scholarly journals The Emerging Role of Peptides and Lipids as Antimicrobial Epidermal Barriers and Modulators of Local Inflammation

2012 ◽  
Vol 25 (4) ◽  
pp. 167-181 ◽  
Author(s):  
N.K. Brogden ◽  
L. Mehalick ◽  
C.L. Fischer ◽  
P.W. Wertz ◽  
K.A. Brogden
Keyword(s):  
Local Inflammation

scholarly journals Does the Interaction between Local and Systemic Inflammation Provide a Link from Psychology and Lifestyle to Tissue Health in Musculoskeletal Conditions?

2021 ◽  
Vol 22 (14) ◽  
pp. 7299
Author(s):  
David M. Klyne ◽  
Mary F. Barbe ◽  
Greg James ◽  
Paul W. Hodges
Keyword(s):  
Connective Tissue ◽  
Systemic Inflammation ◽  
Molecular Basis ◽  
Tissue Level ◽  
Lifestyle Factors ◽  
Local Inflammation ◽  
Musculoskeletal Conditions ◽  
Tissue Biology ◽  
Mind And Body

Musculoskeletal conditions are known to involve biological, psychological, social and, often, lifestyle elements. However, these domains are generally considered in isolation from each other. This siloed approach is unlikely to be adequate to understand the complexity of these conditions and likely explains a major component of the disappointing effects of treatment. This paper presents a hypothesis that aims to provide a foundation to understand the interaction and integration between these domains. We propose a hypothesis that provides a plausible link between psychology and lifestyle factors with tissue level effects (such as connective tissue dysregulation/accumulation) in musculoskeletal conditions that is founded on understanding the molecular basis for interaction between systemic and local inflammation. The hypothesis provides plausible and testable links between mind and body, for which empirical evidence can be found for many aspects. We present this hypothesis from the perspective of connective tissue biology and pathology (fibrosis), the role of inflammation locally (tissue level), and how this inflammation is shaped by systemic inflammation through bidirectional pathways, and various psychological and lifestyle factors via their influence on systemic inflammation. This hypothesis provides a foundation for new consideration of the development and refinement of personalized multidimensional treatments for individuals with musculoskeletal conditions.

scholarly journals ROLE OF INNATE IMMUNITY FACTORS IN PERIODONTITIS PATHOGENESIS

2016 ◽  
pp. 100-107 ◽  
Author(s):  
L. V. Gankovskaya ◽  
N. M. Khelminskaya ◽  
E. A. Molchanova ◽  
O. A. Svitich
Keyword(s):  
Innate Immunity ◽  
Molecular Mechanisms ◽  
Subsequent Development ◽  
Cell Populations ◽  
Immune Protection ◽  
Local Inflammation ◽  
Tissue Destruction ◽  
Inflammation Reaction ◽  
Pro Inflammatory Cytokines

Chronic generalized periodontitis (CGP) is a disease of periodontium tissues supporting tooth induced by bacteria, that is characterized by the presence of processes of inflammation with destruction ofbone tissue. The knowledge of molecular mechanisms of CGP pathogenesis facilitates creation of the most effective methods of therapy of this disease. Bacterial infection is a primary factor in periodontitis etiology, however is not sufficient for its start and subsequent development. It is known, that bacterial factors induce a local inflammation reaction and activate the system of innate immunity through activation of Toll-like receptors (TLR), located on the surface of resident cells and leukocytes. Activation of these cells results in production of pro-inflammatory cytokines and recruitment of phagocytes and lymphocytes into the inflammation zone. In review we examined the known data regarding factors of immune protection of periodontium including cell populations and cytokines, as well as mechanisms of tissue destruction, that support the tooth. Perspectives of therapy are also discussed.

scholarly journals Pharmacokinetic, Pharmacogenetic, and Other Factors Influencing CNS Penetration of Antiretrovirals

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Jacinta Nwamaka Nwogu ◽  
Qing Ma ◽  
Chinedum Peace Babalola ◽  
Waheed Adeola Adedeji ◽  
Gene D. Morse ◽  
...  
Keyword(s):  
Neurological Complications ◽  
Hiv Treatment ◽  
Sub Saharan Africa ◽  
Drug Penetration ◽  
Local Inflammation ◽  
Factors Influencing ◽  
Immunodeficiency Virus ◽  
Sub Saharan ◽  
Cns Penetration

Neurological complications associated with the human immunodeficiency virus (HIV) are a matter of great concern. While antiretroviral (ARV) drugs are the cornerstone of HIV treatment and typically produce neurological benefit, some ARV drugs have limited CNS penetration while others have been associated with neurotoxicity. CNS penetration is a function of several factors including sieving role of blood-brain and blood-CSF barriers and activity of innate drug transporters. Other factors are related to pharmacokinetics and pharmacogenetics of the specific ARV agent or mediated by drug interactions, local inflammation, and blood flow. In this review, we provide an overview of the various factors influencing CNS penetration of ARV drugs with an emphasis on those commonly used in sub-Saharan Africa. We also summarize some key associations between ARV drug penetration, CNS efficacy, and neurotoxicity.

IL-1β mediates leptin induction during inflammation

1998 ◽  
Vol 274 (1) ◽  
pp. R204-R208 ◽  
Author(s):  
Raffaella Faggioni ◽  
Giamila Fantuzzi ◽  
John Fuller ◽  
Charles A. Dinarello ◽  
Kenneth R. Feingold ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Host Response ◽  
Tumor Necrosis ◽  
Local Inflammation ◽  
Protein Levels ◽  
Infection And Inflammation ◽  
Leptin Expression ◽  
Necrosis Factor

Interleukins (IL) are key mediators of the host response to infection and inflammation. Leptin is secreted by adipose tissue and plays an important role in the control of food intake. Administration of lipopolysaccharide (LPS), tumor necrosis factor (TNF), or IL-1 acutely increases leptin mRNA and protein levels. To investigate the role of IL-1β and IL-6 in leptin expression during inflammation, we used IL-1β-deficient (−/−) and IL-6 −/− mice. Mice were injected intraperitoneally with LPS or subcutaneously with turpentine, as models of systemic or local inflammation, respectively. In IL-1β +/+ mice, both LPS and turpentine increased leptin mRNA and circulating leptin. In contrast, neither LPS nor turpentine increased leptin levels in IL-1β −/− mice. In IL-6 +/+ or IL-6 −/− mice, turpentine increased leptin protein to comparable levels. We conclude that IL-1β is essential for leptin induction by both LPS and turpentine in mice, but IL-6 is not.

scholarly journals The Role of Hepatic Invariant NKT Cells in Systemic/Local Inflammation and Mortality during Polymicrobial Septic Shock

2009 ◽  
Vol 182 (4) ◽  
pp. 2467-2475 ◽  
Author(s):  
Caroline K. Hu ◽  
Fabienne Venet ◽  
David S. Heffernan ◽  
Yvonne L. Wang ◽  
Brian Horner ◽  
...  
Keyword(s):  
Septic Shock ◽  
Nkt Cells ◽  
Local Inflammation ◽  
Invariant Nkt Cells

scholarly journals Anti-inflammatory and pro-resolving role of mast cells during resolution of local inflammation.

2021 ◽  
Author(s):  
◽  
Lisa Kornstädt
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
The Body ◽  
Type I ◽  
Local Inflammation ◽  
Ontology Term ◽  
Resolution Of Inflammation ◽  
Macrophage Phagocytosis ◽  
Anti Inflammatory

Mast cells are long-lived tissue-resident leukocytes, located most abundantly in the skin and mucosal surfaces. They belong to the first line of defence of the body, protecting against invading pathogens, toxins and allergens. Their secretory granules are densely packed with a plethora of mediators, which can be released immediately upon activation of the cell. Next to their role in IgE-mediated allergic diseases and in promoting inflammation, potential anti-inflammatory functions have been assigned to mast cells, depending on the biological setting. The aim of this thesis was to contribute to a better understanding of the role of mast cells during the resolution of a local inflammation. Therefore, in a first of step a suitable model of a local inflammation had to be identified. Since comparison of the two Toll-like receptor (TLR)-agonists zymosan and lipopolysaccharide (LPS), which are most commonly used to locally induce inflammation, revealed a systemic response after LPS-injection and a local inflammation after zymosan-injection, the TLR2 agonist zymosan was chosen for the subsequent experiments. Multi epitope ligand cartography (MELC) combined with statistical neighbourhood analysis showed that mast cells are located in an anti-inflammatory microenvironment next to M2 macrophages during resolution of inflammation, while neutrophils and M1 macrophages are located in the zymosan-filled core of the inflammation. Furthermore, infiltrating neutrophils during peak inflammation and an increasing population of macrophages phagocytosing neutrophils during resolution of inflammation could be observed. MELC as well as flow cytometry analysis of mast cell-deficient mice revealed a decreased phagocytosing activity of macrophages in the absence of mast cells. As an untargeted approach to identify mast cell-derived mediators induced by zymosan, mRNA sequencing of bone marrow-derived mast cells (BMMCs) was performed. Gene ontology term analysis of the sequencing data revealed the induction of the type I interferon (IFN) pathway as the dominant response. Contradicting previous studies, I could validate the production of IFN-β by mast cells in response to zymosan and LPS in vitro. Furthermore IFN-β expression by mast cells was also detected in vivo. In accordance with previous studies regarding other cell types the release of IFN-β by mast cells depends on endosomal signaling. The potential of IFN-β to enhance the phagocytosing activity of macrophages has been demonstrated recently. Besides IFN-β, various other mediators with reported enhancing effects on macrophage phagocytosis were also induced by zymosan in BMMCs, including Interleukin (IL)-1β, IL-4, IL-13, and Prostaglandin (PG) E2. Thus, either one of these mediators alone or a combination of them could promote macrophage phagocytosis. In conclusion, I herein present mast cells as a novel source for IFN-β induced by non-viral TLR ligands and demonstrate their enhancing effect on macrophage phagocytosis, thereby contributing to the resolution of inflammation.

scholarly journals Mast cells in collagen diseases

2019 ◽  
Vol 3 (2) ◽  
pp. 69
Author(s):  
Naoya Mikita ◽  
Yutaka Inaba ◽  
Takashi Yoshimasu ◽  
Nobuo Kanazawa ◽  
Fukumi Furukawa
Keyword(s):  
Rheumatoid Arthritis ◽  
Multiple Sclerosis ◽  
Mast Cells ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Allergic Diseases ◽  
Local Inflammation ◽  
Systemic Lupus ◽  
Cytokines And Chemokines

Mast cells are involved in many immune reactions and diseases through 1) the expressions of several receptors, 2) productions of various mediators such as histamine, cytokines, and chemokines, 3) direct interactions with immune cells. Besides allergic diseases, mast cells have been also assumed to be involved in autoimmune diseases such as bullous pemphigoid, rheumatoid arthritis, and multiple sclerosis. Moreover, several studies reported the involvement of mast cells in collagen disease. In this article, we review recent findings about the role of mast cells especially in systemic lupus erythematosus and systemic sclerosis. In these diseases, mast cells seem to be involved in local inflammation and tissue damage partially in the targeted organ rather than the development of autoimmunity including production of autoantibodies.

A Potential Role of Adhesion Molecules on Lung Metastasis Enhanced by Local Inflammation

2020 ◽  
Vol 40 (11) ◽  
pp. 6171-6178
Author(s):  
HIROYUKI HORIGUCHI ◽  
HIRONORI TSUJIMOTO ◽  
NARIYOSHI SHINOMIYA ◽  
YUSUKE MATSUMOTO ◽  
HIDEKAZU SUGASAWA ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Lung Metastasis ◽  
Potential Role ◽  
Local Inflammation
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