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The Pituitary Gland, Psychoneuroimmunology and Infection
Published in Herman Friedman, Thomas W. Klein, Andrea L. Friedman, Psychoneuroimmunology, Stress, and Infection, 2020
Istvan Berczi, Andor Szentivanyi
A lipopolysaccharide binding protein (LBP) was isolated from human and rabbit serum. LBP is a 60 kd glycoprotein and normally is present at 0.5 µg/ml concentration in the serum, but it will rise up to 50 µg/ml, during an acute phase response. LBP is capable of opsonizing of LPS bearing particles which suggests that this protein is necessary for the activation of the complement system by LPS. LBP-LPS complexes were as much as 1,000 fold more active than LPS alone in the induction of TNF or IL-1β. LBP was found to be related to another LPS binding protein of neutrophils called bacterial permeability increasing protein. A 55 kd glycoprotein called CD14 which serves as the receptor for LPS-LBP on monocytes and macrophages. CD14 does not contain a transmembrane domain but holds onto the cell surface by a phosphatidylinositol glycane anchor.91 Other LPS binding proteins have also been identified on various cell types. B lymphocytes do not possess CD14, yet they respond to stimulation by LPS with proliferation and polyclonal immunoglobulin secretion. LPS regulates transcription of IC gene mRNA by the stimulation of the cis-acting nuclear factor NF-KB or OTF-2.91 B lymphocytes of C3H/HeJ mice cannot be activated by LPS for proliferation and polyclonal immunoglobulin secretion. Such mice respond poorly to infection with gram-negative bacteria.72
Heterogeneity Among CD36+ Cells in Normal and Diseased Human Skin
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Of all the macrophage-associated molecules which have been studied thus far, the CD14 antigen and those belonging to the CD11/CD18 complex appear to be some of the more susceptible to differential modulation. However, due to conflicting data in various experimental systems, it is difficult to directly extrapolate published findings to the dermal macrophage population. For example, CD14 is known to bind complexes of lipopolysaccharide (LPS) and LPS-binding protein,114 and thus, may function in the clearance of Gram-negative pathogens during infection. Some investigators reported that IFN-γ and granulocyte macrophage colony-stimulating factor (GM-CSF) downregulate CD14 antigen expression on cultured peripheral blood monocytes,115–117 with a concomitant increase in MHC class II expression, and suggested that this was an activation phenotype for monocytes and macrophages.115 Conversely, others failed to detect an IFN-γ-induced reduction of CD14 antigen on monocytes.118 Preliminary observations in a limited number of biopsies from both AD and psoriatic patients indicated that CD 14 expression on dermal macrophages was enhanced rather than decreased, as compared to noninflamed skin. While these results are contradictory to some in vitro experiments,115–117 one must consider that the cytokine network in vivo is much more complex and additional investigations are obviously necessary to resolve this issue.
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
The role of innate immune response has been suggested in the induction of the early phase of inflammation and stimulation of process of fibrosis.4 The innate immune system plays an important role in the pathogenesis mediated through mast cells, NK cells, macrophages, and DCs.3 The chronic exposure of bacterial lipopolysaccharide (LPS) causes overexpression of the Toll-like receptor (TLR)-4, co-receptors CD14, and MD2 in the lesioned skin of patients with diffuse cutaneous SSc (dcSSc). The CD14 expression can be used as a prognostic marker as it showed significant correlation with progressive and regressive skin disease. The chronic exposure of lipopolysaccharides also showed overexpression of proinflammatory chemokines, and recruitment and activation of macrophages and upregulation of TGF-β signature genes through the Toll-like receptor-4 (TLR4) activation and subsequent myeloid differentiation primary response 88 (MyD88) signaling pathway.4
A review on the reciprocal interactions between neuroinflammatory processes and substance use and misuse, with a focus on alcohol misuse
Published in The American Journal of Drug and Alcohol Abuse, 2023
Anny Gano, Terrence Deak, Ricardo Marcos Pautassi
Moreover, as we already anticipated it has been shown that one of the most severe consequences of AUD, namely the development of liver disease, is dependent upon genes associated with inflammation. More in detail, specific polymorphisms in the Cluster of Differentiation 14 (CD14) were associated, in Indian (68) or Greek (69) patients, with greater susceptibility to liver disease induced by alcohol use. CD14 is a pattern-recognition receptor, associated with inflammatory responses via cytokine production. Direct support for a link between cytokine gene variations and proclivity to AUD, independently of alcohol-induced liver disease, has been provided by Marcos, et al. (70). These researchers found that polymorphisms of IL-10 were associated with a diagnosis of AUD but not with greater risk of alcohol-induced liver disease. Similarly, it has been shown that Spanish men with an AUD diagnosis exhibit polymorphism in the interleukin-1 receptor antagonist gene (IL1RN) (71). Future studies should address whether these polymorphisms are associated with a loss-of-function or gain-of-function, pertinent to understand its potential implication in AUD.
Lactobacillus plantarum-derived extracellular vesicles induce anti-inflammatory M2 macrophage polarization in vitro
Published in Journal of Extracellular Vesicles, 2020
Wanil Kim, Eun Jung Lee, Il-Hong Bae, Kilsun Myoung, Sung Tae Kim, Phil June Park, Kyung-Ha Lee, An Vuong Quynh Pham, Jaeyoung Ko, Sang Ho Oh, Eun-Gyung Cho
Considering that LEVs induced cytokines including IL-1β, GM-CSF and IL-10, which are primarily secreted by macrophages [35,36], in cultured human skin tissues (Figure 2(c); Supplementary Figure S3b), we postulated that they may influence monocyte differentiation and macrophage activation. The mature yet inactive state of macrophages (naïve M0) are differentiated from monocytes that have migrated into tissues and are subsequently polarized into pro-inflammatory M1, or anti-inflammatory and tissue-repairing M2 macrophages, all of which secrete IL-10 [21,35,37]. Once monocytes become differentiated into the macrophage lineage, they reportedly express several markers including cluster of differentiation 14 (CD14), intercellular adhesion molecule 1 (ICAM-1) and C-C chemokine receptor type 2 (CCR2) in different patterns. CD14, as a co-receptor of TLR4, detects bacterial LPS and is highly expressed in monocytes and most tissue macrophages [38]. ICAM1, one of the specific markers of activated macrophages, participates in the binding of immune cells to endothelial cells for extravasation [39,40]. Meanwhile, CCR2, a receptor for CCL2 (monocyte chemoattractant protein-1), has a unique role in monocyte chemotaxis and is lost upon monocyte differentiation [41]. Thus, as a first step, we investigated whether LEV treatment can induce the differentiation of human THP1 monocytic cells towards the macrophage lineage by examining the expression patterns of these genes.
NHDL, a recombinant VL/VH hybrid antibody control for IgG2/4 antibodies
Published in mAbs, 2020
Corinna Lau, Martin Berner McAdam, Grethe Bergseth, Algirdas Grevys, Jack Ansgar Bruun, Judith Krey Ludviksen, Hilde Fure, Terje Espevik, Anders Moen, Jan Terje Andersen, Tom Eirik Mollnes
Since the IgG2/4 backbone is already used in a marketed product, we constructed two such antibodies in our laboratory for neutralization of human and porcine CD14 in different sepsis models, and reported the results of studies exploring their properties.12,24,25 CD14 is a cofactor of several Toll-like receptors (TLRs), including TLR2 and TLR4, that are the second branch of innate immunity against pathogenic and endogenous danger. CD14 facilitates pattern recognition of mainly acylated structural components like Gram-negative bacterial lipopolysaccharide (LPS), and induces the expression of proinflammatory cytokines and type I interferons through TLR signaling.26–29 Recently, increased plasma levels of a 13 kDa soluble CD14 subtype (sCD14-ST; presepsin) have emerged as an early sepsis marker.30 Although the blocking of CD14 has been shown to be beneficial in various experimental sepsis models, the strategy has failed in clinical trials. Due to signaling crosstalk between CD14/TLRs and complement, a more potent therapeutic strategy to treat sepsis, however, seems to be the combined inhibition of CD14 and complement, as successfully demonstrated in mice and porcine models.25,31,32 This approach may also be effective in the treatment of acute sterile inflammatory conditions like trauma and ischemia-reperfusion injury.32,33