Cytokine Production in Lipopolysaccharide-exposed Rat Lung Pericytes

Edelman, David A.; Yang, Jiang; Tyburski, James G.; Wilson, Robert F.; Steffes, Christopher P.

doi:10.1097/ta.0b013e31802dd712

Cited by 40 publications

(30 citation statements)

References 27 publications

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“…Reduction of NF-κB, ERK1/2 and JNK activation in adipose tissue of rAd-GLP-1-treated mice Activation of NF-κB is involved mainly in the expression of inflammatory responsive genes such as Il6 and Tnfa [20,21]. As pro-inflammatory cytokine production is reduced by rAd-GLP-1 treatment, we used EMSA to examine the activation of NF-κB in epididymal fat at 2 weeks after rAd-GLP-1 treatment.…”

Section: Resultsmentioning

confidence: 99%

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Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

et al. 2012

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Aims/hypothesis Obesity and insulin resistance are associated with low-grade chronic inflammation. Glucagon-like peptide-1 (GLP-1) is known to reduce insulin resistance. We investigated whether GLP-1 has anti-inflammatory effects on adipose tissue, including adipocytes and adipose tissue macrophages (ATM). Methods We administered a recombinant adenovirus (rAd) producing GLP-1 (rAd-GLP-1) to an ob/ob mouse model of diabetes. We examined insulin sensitivity, body fat mass, the infiltration of ATM and metabolic profiles. We analysed the mRNA expression of inflammatory cytokines, lipogenic genes, and M1 and M2 macrophage-specific genes in adipose tissue by real-time quantitative PCR. We also examined the activation of nuclear factor κB (NF-κB), extracellular signalregulated kinase 1/2 and Jun N-terminal kinase (JNK) in vivo and in vitro. Results Fat mass, adipocyte size and mRNA expression of lipogenic genes were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Macrophage populations (F4/80 + and F4/80 + CD11b + CD11c + cells), as well as the expression and production of IL-6, TNF-α and monocyte chemoattractant protein-1, were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Expression of M1-specific mRNAs was significantly reduced, but that of M2-specific mRNAs was unchanged in rAd-GLP-1-treated ob/ob mice. NF-κB and JNK activation was significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Lipopolysaccharide-induced inflammation was reduced by the GLP-1 receptor agonist, exendin-4, in 3T3-L1 adipocytes and ATM. Conclusions/interpretation We suggest that GLP-1 reduces macrophage infiltration and directly inhibits inflammatory pathways in adipocytes and ATM, possibly contributing to the improvement of insulin sensitivity.

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Section: Resultsmentioning

confidence: 99%

“…4a). Because ERK1/2 and JNK are involved in NF-κB activation [21][22][23], we examined the activation of ERK1/2 and JNK in epididymal fat by western blot. We found that phosphorylation of ERK1/2 and JNK was decreased in rAd-GLP-1-treated ob/ob mice compared with untreated, rAd-βgal-treated and pair-fed ob/ob mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

et al. 2012

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“…The significance of pericytes in the regulation of T cell responses is further strengthened from observations that immunomodulatory cytokines/growth factors and adhesion molecules may be secreted or elaborated from pericytes under certain conditions (17)(18)(19). Recently, elegant work by Stark et al (20) established the instructive role of NG2 + pericytes on innate myeloid leukocytes for their homing into sites of inflammation as a consequence of upregulating ICAM-1 expression and macrophage migration inhibitory factor-mediated signaling.…”

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Tumor-Derived Vascular Pericytes Anergize Th Cells

Bose

Barik

Banerjee

et al. 2013

The Journal of Immunology

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Immune evasion within the tumor microenvironment supports malignant growth and is also a major obstacle for successful immunotherapy. Multiple cellular components and soluble factors coordinate to disrupt protective immune responses. Although stromal cells are well-known for their parenchymal supportive roles in cancer establishment and progression, we demonstrate for the first time, to our knowledge, that tumor-derived vascular pericytes negatively influence CD4+ T cell activation and proliferation, and promote anergy in recall response to Ag by CD4+CD44+ T cells via regulator of G protein signaling 5– and IL-6–dependent pathways. Our data support a new specific role for tumor-derived pericytes in the immune evasion paradigm within the tumor microenvironment and suggest the targeting of these cell populations in the context of successful immunotherapeutics for the treatment of cancer.

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“…In a series of pioneering works by Edelman et al (13)(14)(15), the authors demonstrated the expression of TLR4 by Western blotting in rat lung pericytes (13) as well as increased vessel permeability (14) and production of IL-1␤ (15) in LPS-treated pericytes, suggesting for the first time an active role of pericytes in the inflammatory cascade. More recently, the release of nitric oxide and several cytokines and chemokines by mouse brain vascular pericytes in response to LPS has been reported (16).…”

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confidence: 99%

Lipopolysaccharide Activates Toll-like Receptor 4 (TLR4)-mediated NF-κB Signaling Pathway and Proinflammatory Response in Human Pericytes

Guijarro‐Muñoz

Compte

Álvarez-Cienfuegos

et al. 2014

Journal of Biological Chemistry

255

201

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Background: Endothelial cells are well known inflammatory effectors, but TLR4 expression and function in human pericytes have not been addressed. Results: Pericytes express TLR4, and stimulation with LPS or HMGB1 promotes cytokine and chemokine secretion and overexpression of adhesion molecules via NF-B. Conclusion: TLR4 activation in pericytes triggers a proinflammatory and proangiogenic program. Significance: Pericytes are active players in inflammatory responses beyond their homeostatic role.

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Cytokine Production in Lipopolysaccharide-exposed Rat Lung Pericytes

Cited by 40 publications

References 27 publications

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

Tumor-Derived Vascular Pericytes Anergize Th Cells

Lipopolysaccharide Activates Toll-like Receptor 4 (TLR4)-mediated NF-κB Signaling Pathway and Proinflammatory Response in Human Pericytes

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