Role of Cytokines in the Maturation and Function of Macrophages

Keisari, Yona; Robin, Guy; Nissimov, L.; Wang, Hongbin; Mesika, Adi; Dimri, Rachel; Ofek, Itzhak

doi:10.1007/0-306-46831-x_7

Cited by 4 publications

(3 citation statements)

References 76 publications

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“…demonstrates that these cells also showed a dramatic increase in surface CD36 expression that correlated with this differentiation process. Thus, THP‐1 cells appear to possess the same characteristics as normal human monocytes of increased CD36 expression as they differentiate into macrophages 18,19 …”

Section: Resultsmentioning

confidence: 99%

Peroxisome‐proliferator‐activated‐receptor gamma (PPARγ) independent induction of CD36 in THP‐1 monocytes by retinoic acid

Han

Sidell

2002

Immunology

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SUMMARYRetinoic acid (RA) has been shown to regulate cellular growth and differentiation of a variety of cell types, including cells of the myelomonocytic lineage. We used the monocytic leukaemia cell line THP-1, which differentiates to macrophages in response to phorbol 12-myristate 13-acetate (PMA), to investigate the regulation by RA of genes in the scavenger receptor type B family (CD36) in human monocyte/macrophages. Reverse transcription-polymerase chain reaction and flow cytometry demonstrated that, like PMA and the natural peroxisomeproliferator-activated receptor-c (PPARc) ligand 15d-PGJ2, RA induced CD36 gene expression in these cells. Moreover, RA plus 15d-PGJ2 further enhanced CD36 protein and mRNA levels over that seen with the RA or PPARc compounds alone. The PPARc antagonist GW9662 was shown to block completely PPARc-ligand induction of CD36 gene expression, but had little effect on the action of RA. Our data indicated that RXR-and RAR-specific ligands (LG153 and TTNPB, respectively) were each alone able to increase CD36 mRNA and surface protein levels. By using calphostin C, a specific protein kinase C (PKC) inhibitor, we demonstrated that induction of CD36 by PMA, as well as by PPARc and RXR ligands were dependent upon PKC activation. In contrast, activation of CD36 through the RAR pathway was not affected by inhibition of PKC activity. Taken together, these data demonstrate that RA can up-regulate CD36 expression in human monocytes/macrophages. This regulation appears to be predominantly mediated through the RAR/RXR pathway of action and, unlike previously described methods of CD36 modulation, is independent of PPARc and PKC signalling. This study suggests a possible role for RA in physiological processes involving the scavenger receptor function in cells of the monocyte/ macrophage lineage.

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Section: Resultsmentioning

confidence: 99%

Peroxisome‐proliferator‐activated‐receptor gamma (PPARγ) independent induction of CD36 in THP‐1 monocytes by retinoic acid

Han

Sidell

2002

Immunology

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“…The mononuclear fraction was separated on Ficoll-Hypaque (19), and adherent monocyte monolayers (5 ϫ 10 6 cells/ml in a tissue culture flask with a surface area of 75 cm 2 ) were reconstituted with RPMI-1640 supplemented with 100 g/ml of streptomycin, 100 U/ml of penicillin, 300 g/ml of glutamine, and 10% newborn bovine serum. Cultured cells were further incubated for 10 to 14 days in the presence of 100 U/ml of granulocyte-macrophage colony-stimulating factor (Behringwerke, Marburg, Germany) to obtain monocyte-derived macrophages (MoDM) and to promote MR expression (21).…”

Section: Animalsmentioning

confidence: 99%

NoncapsulatedKlebsiella pneumoniaeBearing Mannose-Containing O Antigens Is Rapidly Eradicated from Mouse Lung and Triggers Cytokine Production by Macrophages following Opsonization with Surfactant Protein D

et al. 2005

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To better understand the relationship between the surface polysaccharides of pulmonary pathogens and components of the lung innate immune system, we employed selected serotypes of Klebsiella pneumoniae expressing distinct capsular polysaccharides and/or O antigen in a murine model of K. pneumoniae infection. In addition, we examined the effect of surfactant protein D (SP-D) on the cytokine response of human monocyte-derived macrophages to these serotypes in vitro. Noncapsulated mannose-containing O3 serotypes (K50/n and K55/n), which react efficiently with SP-D in vitro, triggered high levels of interleukin-1␤ (IL-1␤) and IL-6 production. In vivo, they were more efficiently cleared from the lungs of mice but not from macrophage-depleted mice. They also were more efficiently internalized by alveolar macrophages in vivo. In contrast, galactose-containing O1 serotypes (K2/n and K21a/n), which interact poorly with SP-D, exhibited significantly lower cytokine production and less efficient pulmonary clearance and were ineffectively internalized by alveolar macrophages. These findings are consistent with in vitro results showing that production of IL-1␤ and IL-6 mRNA and IL-6 protein by human macrophages exposed to mannose-bearing Klebsiella O serotypes is significantly increased by SP-D. Thus, survival of inhaled bacteria in the lung depends partially on the lipopolysaccharide structure of the bacteria and their interactions with innate immunity components. We speculate that an imbalance of host SP-D and therefore cytokine levels may result in high susceptibility of the host to the pathogen.

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“…In our initial experiments to investigate regulation of CD36 expression on cells of the monocyte/macrophage lineage, we have utilized the well‐characterized human monocyte cell line THP‐1, which can be induced to differentiate into macrophages by a variety of stimuli including PMA, GM‐CSF, and IL‐4 21,25,26. To assess surface protein levels of CD36, cells were stained with R ‐phycoerythrin ( R ‐PE)‐conjugated mouse antihuman CD36 monoclonal antibody (PharMingen) and analyzed by flow cytometry.…”

Section: Regulation Of Cd36 Expression On Nonadherent Monocytes/macromentioning

confidence: 99%

Regulation and Modulation of Abnormal Immune Responses in Endometriosis

Sidell

Han

Parthasarathy

2002

Annals of the New York Academy of Sciences

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There is ample evidence demonstrating that endometriosis is accompanied by inflammatory reactions in the peritoneum, resulting in abnormal levels of a variety of cytokines and chemokines in the peritoneal fluid. Among the immunological parameters that have been shown to be altered in the peritoneal cavity of women with endometriosis, an increase in the number of activated nonadherent macrophages that show reduced surface expression of scavenger receptors has been observed. The cause-and-effect relationship between aberrant peritoneal macrophage activity and endometriosis is still unknown. We have demonstrated that steroid hormone receptor agonists and antagonists [e.g., retinoids, antiglucocorticoids, ligands to peroxisome proliferator activated receptors (PPARs)] can regulate macrophage functions in ways that could either suppress or stimulate the growth of ectopic endometrial lesions. Our studies include a number of relevant findings: (1) RU486, acting as an antioxidant, can suppress activation of NFkappaB, a nuclear transcription factor that affects the expression of several inflammatory genes such as those for MCP-1, GM-CSF, CSF-1, and various adhesion molecules; (2) IL-6 secretion from a variety of cell types including endometrial cells is inhibited by retinoic acid; and (3) retinoids and PPARgamma ligands can upregulate the expression of scavenger receptors in cells of the monocyte/macrophage lineage. These observations, combined with the possibility that macrophage activity may play a fundamental role in endometriosis, suggest that pharmacologic manipulation of macrophage function may provide a novel mechanism for treating this disease.

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Role of Cytokines in the Maturation and Function of Macrophages

Cited by 4 publications

References 76 publications

Peroxisome‐proliferator‐activated‐receptor gamma (PPARγ) independent induction of CD36 in THP‐1 monocytes by retinoic acid

Peroxisome‐proliferator‐activated‐receptor gamma (PPARγ) independent induction of CD36 in THP‐1 monocytes by retinoic acid

NoncapsulatedKlebsiella pneumoniaeBearing Mannose-Containing O Antigens Is Rapidly Eradicated from Mouse Lung and Triggers Cytokine Production by Macrophages following Opsonization with Surfactant Protein D

Regulation and Modulation of Abnormal Immune Responses in Endometriosis

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