scholarly journals Mecanismos de control neuroinmune y la vía colinérgica antiinflamatoria

Tequio ◽  
2018 ◽  
Vol 1 (2) ◽  
pp. 35-49
Author(s):  
Yobana Pérez-Cervera ◽  
Rafael Torres Rosas

The innate immune system is the first line of defense involved in protecting against external pathogens and is crucial for survival. However, uncontrolled activation of the immune system can result in more damage than the factor that triggered them, causing atrophic scarring, chronic inflammation and even Systemic inflammation events such as Lupus, arthritis, Crohn’s disease or sepsis. Fortunately, there are neuronal mechanisms of inflammatory control which could be part of new therapeutic strategies to be studied for a better control of this type of pathologies. In the last decade, the cholinergic pathway has been described as part of the neuronal mechanisms that can be exogenous activated for the non-pharmacological control of inflammatory diseases, the aim of this review is to present the evidence in basic research and encourage the research in medical practice.

Microbiology ◽  
2006 ◽  
Vol 152 (2) ◽  
pp. 285-293 ◽  
Author(s):  
Gavin K. Paterson ◽  
Tim J. Mitchell

The innate immune system provides a non-specific first line of defence against microbes and is crucial both in the development and effector stages of subsequent adaptive immune responses. Consistent with its importance, study of the innate immune system is a broad and fast-moving field. Here we provide an overview of the recent key advances made in this area with relation to the important pathogen Streptococcus pneumoniae (the pneumococcus).


2019 ◽  
Vol 12 (581) ◽  
pp. eaax3521 ◽  
Author(s):  
Nelson O. Gekara ◽  
Hui Jiang

Cyclic cGMP-AMP synthase (cGAS) alerts the innate immune system to the presence of foreign or damaged self-DNA inside the cell and is critical for the outcome of infections, inflammatory diseases, and cancer. Two studies now demonstrate that cGAS activation is regulated by differential subcellular localization through its non-enzymatic, N-terminal domain.


Antibiotics ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 94 ◽  
Author(s):  
Ashley S. Brott ◽  
Anthony J. Clarke

The peptidoglycan sacculus of both Gram-positive and Gram-negative bacteria acts as a protective mesh and provides structural support around the entirety of the cell. The integrity of this structure is of utmost importance for cell viability and so naturally is the first target for attack by the host immune system during bacterial infection. Lysozyme, a muramidase and the first line of defense of the innate immune system, targets the peptidoglycan sacculus hydrolyzing the β-(1→4) linkage between repeating glycan units, causing lysis and the death of the invading bacterium. The O-acetylation of N-acetylmuramoyl residues within peptidoglycan precludes the productive binding of lysozyme, and in doing so renders it inactive. This modification has been shown to be an important virulence factor in pathogens such as Staphylococcus aureus and Neisseria gonorrhoeae and is currently being investigated as a novel target for anti-virulence therapies. This article reviews interactions made between peptidoglycan and the host immune system, specifically with respect to lysozyme, and how the O-acetylation of the peptidoglycan interrupts these interactions, leading to increased pathogenicity.


2021 ◽  
Vol 12 ◽  
Author(s):  
Richard Felix Kraus ◽  
Michael Andreas Gruber

Neutrophils (polymorphonuclear cells; PMNs) form a first line of defense against pathogens and are therefore an important component of the innate immune response. As a result of poorly controlled activation, however, PMNs can also mediate tissue damage in numerous diseases, often by increasing tissue inflammation and injury. According to current knowledge, PMNs are not only part of the pathogenesis of infectious and autoimmune diseases but also of conditions with disturbed tissue homeostasis such as trauma and shock. Scientific advances in the past two decades have changed the role of neutrophils from that of solely immune defense cells to cells that are responsible for the general integrity of the body, even in the absence of pathogens. To better understand PMN function in the human organism, our review outlines the role of PMNs within the innate immune system. This review provides an overview of the migration of PMNs from the vascular compartment to the target tissue as well as their chemotactic processes and illuminates crucial neutrophil immune properties at the site of the lesion. The review is focused on the formation of chemotactic gradients in interaction with the extracellular matrix (ECM) and the influence of the ECM on PMN function. In addition, our review summarizes current knowledge about the phenomenon of bidirectional and reverse PMN migration, neutrophil microtubules, and the microtubule organizing center in PMN migration. As a conclusive feature, we review and discuss new findings about neutrophil behavior in cancer environment and tumor tissue.


Author(s):  
Malini Bhole

Neutrophils are an important component of the innate immune system, forming the first line of defence against bacterial invasion. Abnormalities in either neutrophil numbers or function lead to immunodeficiency disorders affecting the innate immune system, with a predisposition towards developing serious and often life-threatening infections. Alterations in neutrophil numbers and function may also be noted secondary to systemic diseases, where they may act as markers for ongoing disease processes. Most of the primary neutrophil disorders discussed in this chapter will present in childhood. In adults, acquired neutropenia is the commonest neutrophil abnormality encountered in clinical practice, although, rarely, some primary neutrophil defects may present.


2021 ◽  
pp. practneurol-2021-003031
Author(s):  
William K Diprose ◽  
Anthony Jordan ◽  
Neil E Anderson

Autoinflammatory syndromes result in a defective innate immune system. They are characterised by unexplained fever and systemic inflammation involving the skin, muscle, joints, serosa and eyes, along with elevated acute phase reactants. Autoinflammatory syndromes are increasingly recognised as a cause of neurological disease with a diverse range of manifestations. Corticosteroids, colchicine and targeted therapies are effective if started early, and hence the importance of recognising these syndromes. Here, we review the neurological features of specific autoinflammatory syndromes and our approach (as adult neurologists) to their diagnosis.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Zhen Wang ◽  
Ying Zheng

The innate immune system is the first line of defense against microbial pathogens. The activated innate immune system plays important roles in eliciting antimicrobial defenses. Despite the benefits of innate immune responses, excessive inflammation will cause host damage. Thus, tight regulation of these processes is required for the maintenance of immune homeostasis. Recently, a new class of long noncoding RNAs (lncRNAs) has emerged as important regulators in many physiological and pathological processes. Dysregulated lncRNAs have been found to be associated with excessive or uncontrolled inflammation. In this brief review, we summarize the roles of functional lncRNAs in regulating innate immune responses. We also discuss the roles of lncRNAs in macrophage polarization, an important molecular event in the innate immune responses.


2021 ◽  
Vol 12 ◽  
Author(s):  
Hélène Duez ◽  
Benoit Pourcet

The innate immune system is the first line of defense specialized in the clearing of invaders whether foreign elements like microbes or self-elements that accumulate abnormally including cellular debris. Inflammasomes are master regulators of the innate immune system, especially in macrophages, and are key sensors involved in maintaining cellular health in response to cytolytic pathogens or stress signals. Inflammasomes are cytoplasmic complexes typically composed of a sensor molecule such as NOD-Like Receptors (NLRs), an adaptor protein including ASC and an effector protein such as caspase 1. Upon stimulation, inflammasome complex components associate to promote the cleavage of the pro-caspase 1 into active caspase-1 and the subsequent activation of pro-inflammatory cytokines including IL-18 and IL-1β. Deficiency or overactivation of such important sensors leads to critical diseases including Alzheimer diseases, chronic inflammatory diseases, cancers, acute liver diseases, and cardiometabolic diseases. Inflammasomes are tightly controlled by a two-step activation regulatory process consisting in a priming step, which activates the transcription of inflammasome components, and an activation step which leads to the inflammasome complex formation and the subsequent cleavage of pro-IL1 cytokines. Apart from the NF-κB pathway, nuclear receptors have recently been proposed as additional regulators of this pathway. This review will discuss the role of nuclear receptors in the control of the NLRP3 inflammasome and the putative beneficial effect of new modulators of inflammasomes in the treatment of inflammatory diseases including colitis, fulminant hepatitis, cardiac ischemia–reperfusion and brain diseases.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Todd V. Brennan ◽  
Keri E. Lunsford ◽  
Paul C. Kuo

Studies of the immune mechanisms of allograft rejection have predominantly focused on the adaptive immune system that includes T cells and B cells. Recent investigations into the innate immune system, which recognizes foreign antigens through more evolutionarily primitive pathways, have demonstrated a critical role of the innate immune system in the regulation of the adaptive immune system. Innate immunity has been extensively studied in its role as the host's first-line defense against microbial pathogens; however, it is becoming increasingly recognized for its ability to also recognize host-derived molecules that result from tissue damage. The capacity of endogenous damage signals acting through the innate immune system to lower immune thresholds and promote immune recognition and rejection of transplant grafts is only beginning to be appreciated. An improved understanding of these pathways may reveal novel therapeutic targets to decrease graft alloreactivity and increase graft longevity.


Author(s):  
Aleksejs Zavorins ◽  
Jūlija Voicehovska ◽  
Jānis Ķīsis ◽  
Aivars Lejnieks

Abstract Rosacea is a chronic inflammatory skin disease characterised by transient or persistent erythema, telangiectasia, papules, and pustules that predominantly involve central regions of the face. Recent studies have shown a possible clinical association between rosacea and cardiovascular diseases (CVDs). Rosacea and atherosclerosis are both known to have alterations in the innate immune system, enhanced oxidative and endoplasmic reticulum stress. The aim of this review is to delve deep into the pathogenesis of rosacea and atherosclerosis to uncover possible pathogenic overlaps between these chronic inflammatory diseases.


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