scholarly journals Intestinal transcriptomes in Kazakh sheep with different haplotypes after experimental Echinococcus granulosus infection

Parasite ◽  
2021 ◽  
Vol 28 ◽  
pp. 14
Author(s):  
Xin Li ◽  
Song Jiang ◽  
Xuhai Wang ◽  
Bin Jia
Keyword(s):  
Immune Response ◽  
Echinococcus Granulosus ◽  
Adaptive Response ◽  
Tumor Necrosis ◽  
Function Analysis ◽  
Innate Immune ◽  
Intestinal Tissue ◽  
Lectin Receptors ◽  
Differential Expression Genes ◽  
Necrosis Factor

Cystic echinococcosis (CE) is a chronic zoonosis caused by infection with the larval stage of the cestode Echinococcus granulosus. As the intermediate host, sheep are highly susceptible to this disease. Our previous studies have shown that sheep with haplotype MHC Mva Ibc-Sac IIab-Hin1I ab were resistant to CE infection, while their counterparts without this haplotype were not. In order to reveal the molecular mechanism of resistance in Kazakh sheep, after selecting the differential miRNA in our previous study, herein, transcriptome analyses were conducted to detect the differential expression genes in the intestinal tissue of Kazakh sheep with resistant and non-resistant MHC haplotypes, after peroral infection with E. granulosus eggs. A total of 3835 differentially expressed genes were identified between the two groups, with 2229 upregulated and 1606 downregulated. Further function analysis showed that the most significant genes were related to both innate immune response and adaptive response participating in the defense against E. granulosus infection and the metabolic changes associated with it. The results suggest that genes related to lectin receptors, NK cells activation, chemokines, and tumor necrosis factor, may play important roles in the response of intestinal tissue to E. granulosus.

scholarly journals Innate Immune Response to Anaplasma phagocytophilum Contributes to Hepatic Injury

2006 ◽  
Vol 13 (7) ◽  
pp. 806-809 ◽  
Author(s):  
Diana G. Scorpio ◽  
Friederike D. von Loewenich ◽  
Heike Göbel ◽  
Christian Bogdan ◽  
J. Stephen Dumler
Keyword(s):  
Immune Response ◽  
Anaplasma Phagocytophilum ◽  
Tumor Necrosis ◽  
Hepatic Injury ◽  
No Synthase ◽  
Innate Immune ◽  
Host Responses ◽  
Toll Like Receptor ◽  
Phagocyte Oxidase ◽  
Necrosis Factor

ABSTRACT In mice, Anaplasma phagocytophilum control is independent of phagocyte oxidase (phox), inducible NO synthase (NOS2), tumor necrosis factor (TNF), and MyD88 Toll-like receptor signaling. We show that despite evasion of these host responses, phox, NOS2, TNF, and MyD88 are activated and contribute to inflammation and hepatic injury more than A. phagocytophilum itself.

scholarly journals Lack of Proinflammatory Cytokine Interleukin-6 or Tumor Necrosis Factor Receptor-1 Results in a Failure of the Innate Immune Response after Bacterial Meningitis

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Lea-Jessica Albrecht ◽  
Simone C. Tauber ◽  
Julika Merres ◽  
Eugenia Kress ◽  
Matthias B. Stope ◽  
...  
Keyword(s):  
Immune Response ◽  
Streptococcus Pneumoniae ◽  
Tumor Necrosis Factor ◽  
Bacterial Meningitis ◽  
Innate Immune Response ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Innate Immune ◽  
Wild Type ◽  
Necrosis Factor

The most frequent pathogen that causes bacterial meningitis is the Gram-positive bacteriumStreptococcus pneumoniae. By entering the brain, host cells will be activated and proinflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) are released. The goal of the current study was to examine the interaction between IL-6 and TNFR1 as receptor for TNF-αand the innate immune response in vivo in a model ofStreptococcus pneumoniae-induced meningitis. For the experiments IL-6−/−, TNFR1−/−, and TNFR1-IL-6−/−KO mice were used. Our results revealed higher mortality rates and bacterial burden after infection in TNFR1−/−, IL-6−/−, and TNFR1-IL-6−/−mice and a decreased immune response including lower neutrophil infiltration in the meninges of TNFR1−/−and TNFR1-IL-6−/−mice in contrast to IL-6−/−and wild type mice. Furthermore, the increased mortality of TNFR1−/−and TNFR1-IL-6−/−mice correlated with decreased glial cell activation compared to IL-6−/−or wild type mice after pneumococcal meningitis. Altogether, the results show the importance of TNFR1 and IL-6 in the regulation of the innate immune response. The lack of TNFR1 and IL-6 results in higher mortality by weakened immune defence, whereas the lack of TNFR1 results in more severe impairment of the innate immune response than the lack of IL-6 alone.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) improves the innate immune response and enhances survival in murine polymicrobial sepsis

2010 ◽  
Vol 38 (11) ◽  
pp. 2169-2174 ◽  
Author(s):  
Katharina Cziupka ◽  
Alexandra Busemann ◽  
Lars Ivo Partecke ◽  
Christian Pötschke ◽  
Matthias Rath ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Innate Immune Response ◽  
Tumor Necrosis ◽  
Innate Immune ◽  
Polymicrobial Sepsis ◽  
Necrosis Factor

scholarly journals Still’s Disease in the Constellation of Hyperinflammatory Syndromes: A Link with Kawasaki Disease?

2021 ◽  
Vol 10 (15) ◽  
pp. 3244
Author(s):  
Perrine Dusser ◽  
Isabelle Koné-Paut
Keyword(s):  
Immune Response ◽  
Kawasaki Disease ◽  
Innate Immune Response ◽  
Adaptive Response ◽  
Genetic Factors ◽  
Innate Immune ◽  
Cytokine Storm ◽  
Still’S Disease ◽  
Still's Disease ◽  
Excessive Activation

Still’s disease and Kawasaki disease (KD) today belong to the group of cytokine storm syndromes, a pathophysiological set related to excessive activation of the innate immune response. We present here a personal vision of what can link these two diseases, taking up their concepts at their beginning. By their many clinical and physiopathological similarities, we conclude that they constitute a common spectrum whose fate is modified by subtle differences in terms of adaptive response that could, in part, be driven by genetic factors.

scholarly journals Human Immunodeficiency Virus Infection Alters Tumor Necrosis Factor Alpha Production via Toll-Like Receptor-Dependent Pathways in Alveolar Macrophages and U1 Cells

2008 ◽  
Vol 82 (16) ◽  
pp. 7790-7798 ◽  
Author(s):  
Marlynne Q. Nicol ◽  
Jean-Marie Mathys ◽  
Albertina Pereira ◽  
Kevin Ollington ◽  
Michael H. Ieong ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Innate Immune ◽  
Hiv Positive ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Human immunodeficiency virus (HIV)-positive persons are predisposed to pulmonary infections, even after receiving effective highly active antiretroviral therapy. The reasons for this are unclear but may involve changes in innate immune function. HIV type 1 infection of macrophages impairs effector functions, including cytokine production. We observed decreased constitutive tumor necrosis factor alpha (TNF-α) concentrations and increased soluble tumor necrosis factor receptor type II (sTNFRII) in bronchoalveolar lavage fluid samples from HIV-positive subjects compared to healthy controls. Moreover, net proinflammatory TNF-α activity, as measured by the TNF-α/sTNFRII ratio, decreased as HIV-related disease progressed, as manifested by decreasing CD4 cell count and increasing HIV RNA (viral load). Since TNF-α is an important component of the innate immune system and is produced upon activation of Toll-like receptor (TLR) pathways, we hypothesized that the mechanism associated with deficient TNF-α production in the lung involved altered TLR expression or a deficit in the TLR signaling cascade. We found decreased Toll-like receptor 1 (TLR1) and TLR4 surface expression in HIV-infected U1 monocytic cells compared to the uninfected parental U937 cell line and decreased TLR message in alveolar macrophages (AMs) from HIV-positive subjects. In addition, stimulation with TLR1/2 ligand (Pam3Cys) or TLR4 ligand (lipopolysaccharide) resulted in decreased intracellular phosphorylated extracellular signal-regulated kinase and subsequent decreased transcription and expression of TNF-α in U1 cells compared to U937 cells. AMs from HIV-positive subjects also showed decreased TNF-α production in response to these TLR2 and TLR4 ligands. We postulate that HIV infection alters expression of TLRs with subsequent changes in mitogen-activated protein kinase signaling and cytokine production that ultimately leads to deficiencies of innate immune responses that predispose HIV-positive subjects to infection.

The Effect of the Tumor Necrosis Factor DNA on the Immune Response in DNA Immunization against the Herpes Simplex Virus

2004 ◽  
Vol 38 (2) ◽  
pp. 281-288 ◽  
Author(s):  
R. R. Klimova ◽  
A. Yu. Kozlov ◽  
L. N. Shingarova ◽  
O. V. Nekrasova ◽  
E. F. Boldyreva ◽  
...  
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Dna Immunization ◽  
Simplex Virus ◽  
Necrosis Factor

scholarly journals Differential Gamma Interferon- and Tumor Necrosis Factor Alpha-Driven Cytokine Response Distinguishes Acute Infection of a Metatherian Host with Toxoplasma gondii and Neospora caninum

2017 ◽  
Vol 85 (6) ◽  
Author(s):  
Shannon L. Donahoe ◽  
David N. Phalen ◽  
Bronwyn M. McAllan ◽  
Denis O'Meally ◽  
Milton M. McAllister ◽  
...  
Keyword(s):  
Immune Response ◽  
Toxoplasma Gondii ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Neospora Caninum ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Toxoplasma gondii and Neospora caninum (both Apicomplexa) are closely related cyst-forming coccidian parasites that differ significantly in their host ranges and ability to cause disease. Unlike eutherian mammals, Australian marsupials (metatherian mammals) have long been thought to be highly susceptible to toxoplasmosis and neosporosis because of their historical isolation from the parasites. In this study, the carnivorous fat-tailed dunnart (Sminthopsis crassicaudata) was used as a disease model to investigate the immune response and susceptibility to infection of an Australian marsupial to T. gondii and N. caninum. The disease outcome was more severe in N. caninum-infected dunnarts than in T. gondii-infected dunnarts, as shown by the severity of clinical and histopathological features of disease and higher tissue parasite burdens in the tissues evaluated. Transcriptome sequencing (RNA-seq) of spleens from infected dunnarts and mitogen-stimulated dunnart splenocytes was used to define the cytokine repertoires. Changes in mRNA expression during the time course of infection were measured using quantitative reverse transcription-PCR (qRT-PCR) for key Th1 (gamma interferon [IFN-γ] and tumor necrosis factor alpha [TNF-α]), Th2 (interleukin 4 [IL-4] and IL-6), and Th17 (IL-17A) cytokines. The results show qualitative differences in cytokine responses by the fat-tailed dunnart to infection with N. caninum and T. gondii. Dunnarts infected with T. gondii were capable of mounting a more effective Th1 immune response than those infected with N. caninum, indicating the role of the immune response in the outcome scenarios of parasite infection in this marsupial mammal.

scholarly journals REDUCTION OF TUMOR NECROSIS FACTOR-ALPHA AND INTERFERON-GAMMA CONCENTRATION ON TUBERCULOSIS WITH DIABETES MELLITUS AS A MARKER IN DECREASE IMMUNE SYSTEM

2019 ◽  
pp. 151-154
Author(s):  
NELLY MARISSA ◽  
NUR RAMADHAN ◽  
SARI HANUM ◽  
MARLINDA ◽  
EKA FITRIA ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Immune Response ◽  
Tumor Necrosis Factor ◽  
Interferon Gamma ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

Objective: This study aimed to determine the decreased immune response of tuberculosis (TB) with diabetes mellitus (DM) patients. Methods: A total of 105 TB patients who were undergoing treatment at health centers and hospitals in Banda Aceh and Aceh Besar were included in this study. Data collection was carried out by interviewed to obtained demographic and respondent categories based on the diagnosis. Measurements of height and weight were also conducted to obtain body mass index data. 5 mL peripheral blood was taken from each respondent group into a TB with DM (TB+DM) and TB without DM (TB-DM). The blood tested usage tumor necrosis factor-alpha (TNF-α) level using enzyme-linked immunosorbent assay and interferon-gamma (IFN-γ) using IFN-γ release assay. Results: The average concentration of both TNF-α and IFN-γ was higher in TB-DM group (TNF-a 5.2 pg/mL; IFN-g 1.5 IU/mL) than in TB+DM group (TNF-a 2.06 pg/mL; IFN-g 2.86 IU/mL). There were significant differences in TNF-α between the two groups but no significant differences in IFN-γ protein concentration. Conclusion: The immune response of TB patients with DM symptoms was markedly reduced by the decreased expression of TNF-α and IFN-γ.

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