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Proinflammatory Peptides in Relation to Other Inflammatory Mediators
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Pierangelo Geppetti, Costanza Emanueli, Michela Figini, Domenico Regoli
The presence of tachykinin receptors on resident or circulating inflammatory cells have been proposed. Although conflicting results have been reported in the past regarding the presence of tachykinin receptors in leukocytes and particularly lymphocytes, more consistent findings indicate that cells of the monocytic lineage in the lung and outside the lung cause the release of diverse inflammatory mediators via activation of specific tachykinin receptors. Mononuclear phagocytes, either as monocytes circulating in the bloodstream or as tissue macrophages, modulate the host defense response through their ability to present antigens and the release of soluble mediators. Interleukin-1 (IL-1), TNF-α, and IL-6 were released from human blood monocytes by SP, an effect that was blocked by a SP receptor antagonist (48–50). Stimulation by naturally occurring tachykinins and by selective NK2 receptor agonists caused a respiratory burst-dependent release of superoxide anion (51) and gelantinase production (52) from rat pulmonary macrophages, thus suggesting that NK2 receptors were involved. “Nonclassical” tachykinin receptors have been proposed to be involved in cytokine release from microglia cells and macrophages (53,54).
Conclusions
Published in Miroslav Holub, Immunology of Nude Mice, 2020
Phagocytic systems and monokines secreted by mononuclear phagocytes are the main compensatory measure for the T deficiency. Mononuclear phagocytes are already stimulated prenatally and, in the postnatal period, the gut microflora provides an additional and steady activating effect on the mononuclear and, through it, on polymorphonuclear phagocyte systems.
Role of Macrophages and Microglia in the Injured CNS
Published in Martin Berry, Ann Logan, CNS Injuries: Cellular Responses and Pharmacological Strategies, 2019
Mononuclear phagocytes is a generic, descriptive term for a major cell population of the immune system capable of phagocytosis. These cells are found in every organ, and are often referred to as tissue-specific macrophages. Examples of these include Kupffer’s cells of the liver, alveolar macrophages of the lung, and monocytes of the blood. Although there is little doubt that tissue-specific macrophages are ontogenetically related and possibly of the same lineage with a common primordial precursor cell, in the case of microglia it is unlikely that they are continuously being replenished by monocyte-like precursor cells from the blood stream, as claimed by the central dogma of the mononuclear phagocyte system (see below).
Effect of inflammation on cytochrome P450-mediated arachidonic acid metabolism and the consequences on cardiac hypertrophy
Published in Drug Metabolism Reviews, 2023
Mohammed A. W. ElKhatib, Fadumo Ahmed Isse, Ayman O. S. El-Kadi
The contribution of inflammatory cells to CH is well established. Macrophages (Mϕ) are mononuclear phagocytes that exert pivotal functions in tissue repair and remodeling, and regulation of adaptive and innate immunity (Murray and Wynn 2011; Takeda and Manabe 2011). In the heart, the two Mϕ phenotypes that are present are pro-inflammatory M1 and anti-inflammatory M2 (Mosser and Edwards 2008; Takeda and Manabe 2011). Regarding M1, it exacerbates cardiac inflammation through cytokine release and enhanced apoptosis, as well as its implication in cardiac remodeling (Takeda and Manabe 2011; Van den Akker et al. 2013; Fernández-Velasco et al. 2014). On the other hand, M2 attenuates inflammation and induces cardiac reparative cascades and angiogenesis (Van den Akker et al. 2013). A robust association between Mϕ and CH was created, however, reports have demonstrated that depletion of Mϕ exacerbates cardiac dysfunction following CH, proposing a pivotal undetermined contribution to both CH development and outcomes (Takeda and Manabe 2011). In summary, inflammation is a potential intervention target in CH development for discovering novel therapeutic agents that can improve the cardiac functions (Heymans et al. 2009; Hofmann and Frantz 2013).
Macrophage membrane biomimetic drug delivery system: for inflammation targeted therapy
Published in Journal of Drug Targeting, 2023
Yulu Zhang, Yu Long, Jinyan Wan, Songyu Liu, Ai Shi, Dan Li, Shuang Yu, Xiaoqiu Li, Jing Wen, Jie Deng, Yin Ma, Nan Li
The release mechanism of the MM-nano-DDS in target tissues is a major and difficult task in the research. As the pharmacokinetics properties of the drug in terms of dose and event specificity, the use of cellular responses to various conditions can provide the desired trigger release [36]. There are three main modes of drug release from MM-NP: MM-NP is phagocytosed by cells and the surface cell membrane ruptures leading to drug release; due to stimulation of the extracellular microenvironment, which drives drug-triggered release; or drug release by diffusion through the cell membrane [37]. Mononuclear phagocytes are known to produce and store various compounds in intracellular vesicles and release them through exocytosis at disease sites. Therefore, when macrophages are used as drug delivery vehicles, a similar mechanism can trigger cellular nanocarriers to release drugs. Normally, the drug release rate of MM-NPs is slightly lower than that of uncoated NPs, probably due to the fact that MM-NPs are coated with a cell membrane. When the drug is released, the cell membrane acts as a barrier and therefore can slow down the release of the drug to a certain extent [32,38].
Epigenetic regulation by gut microbiota
Published in Gut Microbes, 2022
Vivienne Woo, Theresa Alenghat
Immune cells similarly undergo broad histone modifications in response to microbial colonization. Non-mucosal mononuclear phagocytes (macrophages and dendritic cells) require microbial signals to epigenetically and transcriptionally activate genes involved in interferon (IFN) signaling and initiating normal T cell responses.61,62 Specifically, GF or antibiotic-treated mice have decreased H3K4me3 (activating) at genes involved in pro-inflammatory responses including type I IFNs and increased H3K27me3 (repressive) at metabolic pathways compared to microbiota-exposed cells. The microbiota further maintain this anti-inflammatory phenotype in macrophages through HDAC3-mediated histone deacetylation of the pro-inflammatory cytokine IL-12β.63 Similar changes in chromatin accessibility defined by differential H3K4me2 enrichment were shown at lineage-defining regulatory elements in innate lymphoid cells (ILCs) to favor an ILC3 phenotype over ILC1 or ILC2 in response to the microbiota.64 Ethionine was recently discovered as a novel microbiota-derived metabolite produced by the commensal bacterium Lactobacillus reuteri through a 2-carbon folate cycle.43 In agreement with previous reports that ethionine inhibits histone methylation,65 mass spectrometric analyses revealed that human monocytic THP-1 cells treated with ethionine preferentially incorporated ethyl groups into lysine residues of histone H3 (K9/K10/K26) instead of methyl groups. Moreover, ethionine-treated monocytes failed to activate NF-kB signaling or TNF-α expression in response to LPS treatment.43