The role of serpin protein on the natural immune defense against pathogen infection in Lampetra japonica

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

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Special Issue: The Role of Complement in Cancer Immunotherapy

Antibodies ◽

10.3390/antib10030029 ◽

2021 ◽

Vol 10 (3) ◽

pp. 29

Author(s):

Ronald P. Taylor

Keyword(s):

Cancer Immunotherapy ◽

Complement System ◽

Immune Defense ◽

Special Issue ◽

The Complement System ◽

Critical Aspects

The complement system plays an important role in critical aspects of immune defense and in the maintenance of homeostasis in the bloodstream, as well as in essentially all tissues and organs [...]

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A role of hexokinases in plant resistance to oxidative stress and pathogen infection

Journal of Plant Biology ◽

10.1007/bf03036136 ◽

2008 ◽

Vol 51 (5) ◽

pp. 341-346 ◽

Cited By ~ 28

Author(s):

Sujon Sarowar ◽

Jae -Yong Lee ◽

Eu -Ree Ahn ◽

Hyun -Sook Pai

Keyword(s):

Oxidative Stress ◽

Plant Resistance ◽

Pathogen Infection

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Emerging Role of Exosomes in Tuberculosis: From Immunity Regulations to Vaccine and Immunotherapy

Frontiers in Immunology ◽

10.3389/fimmu.2021.628973 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yin-Fu Sun ◽

Jiang Pi ◽

Jun-Fa Xu

Keyword(s):

Immune Responses ◽

Delivery System ◽

Immune Modulation ◽

Immune Cell ◽

Critical Role ◽

Cell Communication ◽

Immune Defense ◽

Research Progress ◽

Recent Research Progress

Exosomes are cell-derived nanovesicles carrying protein, lipid, and nucleic acid for secreting cells, and act as significant signal transport vectors for cell-cell communication and immune modulation. Immune-cell-derived exosomes have been found to contain molecules involved in immunological pathways, such as MHCII, cytokines, and pathogenic antigens. Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), remains one of the most fatal infectious diseases. The pathogen for tuberculosis escapes the immune defense and continues to replicate despite rigorous and complicate host cell mechanisms. The infected-cell-derived exosomes under this circumstance are found to trigger different immune responses, such as inflammation, antigen presentation, and activate subsequent pathways, highlighting the critical role of exosomes in anti-MTB immune response. Additionally, as a novel kind of delivery system, exosomes show potential in developing new vaccination and treatment of tuberculosis. We here summarize recent research progress regarding exosomes in the immune environment during MTB infection, and further discuss the potential of exosomes as delivery system for novel anti-MTB vaccines and therapies.

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Changes in Photosynthesis Could Provide Important Insight into the Interaction between Wheat and Fungal Pathogens

International Journal of Molecular Sciences ◽

10.3390/ijms22168865 ◽

2021 ◽

Vol 22 (16) ◽

pp. 8865

Author(s):

Huai Yang ◽

Peigao Luo

Keyword(s):

Fungal Pathogens ◽

Puccinia Striiformis ◽

Early Stage ◽

Acquired Resistance ◽

Immune Defense ◽

Pathogen Infection ◽

Resistance Level ◽

Growth Environment ◽

Expression Of Genes ◽

Host Materials

Photosynthesis is a universal process for plant survival, and immune defense is also a key process in adapting to the growth environment. Various studies have indicated that these two processes are interconnected in a complex network. Photosynthesis can influence signaling pathways and provide both materials and energy for immune defense, while the immune defense process can also have feedback effects on photosynthesis. Pathogen infection inevitably leads to changes in photosynthesis parameters, including Pn, Gs, and Ci; biochemical materials such as SOD and CAT; signaling molecules such as H2O2 and hormones; and the expression of genes involved in photosynthesis. Some researchers have found that changes in photosynthesis activity are related to the resistance level of the host, the duration after infection, and the infection position (photosynthetic source or sink). Interactions between wheat and the main fungal pathogens, such as Puccinia striiformis, Blumeria graminis, and Fusarium graminearum, constitute an ideal study system to elucidate the relationship between changes in host photosynthesis and resistance levels, based on the accessibility of methods for artificially controlling infection and detecting changes in photosynthesis, the presence of multiple pathogens infecting different positions, and the abundance of host materials with various resistance levels. This review is written only from the perspective of plant pathologists, and after providing an overview of the available data, we generally found that changes in photosynthesis in the early stage of pathogen infection could be a causal factor influencing acquired resistance, while those in the late stage could be the result of resistance formation.

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Role of copper in defending against bacterial infection

10.32469/10355/47147 ◽

2015 ◽

Author(s):

◽

Erik Ladomersky

Keyword(s):

Bacterial Infection ◽

Host Defense ◽

Immune Defense ◽

Copper Proteins ◽

University Of Missouri ◽

Susceptibility To Infection ◽

Essential Nutrient ◽

The University ◽

The Relationship

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Copper is an essential nutrient. It plays an important role in development, pigmentation, neurological function, and immune defense. Copper deficiency is known to make host's more susceptible to infection. In this work we show that two copper proteins, ATP7A and ceruloplasmin, are important for host defense against bacterial infection. Studies have shown ATP7A is responsible for increasing copper concentrations inside the phagosome. Our study sheds light on the role of Atp7a and copper in adaptive immunity, and provide a biochemical model for understanding the relationship between copper malnutrition and susceptibility to infection. Iron, another essential nutrient, is linked with copper through the actions of copper-dependent proteins which play a role in maintaining normal iron levels in the blood. One of these proteins is ceruloplasmin, a protein that is also upregulated during infection. Our study sheds light onto why this protein is necessary for host defense against Salmonella infection.

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Review on the Role of Host Immune Response in Protection and Immunopathogenesis during Cutaneous Leishmaniasis Infection

Journal of Immunology Research ◽

10.1155/2020/2496713 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12

Author(s):

Teshager Dubie ◽

Yasin Mohammed

Keyword(s):

Immune Response ◽

Cutaneous Leishmaniasis ◽

Proinflammatory Cytokines ◽

Parasitic Infection ◽

Host Immune Response ◽

Immune Defense ◽

Host Cells ◽

Infected Host ◽

Major Public Health Problem

Cutaneous leishmaniasis (CL) is a major public health problem worldwide and spreads to human via the bite of sand flies during blood meal. Following its inoculation, the promastigotes are immediately taken up by phagocytic cells and these leishmania-infected host cells produce proinflammatory cytokines that activate other immune cells and these infected host cells produce more cytokines and reactive nitrogen and oxygen species for efficient control of leishmania infection. Many experimental studies showed that resistance to infection with leishmania paraites is associated with the production of proinflammatory cytokines and activation of CD4+ Th1 response. On the other hand, vulnerability to this parasitic infection is correlated to production of T helper 2 cytokines that facilitate persistence of parasites and disease progression. In addition, some studies have also indicated that CD8+ T cells play a vital role in immune defense through cytokine production and their cytotoxic activity and excessive production of proinflammatory mediators promote amplified recruitment of cells. This could be correlated with excessive inflammatory reaction and ultimately resulted in tissue destruction and development of immunopathogenesis. Thus, there are contradictions regarding the role of immune responses in protection and immunopathogenesis of CL disease. Therefore, the aim of this paper was to review the role of host immune response in protection and its contribution to disease severity for CL infection. In order to obtain more meaningful data regarding the nature of immune response to leishmania, further in-depth studies focused on immune modulation should be conducted to develop better therapeutic strategies.

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Antiapoptotic activity of Chlamydia trachomatis Pgp3 protein involves activation of the ERK1/2 pathway mediated by upregulation of DJ-1 protein

Pathogens and Disease ◽

10.1093/femspd/ftaa003 ◽

2019 ◽

Vol 77 (9) ◽

Cited By ~ 1

Author(s):

Fangzhen Luo ◽

Mingyi Shu ◽

Silu Gong ◽

Yating Wen ◽

Bei He ◽

...

Keyword(s):

Chlamydia Trachomatis ◽

Hela Cells ◽

Signal Pathway ◽

Immune Defense ◽

Apoptosis Resistance ◽

Host Cell Apoptosis ◽

Pathway Activation ◽

Tnf Α ◽

Antiapoptotic Activity

ABSTRACT Chlamydia trachomatis has evolved strategies to prevent host cell apoptosis to evade the host immune defense. However, the precise mechanisms of antiapoptotic activity of C. trachomatis still need to be clarified. Pgp3, one of eight plasmid proteins of C. trachomatis, has been identified to be closely associated with chlamydial virulence. In this study, we attempted to explore the effects and the mechanisms of Pgp3 protein on apoptosis in HeLa cells; the results showed that Pgp3 increased Bcl-2/Bax ratio and prevented caspase-3 activation to suppress apoptosis induced by TNF-α and cycloheximide (CHX) through ERK1/2 pathway activation. Downregulation of DJ-1 with siRNA-DJ-1(si-DJ-1) reduced ERK1/2 phosphorylation and elevated apoptotic rate significantly in Pgp3-HeLa cells. However, inhibition of ERK1/2 signal pathway with ERK inhibitor PD98059 had little effect on DJ-1 expression. These findings confirm that plasmid protein Pgp3 contributes to apoptosis resistance through ERK1/2 signal pathway mediated by upregulation of DJ-1 expression. Therefore, the present study provided novel insights into the role of Pgp3 in apoptosis and suggested that manipulation of the host apoptosis response could be a new approach for the prevention and treatment of C. trachomatis infection.

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Notch-1 Signaling Modulates Macrophage Polarization and Immune Defense against Mycobacterium avium paratuberculosis Infection in Inflammatory Diseases

Microorganisms ◽

10.3390/microorganisms8071006 ◽

2020 ◽

Vol 8 (7) ◽

pp. 1006 ◽

Cited By ~ 1

Author(s):

Esra’a Keewan ◽

Saleh A. Naser

Keyword(s):

Inflammatory Response ◽

Notch Signaling ◽

Mycobacterium Avium ◽

Macrophage Polarization ◽

Immune Defense ◽

Notch 1 ◽

Macrophage Response ◽

Mycobacterium Avium Paratuberculosis ◽

Vitro Effect

Despite the extensive research on Notch signaling involvement in inflammation, its specific role in macrophage response in autoimmune disease and defense mechanisms against bacterial infection, such as Mycobacterium avium paratuberculosis (MAP), remains unknown. In this study, we investigated the molecular role of Notch-1 signaling in the macrophage response during MAP infection. In particular, we measured the in vitro effect of MAP on Notch-1 signaling and downstream influence on interleukin (IL)-6 and myeloid cell leukemia sequence-1 (MCL-1) and consequent cellular apoptosis, MAP viability, and macrophage polarization. Overall, the data show significant upregulation in Notch-1, IL-6, and MCL-1 in MAP-infected macrophages, parallel with a decrease in apoptosis and elevated pro-inflammatory response in these infected cells. On the contrary, blocking Notch signaling with γ-secretase inhibitor (DAPT) decreased MAP survival and burden, increased apoptosis, and diminished the pro-inflammatory response. In particular, the treatment of infected macrophages with DAPT shifted macrophage polarization toward M2 anti-inflammatory phenotypic response. The outcome of this study clearly demonstrates the critical role of Notch signaling in macrophage response during infection. We conclude that MAP infection in macrophages activates Notch-1 signaling and downstream influence on IL-6 which hijack MCL-1 dependent inhibition of apoptosis leading to its chronic persistence, and further inflammation. This study supports Notch-1 signaling as a therapeutic target to combat infection in autoimmune diseases such as Crohn’s disease and Rheumatoid Arthritis.

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Dengue Virus and the Relationship with MicroRNAs

Dengue Fever in a One Health Perspective ◽

10.5772/intechopen.92453 ◽

2020 ◽

Author(s):

Samir Casseb ◽

Karla de Melo

Keyword(s):

Dengue Virus ◽

Viral Infection ◽

Viral Infections ◽

Immune Defense ◽

Tropical Regions ◽

Denv Serotypes ◽

History Of ◽

Infection Processes ◽

The Relationship

Dengue is an acute febrile disease caused by a virus of the genus Flavivirus, family Flaviviridae, endemic in tropical regions of the globe. The agent is a virus with single-stranded RNA, classified into four distinct dengue virus (DENV) serotypes: DENV-1, DENV-2, DENV-3, and DENV-4. The host’s innate and adaptive immune responses play an essential role in determining the natural history of viral infections, especially in dengue. In this context, it has observed in recent years that the presence of RNA interference (RNAi) in viral infection processes is increasing, as well as immune defense. The context microRNAs (miRNAs) go for stood out, as their presence during viral infection, both in the replication of the virus and in the defense against these infections, becomes increasingly noticeable, therefore, making it increasingly necessary to better understand the role of these small RNAs within viral infection by DENV and what their consequences are in aggravating the consequences of patients affected by this disease.

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