The Impact of Macrophage Membrane Lipid Composition on Innate Immune Response Mechanisms

Schümann, Julia

doi:10.5772/25297

Cited by 3 publications

(7 citation statements)

References 91 publications

(156 reference statements)

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“…Lipids and fatty acids are an abundant component of membranes and are important for signaling transduction after receptor activation, for example PRRs [133,134]. These receptors are often recruited to and activated in lipid rafts, of which the lipid composition shapes PRR-driven signaling.…”

Section: Membranesmentioning

confidence: 99%

Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape

Nouwen

Everts

2020

Cells

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Myeloid cells, including macrophages and dendritic cells, represent an important first line of defense against infections. Upon recognition of pathogens, these cells undergo a metabolic reprogramming that supports their activation and ability to respond to the invading pathogens. An important metabolic regulator of these cells is mammalian target of rapamycin (mTOR). During infection, pathogens use host metabolic pathways to scavenge host nutrients, as well as target metabolic pathways for subversion of the host immune response that together facilitate pathogen survival. Given the pivotal role of mTOR in controlling metabolism and DC and macrophage function, pathogens have evolved strategies to target this pathway to manipulate these cells. This review seeks to discuss the most recent insights into how pathogens target DC and macrophage metabolism to subvert potential deleterious immune responses against them, by focusing on the metabolic pathways that are known to regulate and to be regulated by mTOR signaling including amino acid, lipid and carbohydrate metabolism, and autophagy.

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Section: Membranesmentioning

confidence: 99%

Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape

Nouwen

Everts

2020

Cells

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“…Activated B cells become transformed to plasma cells and synthesize specific antibodies (e.g., IgGs, IgM, IgD, IgA, IgE) and appropriately sensitize or activate other immune cells. In such cases, HI and expression of specific antibodies seem to principally determine which innate immune cells are required for further response processes and for appropriate induction of memory B and T cells [ 3 , 13 , 14 , 27 , 28 , 30 , 35 , 37 , 39 , 44 , 47 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 ].…”

Section: Specialized Shared and Synergistic Features Of Apcsmentioning

confidence: 99%

“…Review of a large amount of data on immune response profiles in target tissues suggests that polarization of immune cells is accompanied by expression of mediators whose effects are different from their non-polarized phenotypes (resting status) in order to act as tumor suppressors (growth-arresting), or tumor promoters (growth-promoting) [ 3 , 39 , 40 , 43 , 44 , 47 , 50 , 56 , 57 , 58 ]. Factors with known dual functions include TLRs, MCP-1-CCL2, M-CSF, TGF-β, GM-CSF, histamine, heparin, TNF-α-TNFR, VEGF, CAMs, MMPs, prostaglandins, surface antigens, adaptor molecules or cell recognition molecules (e.g., CD2, CD11, CD18, CD22, CD25, CD 50, CD54, CD63, CD69, CD88), cytokine suppressor molecules (e.g., S100 family of calcium-binding proteins), enzymes (e.g., tryptase/chymase, neutrophil-derived serine proteases, indolamine 2,3-dioxygenase, lipases or membrane metalloproteases/MMPs), peroxynitrite, cytokines/chemokines, interleukins (e.g., CCL2, CXC, Il-2, IL-3, IL-5, IL-10, IL-12, IL-13) or interferons (e.g., IFN-γ), ECFA, SCF, c-kit, antibodies (e.g., IgE, IgG isotypes, IgA, IgM), platelet-derived growth factor (PDGF) as well as expression products of gene activation pathways (e.g., p53, p27, p70, MAPKs, KRAS, BRAF, ALK, Myc, BCR, ABL, MGMT, TKIs, PI3ks) from mutated DNA, hypo-hyper-methylation products that are reported in chronic diseases or cancer [ 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 12 , 16 , 17 , 18 , 19 , 20 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , ...…”

Section: Interactions and Synergies Between Resident And Recruitedmentioning

confidence: 99%

“…In 1909, observations by Ehrlich that tumor cells are recognized and eliminated by the immune cells were later evolved to the theory of immune surveillance (cancer surveillance), an effective property of immunity to monitor/survey organ systems and destroy those internal or external elements that are useless or threaten the body’s survival [1,2,3]. Since these historical observations a role for inflammation in the genesis and progression of many acute diseases (e.g., sepsis, pneumonia, meningitis or major trauma), allergies (e.g., asthma, emphysema, skin and ocular inflammatory diseases), a wide range of age-associated chronic illnesses, neurodegenerative and autoimmune diseases (e.g., rheumatoid arthritis, atherosclerosis, dementia, Alzheimer’s, multiple sclerosis, hypertension, diabetes, stroke and cardiovascular complications, colitis, gastritis, hepatitis, nephritis, prostatis, pancreatitis, appendicitis, thyroiditis, opthalmitis, Grave’s disease, fibromyalgia, Bechet’s, esophagitis, neuritis, lupus, Parkinson’s, psoriasis) and many cancers (e.g., lung, colon/rectal, breast, cervical, prostate, bladder, liver, gall bladder, appendix, ovarian, thyroid, pancreas, brain, hematologic malignancies) has been reported in the literature [3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,…”

Section: Introductionmentioning

confidence: 99%

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Chronic Inflammation: Synergistic Interactions of Recruiting Macrophages (TAMs) and Eosinophils (Eos) with Host Mast Cells (MCs) and Tumorigenesis in CALTs. M-CSF, Suitable Biomarker for Cancer Diagnosis!

Khatami

2014

Cancers

135

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Ongoing debates, misunderstandings and controversies on the role of inflammation in cancer have been extremely costly for taxpayers and cancer patients for over four decades. A reason for repeated failed clinical trials (90% ± 5 failure rates) is heavy investment on numerous genetic mutations (molecular false-flags) in the chaotic molecular landscape of site-specific cancers which are used for “targeted” therapies or “personalized” medicine. Recently, unresolved/chronic inflammation was defined as loss of balance between two tightly regulated and biologically opposing arms of acute inflammation (“Yin”–“Yang” or immune surveillance). Chronic inflammation could differentially erode architectural integrities in host immune-privileged or immune-responsive tissues as a common denominator in initiation and progression of nearly all age-associated neurodegenerative and autoimmune diseases and/or cancer. Analyses of data on our “accidental” discoveries in 1980s on models of acute and chronic inflammatory diseases in conjunctival-associated lymphoid tissues (CALTs) demonstrated at least three stages of interactions between resident (host) and recruited immune cells: (a), acute phase; activation of mast cells (MCs), IgE Abs, histamine and prostaglandin synthesis; (b), intermediate phase; down-regulation phenomenon, exhausted/degranulated MCs, heavy eosinophils (Eos) infiltrations into epithelia and goblet cells (GCs), tissue hypertrophy and neovascularization; and (c), chronic phase; induction of lymphoid hyperplasia, activated macrophages (Mϕs), increased (irregular size) B and plasma cells, loss of integrity of lymphoid tissue capsular membrane, presence of histiocytes, follicular and germinal center formation, increased ratios of local IgG1/IgG2, epithelial thickening (growth) and/or thinning (necrosis) and angiogenesis. Results are suggestive of first evidence for direct association between inflammation and identifiable phases of immune dysfunction in the direction of tumorigenesis. Activated MFs (TAMs or M2) and Eos that are recruited by tissues (e.g., conjunctiva or perhaps lung airways) whose principal resident immune cells are MCs and lymphocytes are suggested to play crucial synergistic roles in enhancing growth promoting capacities of host toward tumorigenesis. Under oxidative stress, M-CSF may produce signals that are cumulative/synergistic with host mediators (e.g., low levels of histamine), facilitating tumor-directed expression of decoy receptors and immune suppressive factors (e.g., dTNFR, IL-5, IL-10, TGF-β, PGE2). M-CSF, possessing superior sensitivity and specificity, compared with conventional markers (e.g., CA-125, CA-19-9) is potentially a suitable biomarker for cancer diagnosis and technology development. Systematic monitoring of interactions between resident and recruited cells should provide key information not only about early events in loss of immune surveillance, but it would help making informed decisions for balancing the inherent tumoricidal (Yin) and tumorigenic (Yang) properties of immune sy...

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“…Functionally, some lipids behave as innate immune effectors with anti‐microbial properties (Lee et al, ; Fischer et al, ). Lipids also serve as precursors of important signaling molecules such as phosphatidylinositol phosphates (PIPs) derivatives, nuclear receptors agonists (Schürer, ; Fowler et al, ), and extracellular signaling molecules eicosanoids and specialized pro‐resolving mediators (Schumann, ). Several reports link dietary intake of fatty acids to a propensity for developing irritant and allergic skin reactions to chemicals (Wander et al, ; Barman et al, ).…”

mentioning

confidence: 99%

Phospholipidomic Profile Variation on THP‐1 Cells Exposed to Skin or Respiratory Sensitizers and Respiratory Irritant

Martins

Maciel

Silva

et al. 2016

Journal Cellular Physiology

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Occupational exposure to low molecular weight reactive chemicals often leads to development of allergic reactions such as allergic contact dermatitis and respiratory allergies. Further insights into the interaction of these chemicals with physiopathological relevant cellular models might provide the foundations for novel non-animal approaches to safety assessment. In this work we used the human THP-1 cell line to determine phospholipidome changes induced by the skin sensitizer 1-fluoro-2,4-dinitrobenzene (DNFB), the respiratory allergen hexamethylene diisocyanate (HDI), and the irritant methyl salicylate (MESA). We detected that these chemicals differently induce lipid peroxidation and modulate THP-1 IL-1β, IL-12B, IL-8, CD86, and HMOX1 transcription. Decreased phosphatidylethanolamine content was detected in cells exposed to MESA, while profound alterations in the relative abundance of cardiolipin species were observed in cells exposed to DNFB. All chemicals tested induced a decrease in the relative abundance of plasmanyl phosphatidylcholine species PC (O-16:0e/18:1) and phosphatidylinositol species PI (34:1), while increasing PI (38:4). An increased abundance of oleic acid was observed in the phospholipids of cells exposed to DNFB while a decreased abundance of palmitic acid was detected in cells treated with MESA or DNFB. We conclude that both specific and common alterations at phospholipidome levels are triggered by the different chemicals, while not allowing a complete distinction between them using a Canonical Analysis of Principal Coordinates (CAP). The common effects observed at phospholipids level with all the chemicals tested might be related to unspecific cell cytotoxic mechanisms that nevertheless may contribute to the elicitation of specific immune responses. J. Cell. Physiol. 231: 2639-2651, 2016. © 2016 Wiley Periodicals, Inc.

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The Impact of Macrophage Membrane Lipid Composition on Innate Immune Response Mechanisms

Cited by 3 publications

References 91 publications

Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape

Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape

Chronic Inflammation: Synergistic Interactions of Recruiting Macrophages (TAMs) and Eosinophils (Eos) with Host Mast Cells (MCs) and Tumorigenesis in CALTs. M-CSF, Suitable Biomarker for Cancer Diagnosis!

Phospholipidomic Profile Variation on THP‐1 Cells Exposed to Skin or Respiratory Sensitizers and Respiratory Irritant

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