Interactions between TLR2, TLR4, and mannose receptors with gp43 from Paracoccidioides brasiliensis induce cytokine production by human monocytes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Estudo da influência da infecção pelo Mycobacterium tuberculosis sobre a replicação do HIV e a imunidade celular em associação com os polimorfismos dos genes tlr2 e tlr4

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Associação de polimorfismos nos genes TLR2 e TLR4 com risco de câncer colorretal esporádico e influência na expressão gênica

Pós-graduação em Genética - IBILCE

Papel de RAGE e TLR4 na modulação da resposta imune inflamatoria em PBMC de pacientes diabéticos e não diabéticos: (estudo in vitro)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Modulação da proliferação, morte celular e expressão gênica de mediadores inflamatórios pela ativação de RAGE e TLR4 em células da resposta imune inata e adaptativa: papel das vias de sinalização p38 MAPK e NF-kB

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Envolvimento de receptores celulares TLR2 e TLR4 e MR na produção in vitro de citocinas por monócitos humanos estimulados com Paracoccidioides brasiliensis

Pós-graduação em Biologia Geral e Aplicada - IBB

O papel de receptores de imunidade inata βGR, MR, TLR2 e TLR4 no reconhecimento da Candida albicans por monócitos humanos estimulados com polissacarídeos extraídos do cogumelo Agaricus brasiliensis

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Associação entre expressão de receptores TLR2 e TLR4 e produção de TNF-alpha e IL-10 por monócitos de gestantes portadoras de pré-eclâmpsia

Preeclampsia (PE) is a pregnancy specific syndrome characterized by a systemic inflammatory response, with higher intensity than that observed in normal pregnancy. Cells of the immune system, such as monocytes and granulocytes are endogenously activated and secrete high levels of free radicals and inflammatory cytokines. The objective of this study was to assess the activation state of monocytes from pregnant women with preeclampsia by endogenous expression of TLR2 e TLR4 receptors and to correlate the expression of TLR2 and TLR4 on monocytes surface of pregnant women with PE with the production of tumor necrosis factor-alpha (TNF- and interleukin-10 (IL-10) by these cells stimulated or not with peptidoglycan (PG) and lipopolysaccharide (LPS), as agonists agents of TLR2 and TLR4, respectively. We evaluated 15 pregnant women with PE, 15 normotensive pregnant women (NT) and 15 non-pregnant (NP). Peripheral blood monocytes were incubates in the presence or absence of LPS or PG. The supernatant obtained after 18h of culture was aspirated and used for TNF- and IL-10 determination by enzyme immunoassay (ELISA). The endogenous expression of TLR2 and TLR4 receptors was evaluated by flow cytometry. Our results showed significant highly concentrations of TNF- and TLR4 expression in monocytes of preeclamptic women when compared with NT and NP. Normal pregnant women presented higher levels of IL-10 in comparison with PE and NP groups. TLR2 expression was similar in the three groups studied. Therefore, our study highlights the important role of TLR4 in PE and the consequent high production of TNF- by monocytes of these patients, as well as the potential mechanism involving low levels of IL-10 in the pathophysiology of the disease. These observations demonstrate the strong link between the pathology of PE and the immune system of these patients

Modulation of Immune Response by RAGE and TLR4 Signalling in PBMCs of Diabetic and Non-Diabetic Patients

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

RANKL expression is differentially modulated by TLR2 and TLR4 signaling in fibroblasts and osteoblasts

Resident, non-immune cells express various pattern-recognition receptors and produce inflammatory cytokines in response to microbial antigens, during the innate immune response. Alveolar bone resorption is the hallmark of destructive periodontitis and it is caused by the host response to bacteria and their mediators present on the biofilm. The balance between the expression levels of receptor activator of nuclear factorkappa B ligand (RANKL) and osteoprotegerin (OPG) is pivotal for osteoclast differentiation and activity and has been implicated in the progression of bone loss in periodontitis. To assess the contribution of resident cells to the bone resorption mediated by innate immune signaling, we stimulated fibroblasts and osteoblastic cells with LPS from. Escherichia coli (TLR4 agonist), Porphyromonas gingivalis (TLR2 and -4 agonist), and interleukin-1 beta (as a control for cytokine signaling through Toll/IL-1receptor domain) in time-response experiments. Expression of RANKL and OPG mRNA was studied by RT-PCR, whereas the production of RANKL protein and the activation of p38 MAPK and NF-kB signaling pathways were analyzed by western blot. We used biochemical inhibitors to assess the relative contribution of p38 MAPK and NF-kB signaling to the expression of RANKL and OPG induced by TLR2, -4 and IL1β in these cells. Both p38 MAPK and NFkB pathways were activated by these stimuli in fibroblasts and osteoblasts, but the kinetics of this activation varied in each cell type and with the nature of the stimulation. E. coli LPS was a stronger inducer of RANKL mRNA in fibroblasts, whereas LPS from P. gingivalis downregulated RANKL mRNA in periodontal ligament cells but increased its expression in osteoblasts. IL-1β induced RANKL in both cell types and without a marked effect on OPG expression. p38 MAPK was more relevant than NF-kB for the expression of RANKL and OPG in these cell types.

The involvement of TLR2 and TLR4 in cytokine and nitric oxide production in visceral leishmaniasis patients before and after treatment with anti-leishmanial drugs

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Interleukin-18 increases TLR4 and mannose receptor expression and modulates cytokine production in human monocytes

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Melatonin attenuates the TLR4-mediated inflammatory response through MyD88-and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of helicobacter pylori eradication on TLR2 and TLR4 expression in patients with Gastric Lesions

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

TLR2 and TLR4 polymorphisms influence mRNA and protein expression in colorectal cancer

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)