Ovarian cancer and inflammation. Part 1. Pro-inflammatory cytokines.

2018 ◽  
Vol 8 (1) ◽  
pp. 194-201
Author(s):  
KM. Terlikowska ◽  
MA. Strzyż-Skalij ◽  
K. Kryński ◽  
M. Osmólska ◽  
Z. Łada ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Cause Of Death ◽  
Inflammatory Cytokines ◽  
Gynecologic Malignancies ◽  
Cancer Tumor ◽  
Cancer And Inflammation ◽  
Pro Inflammatory Cytokines

Ovarian cancer is the most threatening cause of death among gynecologic malignancies and represents the fifth leading cause of death from all cancers for women. Research reveals that ovarian cancer patients exhibit significant immune responses against the tumor. In this review of the current literature chiefly the interaction of ovarian cancer tumor cells and the immune system is discussed. There is increasingly growing evidence that pro-inflammatory cytokines are involved in intricate complex of mechanisms responsible for tumorigenesis, and delicate balance between pro- and anti-inflammatory cytokines is critical for the antitumor host immune response.

Immune and Inflammatory Responses to Stroke: Good Or Bad?

2008 ◽  
Vol 3 (4) ◽  
pp. 254-265 ◽  
Author(s):  
P. A. McCombe ◽  
S. J. Read
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Therapeutic Option ◽  
Regulatory Lymphocytes ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Inflammatory and immune responses play important roles following ischaemic stroke. Inflammatory responses contribute to damage and also contribute to repair. Injury to tissue triggers an immune response. This is initiated through activation of the innate immune system. In stroke there is microglial activation. This is followed by an influx of lymphocytes and macrophages into the brain, triggered by production of pro-inflammatory cytokines. This inflammatory response contributes to further tissue injury. There is also a systemic immune response to stroke, and there is a degree of immunosuppression that may contribute to the stroke patient's risk of infection. This immunosuppressive response may also be protective, with regulatory lymphocytes producing cytokines and growth factors that are neuroprotective. The specific targets of the immune response after stroke are not known, and the details of the immune and inflammatory responses are only partly understood. The role of inflammation and immune responses after stroke is twofold. The immune system may contribute to damage after stroke, but may also contribute to repair processes. The possibility that some of the immune response after stroke may be neuroprotective is exciting and suggests that deliberate enhancement of these responses may be a therapeutic option.

scholarly journals Klebsiella pneumoniae Lipopolysaccharides Serotype O2afg Induce Poor Inflammatory Immune Responses Ex Vivo

2021 ◽  
Vol 9 (6) ◽  
pp. 1317
Author(s):  
Matteo Bulati ◽  
Rosalia Busà ◽  
Claudia Carcione ◽  
Gioacchin Iannolo ◽  
Giuseppina Di Mento ◽  
...  
Keyword(s):  
Immune Response ◽  
Klebsiella Pneumoniae ◽  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Immune Evasion ◽  
Ex Vivo ◽  
Multidrug Resistant ◽  
Human Monocytes ◽  
Cytokines And Chemokines ◽  
Pro Inflammatory Cytokines

Currently, Klebsiella pneumoniae is a pathogen of clinical relevance due to its plastic ability of acquiring resistance genes to multiple antibiotics. During K. pneumoniae infections, lipopolysaccharides (LPS) play an ambiguous role as they both activate immune responses but can also play a role in immune evasion. The LPS O2a and LPS O2afg serotypes are prevalent in most multidrug resistant K. pneumoniae strains. Thus, we sought to understand if those two particular LPS serotypes were involved in a mechanism of immune evasion. We have extracted LPS (serotypes O1, O2a and O2afg) from K. pneumoniae strains and, using human monocytes ex vivo, we assessed the ability of those LPS antigens to induce the production of pro-inflammatory cytokines and chemokines. We observed that, when human monocytes are incubated with LPS serotypes O1, O2a or O2afg strains, O2afg and, to a lesser extent, O2a but not O1 failed to elicit the production of pro-inflammatory cytokines and chemokines, which suggests a role in immune evasion. Our preliminary data also shows that nuclear translocation of NF-κB, a process which regulates an immune response against infections, occurs in monocytes incubated with LPS O1 and, to a smaller extent, with LPS O2a, but not with the LPS serotype O2afg. Our results indicate that multidrug resistant K. pneumoniae expressing LPS O2afg serotypes avoid an initial inflammatory immune response and, consequently, are able to systematically spread inside the host unharmed, which results in the several pathologies associated with this bacterium.

Ovarian cancer and inflammation. Part 2. Anti-inflammatory cytokines

2018 ◽  
Vol 8 (2) ◽  
pp. 206-209
Author(s):  
K.M. Terlikowska ◽  
B Dobrzycka ◽  
SJ Terlikowski
Keyword(s):  
Ovarian Cancer ◽  
Immune System ◽  
Epithelial Ovarian Cancer ◽  
Inflammatory Cytokines ◽  
Essential Factor ◽  
Tumorigenesis And Progression ◽  
Anti Inflammatory ◽  
Cancer And Inflammation ◽  
Local Cytokine

Inflammation plays a key role in epithelial ovarian cancer tumorigenesis and progression. The growth and progression of epithelial ovarian cancer may be due to local cytokine-induced immunosu-ppression, which may lead to an immunity impairment. Thus, cytokine antagonism may be an essential factor in the treatment of ovarian cancer. Based on the increased knowledge on the role of the immune system in ovarian cancer, major improvements are to be expected of immunotherapy based treatment of this disease. This article aims to summarize the current literature views on the evidence for a role for chronic inflammation with a specific focus on anti-inflammatory cytokines.

scholarly journals The role of pro-inflammatory cytokines in the pathogenesis and progression of neoplasms

2018 ◽  
Vol 72 ◽  
pp. 896-905 ◽  
Author(s):  
Kinga Zielińska ◽  
Konrad Kwasniak ◽  
Jacek Tabarkiewicz ◽  
Bożenna Karczmarek-Borowska
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Host Immune System ◽  
Clinical Observations ◽  
Combined Action ◽  
Progressive Disorder ◽  
Pro Inflammatory Cytokines

Cytokines play an important role in the functioning of the immune system. Studies have reported an increased secretion of inflammatory cytokines by the neoplasms. Inflammation plays a role in the pathogenesis of various diseases; it is also a risk factor for the development and progression of a neoplasm, as exemplified by the development of cancer in the region of the head and neck in response to chronic inflammation caused by irritants present, e.g. in cigarette smoke. Cytokines (IL-1 beta, IL-6, TNF, IL-8, IL-17), which take part in the inflammatory response and are, therefore, strongly involved in the development of cancer. The combined action of cytokines produced by the neoplastic cells via multiple mechanisms, modulates cell response of the host immune system. Clinical observations suggest that cancer patients show a progressive disorder of the immune system, resulting in tumor progression. The mechanisms conducive to the weakening or lack of an immune response to neoplastic antigens contribute to the severity of the invasion of cancerous lesions. Although mechanisms that occur between tumor cells, the micro-environment of the tumor and immune cells of the host are not thoroughly known, previous research point to the importance of this interaction in oncogenesis, which may ultimately affect the prognosis.

scholarly journals The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tian-Yu Lei ◽  
Ying-Ze Ye ◽  
Xi-Qun Zhu ◽  
Daniel Smerin ◽  
Li-Juan Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Immune System ◽  
Immune Responses ◽  
Ischaemic Stroke ◽  
Immune Cells ◽  
Tissue Injury ◽  
Recovery Period ◽  
Vital Functions ◽  
Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

scholarly journals Serum Levels of Pro-inflammatory Cytokines in relationship to outcomes in Children with P. falciparum malaria, in Nnewi-South east Nigeria

1970 ◽  
Vol 42 (2) ◽  
pp. 142-146
Author(s):  
EC Okocha ◽  
NC Ibeh ◽  
EO Ukaejiofor ◽  
JC Ebenebe ◽  
JC Aneke ◽  
...  
Keyword(s):  
Immune Response ◽  
Platelet Count ◽  
Falciparum Malaria ◽  
Inflammatory Cytokines ◽  
Parasite Density ◽  
The Body ◽  
World Health ◽  
Inadequate Response ◽  
Monocyte Count ◽  
Pro Inflammatory Cytokines

Background and Objective: In P. falciparum malaria (PFM) infestation there are marked changes in cytokine production as the body mounts an immune response to it. Hence we set out to study these changes.Methods: A total of 158 cases of PFM among children attending the paediatric unit of our hospital and 56 healthy controls were studied. Children with febrile illness were screened for malaria using 10% Giemsa stained blood smear. Patients with positive smears were recruited; co-infected patients – those infected by another organism in addition to plasmodium specie.- were excluded. Whole blood was collected, some into plain tubes for serum cytokine testing and some into EDTA bottles for complete blood count and parasite density (PD) determination. Controls with asymptomatic parasitaemia were excluded.Results: Using the World Health Organization criteria for defining severe malaria; we identified 15 cases of severe and 143 cases of uncomplicated PFM. Significantly elevated levels of interleukin-1 (IL-1), interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α) were seen in the uncomplicated and severe forms of PFM. It was observed that the elevated cytokine values correlated with PD (in uncomplicated PFM but not in the severe forms). The difference between PD/absolute monocyte count (AMC) ratio was not significant (p=0.13); while PD/platelet count (PC) and PC/ AMC ratios were significant (p=0.01, and 0.03 respectively) when compared between uncomplicated and severe disease.Conclusion: Our data seems to suggest that subjects with an adequate immune response to the parasite density, in terms of pro-inflammatory cytokine levels, presented with uncomplicated disease; while those who have an inadequate response presented with severe disease. The ratios of (PD/PC) and (PC/AMC), in the positive and negative directions respectively, may be predictors of increased disease severity. These observations may have implications for predicting disease outcome and PFM therapy.Key Words: plasmodium falciparum malaria, pro-inflammatory cytokines, Parasite density/Platelet count ratio, Platelet count/Absolute monocyte

scholarly journals Unlocking the Potential of Vaccines Built on Messenger RNA

2021 ◽  
pp. 160-197
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Side Effects ◽  
Immune Responses ◽  
Messenger Rna ◽  
Healthy Tissue ◽  
Therapeutic Approaches ◽  
Inflammatory Reactions ◽  
Discontinuation Of Treatment ◽  
Keywords Cancer

In recent years, immunotherapy has revolutionized the treatment of cancer; however, inflammatory reactions in healthy tissues often have side effects that can be serious and lead to permanent discontinuation of treatment. This toxicity is not yet well understood and is a major obstacle to the use of immunotherapy. When the immune system is so severely activated, the resulting inflammatory reaction can have detrimental effects and sometimes serious damage to healthy tissue. We wanted to know if there was a difference between an optimal immune response that aims to kill cancer and an unwanted response that could affect healthy tissue. Identifying the distinctive elements between these two immune responses allows the development of new, more effective and less toxic therapeutic approaches. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Host F-box protein 22 enhances the uptake of Brucella by macrophages and drives a sustained release of pro-inflammatory cytokines through degradation of the anti-inflammatory effector proteins of Brucella.

2021 ◽  
Author(s):  
Girish Radhakrishnan ◽  
Varadendra Mazumdar ◽  
Kiranmai Joshi ◽  
Binita Roy Nandi ◽  
Swapna Namani ◽  
...  
Keyword(s):  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Effector Proteins ◽  
Host Protein ◽  
Limited Information ◽  
Phagocytic Cells ◽  
Scf Complex ◽  
Enhanced Production ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Brucella species are intracellular bacterial pathogens, causing the world-wide zoonotic disease, brucellosis.  Brucella invade professional and non-professional phagocytic cells, followed by resisting intracellular killing and establishing a replication permissive niche. Brucella also modulate the innate and adaptive immune responses of the host for their chronic persistence. The complex intracellular cycle of Brucella majorly depends on multiple host factors but limited information is available on host and bacterial proteins that play essential role in the invasion, intracellular replication and modulation of host immune responses. By employing an siRNA screening, we identified a role for the host protein, FBXO22 in Brucella -macrophage interaction. FBXO22 is the key element in the SCF E3 ubiquitination complex where it determines the substrate specificity for ubiquitination and degradation of various host proteins.  Downregulation of FBXO22 by siRNA or CRISPR-Cas9 system, resulted diminished uptake of Brucella into macrophages, which was dependent on NF-κB-mediated regulation of phagocytic receptors. FBXO22 expression was upregulated in Brucella -infected macrophages that resulted induction of phagocytic receptors and enhanced production of pro-inflammatory cytokines through NF-κB. Furthermore, we found that FBXO22 recruits the effector proteins of Brucella , including the anti-inflammatory proteins, TcpB and OMP25 for degradation through the SCF complex. We did not observe any role for another F-box containing protein of SCF complex, β-TrCP in Brucella -macrophage interaction. Our findings unravel novel functions of FBXO22 in host-pathogen interaction and its contribution to pathogenesis of infectious diseases.

Introduction to Clinical Immunology: Overview of the Immune Response, Autoimmune Conditions, and Immunosuppressive Therapeutics for Rheumatic Diseases

2016 ◽  
Author(s):  
Steven K. Lundy ◽  
Alison Gizinski ◽  
David A. Fox
Keyword(s):  
Immune Response ◽  
Immune System ◽  
T Cell ◽  
Immune Responses ◽  
Autoimmune Diseases ◽  
Adaptive Immunity ◽  
Cell Populations ◽  
Hematopoietic Stem ◽  
Innate And Adaptive Immunity ◽  
Adaptive Immune

The immune system is a complex network of cells and mediators that must balance the task of protecting the host from invasive threats. From a clinical perspective, many diseases and conditions have an obvious link to improper functioning of the immune system, and insufficient immune responses can lead to uncontrolled acute and chronic infections. The immune system may also be important in tumor surveillance and control, cardiovascular disease, health complications related to obesity, neuromuscular diseases, depression, and dementia. Thus, a working knowledge of the role of immunity in disease processes is becoming increasingly important in almost all aspects of clinical practice. This review provides an overview of the immune response and discusses immune cell populations and major branches of immunity, compartmentalization and specialized immune niches, antigen recognition in innate and adaptive immunity, immune tolerance toward self antigens, inflammation and innate immune responses, adaptive immune responses and helper T (Th) cell subsets, components of the immune response that are important targets of treatment in autoimmune diseases, mechanisms of action of biologics used to treat autoimmune diseases and their approved uses, and mechanisms of other drugs commonly used in the treatment of autoimmune diseases. Figures show the development of erythrocytes, platelets, lymphocytes, and other immune system cells originating from hematopoietic stem cells that first reside in the fetal liver and later migrate to the bone marrow, antigen–major histocompatibility complex recognition by T cell receptor control of T cell survival and activation, and Th cells as central determinants of the adaptive immune response toward different stimuli. Tables list cell populations involved in innate and adaptive immunity, pattern recognition receptors with known ligands, autoantibody-mediated human diseases: examples of pathogenic mechanisms, selected Food and Drug Administration–approved autoimmune disease indications for biologics, and mechanism of action of biologics used to treat autoimmune diseases.   This review contains 3 highly rendered figures, 5 tables, and 64 references.

scholarly journals Extracellular vesicles from human cardiovascular progenitors trigger a reparative immune response in infarcted hearts

2020 ◽  
Author(s):  
Bruna Lima Correa ◽  
Nadia El Harane ◽  
Ingrid Gomez ◽  
Hocine Rachid Hocine ◽  
José Vilar ◽  
...  
Keyword(s):  
Immune Response ◽  
Extracellular Vesicles ◽  
Inflammatory Cytokines ◽  
Nk Cell ◽  
Inflammatory Monocytes ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Aims The cardioprotective effects of human induced pluripotent stem cell-derived cardiovascular progenitor cells (CPC) are largely mediated by the paracrine release of extracellular vesicles (EV). We aimed to assess the immunological behaviour of EV-CPC, which is a prerequisite for their clinical translation. Methods and results Flow cytometry demonstrated that EV-CPC expressed very low levels of immune relevant molecules including HLA Class I, CD80, CD274 (PD-L1), and CD275 (ICOS-L); and moderate levels of ligands of the natural killer (NK) cell activating receptor, NKG2D. In mixed lymphocyte reactions, EV-CPC neither induced nor modulated adaptive allogeneic T cell immune responses. They also failed to induce NK cell degranulation, even at high concentrations. These in vitro effects were confirmed in vivo as repeated injections of EV-CPC did not stimulate production of immunoglobulins or affect the interferon (IFN)-γ responses from primed splenocytes. In a mouse model of chronic heart failure, intra-myocardial injections of EV-CPC, 3 weeks after myocardial infarction, decreased both the number of cardiac pro-inflammatory Ly6Chigh monocytes and circulating levels of pro-inflammatory cytokines (IL-1α, TNF-α, and IFN-γ). In a model of acute infarction, direct cardiac injection of EV-CPC 2 days after infarction reduced pro-inflammatory macrophages, Ly6Chigh monocytes, and neutrophils in heart tissue as compared to controls. EV-CPC also reduced levels of pro-inflammatory cytokines IL-1α, IL-2, and IL-6, and increased levels of the anti-inflammatory cytokine IL-10. These effects on human macrophages and monocytes were reproduced in vitro; EV-CPC reduced the number of pro-inflammatory monocytes and M1 macrophages, while increasing the number of anti-inflammatory M2 macrophages. Conclusions EV-CPC do not trigger an immune response either in in vitro human allogeneic models or in immunocompetent animal models. The capacity for orienting the response of monocyte/macrophages towards resolution of inflammation strengthens the clinical attractiveness of EV-CPC as an acellular therapy for cardiac repair.

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