Effect of angiotensin II and losartan on the phagocytic activity of peritoneal macrophages from Balb/C mice

Belline, Paula; Melo, Patrı́cia da Silva; Haun, Marcela; Palhares, Fernanda Boucault; Bôer, Patrícia Aline; Gontijo, José Antônio Rocha; Figueiredo, José Francisco

doi:10.1590/s0074-02762004000200009

Cited by 11 publications

(5 citation statements)

References 24 publications

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“…Moreover, ANG II suppressed the transcript abundance of AGTR1 and ACE in neutrophils, suggesting that ANG production is autoregulated by a negative feedback loop in these cells. Our data are consistent with previously published reports indicating that: ANG II, via AGTR1 on immune cells, regulates cellular immune responses through a calcineurin‐dependent pathway (Nataraj et al, ); ANG II stimulates phagocytic activity and superoxide production by murine macrophages (Belline et al, ); ANG II activates human neutrophils by enhancing the DNA‐binding activity of NFKB and by increasing the intracellular and extracellular production of superoxide anions and reactive oxygen species through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (El Bekay et al, ); and ANG II, acting via AGTR1, is a strong chemoattractant that stimulates N‐formylmethionyl‐leucyl‐phenylalanine‐dependent neutrophil recruitment in the human lung (Raiden et al, ).…”

Section: Discussionsupporting

confidence: 92%

Angiotensin II increases sperm phagocytosis by neutrophils in vitro: A possible physiological role in the bovine oviduct

Marey

Yousef

Liu

et al. 2016

Molecular Reproduction Devel

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This study aimed to investigate the possible effects of the vasoactive peptide angiotensin II (ANG II), secreted by bovine oviduct epithelial cells, on the in vitro phagocytic activity of polymorphonuclear leukocytes, specifically neutrophils, towards sperm. The measured concentrations of ANG II in oviduct flushes and conditioned medium from primary bovine oviduct epithelial culture ranged from 10(-10) to 10(-11) M. In our experiments, neutrophils were incubated for 2 hr with ANG II (0, 10(-11) , 10(-10) , 10(-9) , and 10(-8) M). Phagocytosis and superoxide production were then assessed by co-incubation of these neutrophils with sperm pretreated to induce capacitation, revealing a dose-dependent increase in both metrics by ANG II. This stimulatory effect of ANG II was eliminated by losartan, an angiotensin receptor type 1 (AGTR1) antagonist. ANG II also suppressed neutrophil transcription of angiotensin converting enzyme-1 (ACE) and AGTR1, but not AGTR2, suggesting the involvement of the AGTR1 receptor-mediated pathway in the response to sperm. Scanning electron microscopy further revealed that incubation of neutrophils with ANG II stimulated the formation of DNA-based extracellular traps for sperm entanglement. The addition of prostaglandin E2 at concentrations found in the oviduct suppressed the ANG II-stimulated phagocytic activity of neutrophils towards sperm. Thus the physiological levels of ANG II stimulate neutrophil phagocytosis of sperm in vitro, and suggest that an angiotensin/prostaglandin E2 system may fine-tune the local immune response that fosters sperm survival in the bovine oviduct. Mol. Reprod. Dev. 83: 630-639, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 92%

Angiotensin II increases sperm phagocytosis by neutrophils in vitro: A possible physiological role in the bovine oviduct

Marey

Yousef

Liu

et al. 2016

Molecular Reproduction Devel

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“…Other cytokines, such as TGF-β2, TGF-β3, platelet-derived growth factor, fibroblast growth factor-2, and connective tissue growth factor69 are involved, together with plasminogen activator inhibitor-1,70 in the initiation of fibrosis. There is also evidence that angiotensin II induces fibronectin expression in mesothelial cells via extracellular-signal-regulated kinase 1 (ERK-1), ERK2 and mitogen-activated protein kinase (MAPK)71,72 and that it takes part in the membrane's cellular immune response 73…”

Section: Introductionmentioning

confidence: 99%

Protective measures against ultrafiltration failure in peritoneal dialysis patients

Aguirre

Abensur

2011

Clinics

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Ultrafiltration failure in patients undergoing peritoneal dialysis is a condition with an incidence that increases over time. It is related to increased cardiovascular morbidity and mortality and is a major cause of the abandonment of the treatment technique. Because the number of patients undergoing renal replacement therapy is increasing with society aging and because approximately 10% of this population is treated with peritoneal dialysis, this matter is becoming more common in everyday practice for clinicians involved in the care of patients with chronic renal failure. In this review, we summarize the available measures used to prevent and treat ultrafiltration failure and the current state of research in the field, both in the experimental and clinical settings, focusing on the possible clinical applications of recent findings.

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“…The reaction was terminated by placing the tubes in ice for 5 min. The production of superoxide anion was monitored spectrophotometrically (UV-1800 UV-VIS spectrophotometer, Shimadju, Japan) at 550 nm in reference to the blank [55]. The amount of superoxide anion production was calculated by the following formula:…”

Section: Assessment Of O 2 − and No Production In Synovial Tissuementioning

confidence: 99%

Neutralization of MMP-2 and TNFR1 Regulates the Severity of S. aureus-Induced Septic Arthritis by Differential Alteration of Local and Systemic Proinflammatory Cytokines in Mice

2017

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Despite advancement in the field of antibiotics septic arthritis remains a serious concern till date. Staphylococcus aureus is the most common bacterium that causes septic arthritis. Severity of this disease is directly correlated with chronic inflammation induced by proinflammatory cytokines like TNF-α, interleukin (IL)-1β, IL-6, and induction of matrix metalloproteinases (MMPs) including MMP-2. The objective of our study was to evaluate the role of MMP-2 and tumor necrosis factor receptor 1 (TNFR1) in the pathogenesis of S. aureus infection-induced septic arthritis. Mice were infected with live S. aureus (5 × 10 cells/ml) followed by administration of MMP-2 inhibitor and TNFR1 antibody. Arthritis index showed highest reduction in severity of arthritis in mice treated with both MMP-2 inhibitor and TNFR1 antibody after infection. Combined neutralization of MMP-2 and TNFR1 led to marked diminution in bacterial count in the combined group. Lowest levels of pro inflammatory cytokines like TNF-α, IL-1β, IL-6, and IFN-γ were observed in both serum and synovial tissues indicating maximum protection in S. aureus arthritis during combination treatment. Increment in the level of IL-10 in the combination group could be positively correlated with the recovery of arthritis. Similarly, expressions of COX-2 and iNOS, markers of acute inflammation were also significantly reduced in the combination group due to resolution of inflammation. Levels of O2 and NO also showed a significant fall in case of the group treated with MMP-2 inhibitor and TNFR1 antibody both. Neutralization of both MMP-2 and TNFR1 caused rapid decline in recruitment of neutrophil and macrophages in the synovial tissues as evident from reduced MPO and MCP-1 levels, respectively, compared to other groups. Overall, it can be suggested that administration of MMP-2 inhibitor and TNFR1 antibody in combination is protective against the severity of inflammation and cartilage destruction associated with S. aureus infection-induced septic arthritis by altering the levels of cytokines.

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Effect of angiotensin II and losartan on the phagocytic activity of peritoneal macrophages from Balb/C mice

Cited by 11 publications

References 24 publications

Angiotensin II increases sperm phagocytosis by neutrophils in vitro: A possible physiological role in the bovine oviduct

Angiotensin II increases sperm phagocytosis by neutrophils in vitro: A possible physiological role in the bovine oviduct

Protective measures against ultrafiltration failure in peritoneal dialysis patients

Neutralization of MMP-2 and TNFR1 Regulates the Severity of S. aureus-Induced Septic Arthritis by Differential Alteration of Local and Systemic Proinflammatory Cytokines in Mice

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