.Methods: In our study, we investigated the protective mechanisms of cangrelor in CLP-induced pulmonary injury in sepsis, using C57BL/6 mouse models.Results: TdT-mediated dUTP Nick-End Labeling (TUNEL) and Masson staining showed that apoptosis and fibrosis in lungs were alleviated by cangrelor treatment. Cangrelor significantly promoted surface expression of CD40L on platelets and inhibited CLP-induced neutrophils in Bronchoalveolar lavage fluid (BALF) (p＜0.001). We also found that cangrelor decreased the inflammatory response in the CLP mouse model and inhibited the expression of inflammatory cytokines, IL-1β (p＜0.01), IL-6 (p＜0.05), and TNF-α (p＜0.001). Western blotting and RT-PCR showed that cangrelor inhibited the increased levels of G-protein-coupled receptor 17 (GPR17) induced by CLP(p＜0.001). Conclusion: Our study indicated that cangrelor repressed the levels of GPR17, followed by a decrease in the inflammatory response and a rise of neutrophils in BALF, potentially reversing CLP-mediated pulmonary injury during sepsis.

Do Different Doses of Talc Influence the Acute Systemic Inflammatory Response in Experimental Pleurodesis

CHEST Journal ◽  
2003 ◽  
Vol 124 (4) ◽  
pp. 80S
Author(s):  
Evaldo Marchi ◽  
F.S. Vargas ◽  
M.M. Acencio ◽  
L Antonangelo ◽  
L.R. Teixeira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Systemic Inflammatory Response ◽  
Different Doses

Chickpea supplementation prior to colitis onset reduces inflammation in dextran sodium sulfate-treated C57Bl/6 male mice

2018 ◽  
Vol 43 (9) ◽  
pp. 893-901 ◽  
Author(s):  
Jennifer M. Monk ◽  
Wenqing Wu ◽  
Laurel H. McGillis ◽  
Hannah R. Wellings ◽  
Amber L. Hutchinson ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Sodium Sulfate ◽  
Clinical Symptoms ◽  
Basal Diet ◽  
Serum Levels ◽  
Dextran Sodium Sulfate ◽  
Male Mice ◽  
Acute Colitis ◽  
Colon Tissue ◽  
Necrosis Factor Alpha

The potential for a chickpea-supplemented diet (rich in fermentable nondigestible carbohydrates and phenolic compounds) to modify the colonic microenvironment and attenuate the severity of acute colonic inflammation was investigated. C57Bl/6 male mice were fed a control basal diet or basal diet supplemented with 20% cooked chickpea flour for 3 weeks prior to acute colitis onset induced by 7-day exposure to dextran sodium sulfate (DSS; 2% w/v in drinking water) and colon and serum levels of inflammatory mediators were assessed. Despite an equal degree of DSS-induced epithelial barrier histological damage and clinical symptoms between dietary groups, biomarkers of the ensuing inflammatory response were attenuated by chickpea pre-feeding, including reduced colon tissue activation of nuclear factor kappa B and inflammatory cytokine production (tumor necrosis factor alpha and interleukin (IL)-18). Additionally, colon protein expression of anti-inflammatory (IL-10) and epithelial repair (IL-22 and IL-27) cytokines were increased by chickpea pre-feeding. Furthermore, during acute colitis, chickpea pre-feeding increased markers of enhanced colonic function, including Relmβ and IgA gene expression. Collectively, chickpea pre-feeding modulated the baseline function of the colonic microenvironment, whereby upon induction of acute colitis, the severity of the inflammatory response was attenuated.

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