China
Africa
Explore chapters and articles related to this topic
Macrophage Inflammatory Protein-1
Published in Jason Kelley, Cytokines of the Lung, 2022
Barbara Sherry, Anthony Cerami
MIP-1 also participates in the host response to inflammation by modulating, through autocrine mechanisms, the activation state of the macrophage. Thioglycollate-elicited peritoneal exudate macrophages, when stimulated with native doublet MIP-1, expressed messages for several inflammatory cytokines, including TNF, IL-1, and IL-6 (Fahey et al., 1991). In addition to inducing specific cytokine mRNAs, MIP-1 stimulated the synthesis and secretion of the corresponding mature proteins. The MIP-1 mediated increases in cytokine mRNAs and protein were both time- and dose-dependent, and cytokine induction by MIP-1 is enhanced significantly in the presence of interferon-gamma. Because enhanced cytokine secretion by macrophages is characteristic of the activated state, we studied the effects of MIP-1 treatment on other parameters of macrophage activation. MIP-1-treated macrophages exhibited enhanced tumor cell-killing activity in coculture assays, but the mechanism of this enhancement is not yet understood (Fahey et al., 1991). In sharp contrast to these apparent “macrophage activating” properties of MIP-1, the cytokine failed to trigger two other components of the activated state, up-regulation of cell surface expression of Ia and the superoxide burst (Fahey et al., 1991). In addition, we separately treated macrophages with recombinant MIP-1α and recombinant MIP-1β peptides alone and found that MIP-1α, but not MIP-1β, reproduces the “activating” effects observed with purified native (doublet) material.
Medicinal Potential of Fenugreek in Neuropathy and Neuroinflammation Associated Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Aman Upaganlawar, Chandrashekhar Upasani, Mayur B. Kale
The pro-inflammatory response mediated by microglia secretes potent ROS such as superoxide radicals and nitric oxide, pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), IL-6, and IL-1β, and neurotrophic factors (Wang et al. 2015). Other inflammatory mediators include the chemokine macrophage inflammatory protein-1α (MIP-1α), interferon-γ (IFN- γ), and compounds such as lipopolysaccharide (LPS) (Appel, Beers, and Zhao 2015).
The Role of Cytokines in Induction of Macrophage Procoagulant Activity
Published in Gary A. Levy, Edward H. Cole, Procoagulant Activity in Health and Disease, 2019
Because of our interest in macrophage migration, our finding that fractions enriched for MPIF activity were chemotactic (see Reference 39 and below), and reports of monocyte procoagulant induction by some chemotactic factors,40,41 we investigated the procoagulant potential of some recently defined chemotactic cytokines. The macrophage-derived murine inflammatory peptides MIP-1 and MIP-242 were generous gifts from S. Wolpe, and macrophage chemotactic proteins MCP-1 and MCP-242 were received from T. Yoshimura. These factors are members of the β-thromboglobulin superfamily including IL-8/neutrophil activating factor. When tested on human Mos or murine exudate Macs, either alone or in combination with LPS or IFNγ, no significant induction of MPCA was observed. In addition, transforming growth factor β (TGFβ), a potent chemoattractant produced by activated macrophages and platelets and recently shown to upmodulate TF expression by murine fibroblasts,44 had no effect on MPCA expression in our studies. Although we find no indication of synergy, the possibility that some chemotactic cytokines may amplify the surface expression of TF, induced by MPIF or LPS as initial signals, via their ability to upregulate the adhesion receptor CDIIb/CDl 8 (Mac-1), as described by Fan and Edgington45 (see Chapter 1 of this volume), is worthy of investigation.
Immunotherapy for SARS-CoV-2: potential opportunities
Published in Expert Opinion on Biological Therapy, 2020
Mehrnoosh Pashaei, Nima Rezaei
Following entry of SARS-CoV-2 into the cells through ACE-2 which is overexpressed in special cells such as lung epithelial cells, especially type II pneumocytes, can activate innate and adaptive immune responses. Infected cells with SARS-CoV-2 release Interleukine-8 (IL-8) to infiltration of alveolar macrophages and mononuclear inflammatory cells to infected tissues, and then T and B lymphocytes responses are triggered. To that end, several signaling pathways play a key role to enhance inflammatory responses, such as Janus kinase transducers (JAK/STAT) that is led macrophage activation syndrome (MAS) and increased secretion of pro-inflammatory cytokines such as IL-1, IL-2, IL-6, IL-7, IL-10, granulocyte-colony-stimulating factor (G-CSF), interferon-γ-inducible protein 10 (IP10), monocyte chemoattractant protein 1 (MCP1), macrophage inflammatory protein 1 alpha (MIP1A) and tumor necrosis factor α (TNF-α). In COVID-19 patients, elevated levels of pro-inflammatory cytokines are associated with immune cell recruitment and then exaggerated inflammation, type II pnemocyte hyperplasia, hyaline membrane formation, and disease progression [18,19].
Multiomic analysis of cytokines in immuno-oncology
Published in Expert Review of Proteomics, 2020
Another separate group of cytokines, termed pro-inflammatory cytokines play a significant role in immuno-oncology [15–18]. The main members of this group are IL-1, IL-6, and TNF-α, and macrophage inflammatory protein 1 alpha (MIP1A). These cytokines have multiple roles in oncology; some from them participate in tumor-stroma interactions (IL-1, IL-6, TNF-α, TGF-β, epidermal growth factor (EGF), and PDGF) [19,20]; some participate in the tumor progression of several cancers (IL-1, IL-6, TNF-α, EGF) [6,21–24], some modulate the immune response as immuno regulatory cytokines (IL-10, IL-17, TGF-b) [2,25,26]; some act though a cancer immunosuppression mechanisms (TNF-α, TGF-β) or participate in cancer escape mechanisms [2,9,19,27–30]. There is evidence that one of the other major mechanisms of the innate immune response to tumors is through the induction of a strong inflammatory response by cytokines [2,19,29]; the inability to suppress chronic inflammation is considered one of the causes of carcinogenesis. About 20% of all cancers are associated with inflammation and with chronic infections [6,22,30]. For example, the most common risk factor for gastric cancer is having a chronic gastric infection with Helicobacter pylori. Chronic inflammation in the epithelium can promote angiogenesis, invasion and metastasis [19,20]. In addition to increasing the proliferation of mutated cells, an inflammatory microenvironment can also increase the degree of mutation [22,31–34].
Coronavirus disease 2019: investigational therapies in the prevention and treatment of hyperinflammation
Published in Expert Review of Clinical Immunology, 2020
Isabelle Amigues, Alexander H Pearlman, Aarat Patel, Pankti Reid, Philip C. Robinson, Rashmi Sinha, Alfred Hj Kim, Taryn Youngstein, Arundathi Jayatilleke, Maximilian Konig
Although no direct evidence implicates proinflammatory cytokines as the cause of lung damage, the observation of patterns of proinflammatory cytokine production in animal and in-vitro models of SARS-CoV-1 and MERS-CoV infection supports the idea of a shared pathophysiology of immune dysregulation. Chu et al. examined the comparative abilities of MERS-CoV and SARS-CoV-1 to trigger a cytokine response in monocyte-derived dendritic cells and found that both induced upregulation of TNF-α and IL-6 during the same time frame that peak viral titers were observed in culture [6]. Zhou et al. similarly examined infectivity and innate immune response-related cytokines in monocyte-derived macrophages (MDMs) and found that MERS-CoV and SARS-CoV-1 showed a sustained induction of MCP-1, MIP-1α, and IL-8, whereas MERS-CoV-infected MDMs produced higher levels of these chemokines [7]. As expected, TNF-α and IL-6 were induced at high levels by both MERS-CoV and SARS-CoV-1. Interestingly, IFN-γ induction in MDMs was much more prominent than IFN-α and IFN-β [7]. Lau et al. examined cytokine profiles in MERS-CoV- and SARS-CoV-1-infected polarized airway epithelial Calu-3 cells and found that both viruses caused a delayed induction of IL-1β, IL-6, and IL-8, with MERS-CoV triggering a stronger response than SARS-CoV-1 [8]. Animal models of MERS and SARS are more heterogeneous in terms of symptom severity, limiting the usefulness of rodent models. However, in more rapidly lethal and systemically symptomatic models, elevations of pro-inflammatory cytokines such as IL-6, IP-10, and IL-8 were observed in lung and brain tissues [9–11].