Influence of interleukin-1β on bradykinin-induced responses in guinea pig peritoneal macrophages

Böckmann, Sabine; Mohrdieck, K.; Paegelow, I.

doi:10.1007/s000110050401

Cited by 5 publications

(3 citation statements)

References 20 publications

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“…It has been previously reported that BK level is increased in the peritoneal exudates induced by carrageenin in rats [40]. In vitro studies informed us that BK performed its effects on peritoneum mainly via BK-B2 receptor [39,[41][42][43]. However, BK-B2 receptors and their relation with peritoneal fibrosis had never been shown in the EPS model.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Systemic Infusion of Bradykinin on Experimental Peritoneal Fibrosis

Yaşar¹,

Uysal²,

Öztop³

et al. 2015

Osmangazi̇ Journal of Medicine

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Background. Bradykinin (BK) is a proinflammatory peptide that is involved in the inflammation and vascular regulation. Recent studies have indicated that stimulation of BK-B2 receptors may attenuate fibrosis in renal and liver injuries and it is also expressed on neutrophils.Objectives. The aim of this study is to investigate the expression of bradykinin-B2 receptors and to explore the effects of systemic infusion of bradykinin (BK) using histochemical and immunohistochemical methods in a rodent model of chlorhexidine gluconate-induced peritoneal fibrosis.Materials and Methods. In this experimental study, twenty-four male SpragueDawley rats (n=24) were divided into three groups; Control, Chlorhexidine Gluconate (CG) and Chlorhexidine Gluconate+Bradykinin treatment (CG+BK). All animals were euthanized at day 21 and peritoneal tissue samples were taken under anesthesia induced by 50 mg/kg s.c. sodium pentothal. Histological assessments were then performed using hematoxylin and eosin, Periodic Acid-Schiff staining; and antibodies against TGF-β1, MMP-2, PAI-1 and bradykinin-B2 (BK-B2) receptors.Results. Thickness of submesothelial layer, neovascularization, polimorphonuclear granulocytes and fibrosis increased in the CG+BK treatment group. While expression of TGF-β1, MMP-2 and PAI-1 was not significantly different than that of the CG group. Staining of BK-B2 receptors was up-regulated in the submesothelial compact zone of the CG+BK treatment group.Conclusions. The results of our study showed that the stimulation of BK-B2 receptors by systemic BK perfusion did not have any antifibrotic effects in the encapsulating peritoneal sclerosis rat models, and actually, it may even promote fibrosis by aggravating inflammation.

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Section: Discussionmentioning

confidence: 99%

The Effects of Systemic Infusion of Bradykinin on Experimental Peritoneal Fibrosis

Yaşar¹,

Uysal²,

Öztop³

et al. 2015

Osmangazi̇ Journal of Medicine

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“…MA express both BKR1 and BKR2 [ 50 ]. BK also induces TNF- α and IL-1 release from murine MA cell lines [ 52 , 53 ] and stimulates prostaglandin E 2 production from rat peritoneal MA [ 54 ] (Fig. 2 ).…”

Section: Innate Immune Systemmentioning

confidence: 99%

Roles of Immune Cells in Hereditary Angioedema

Ferrara

Cristinziano

Petraroli

et al. 2021

Clinic Rev Allerg Immunol

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Hereditary angioedema (HAE) is a rare genetic disease, characterized by recurrent and unexpected potentially life-threatening mucosal swelling. HAE may be further classified into HAE with C1‐inhibitor deficiency (C1‐INH‐HAE) and HAE with normal C1‐INH activity (nlC1‐INH‐HAE), mostly due to mutations leading to increased vascular permeability. Recent evidence implicates also the innate and adaptive immune responses in several aspects of angioedema pathophysiology. Monocytes/macrophages, granulocytes, lymphocytes, and mast cells contribute directly or indirectly to the pathophysiology of angioedema. Immune cells are a source of vasoactive mediators, including bradykinin, histamine, complement components, or vasoactive mediators, whose concentrations or activities are altered in both attacks and remissions of HAE. In turn, through the expression of various receptors, these cells are also activated by a plethora of molecules. Thereby, activated immune cells are the source of molecules in the context of HAE, and on the other hand, increased levels of certain mediators can, in turn, activate immune cells through the engagement of specific surface receptors and contribute to vascular endothelial processes that lead to hyperpemeability and tissue edema. In this review, we summarize recent developments in the putative involvement of the innate and adaptive immune system of angioedema.

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“…During inflammation, nonneuronal cells such as M ϕ produce a variety of chemical mediators that can act on nociceptive neurons [6]. On the other hand, nociceptive mediators such as bradykinin [7, 8] and substance P [9, 10] act on the immune response and M ϕ functions.…”

Section: Introductionmentioning

confidence: 99%

Methotrexate and Cyclosporine Treatments Modify the Activities of Dipeptidyl Peptidase IV and Prolyl Oligopeptidase in Murine Macrophages

Nascimento

Teixeira

Silveira

2008

Clinical and Developmental Immunology

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Analysis of the effects of cyclosporine A (25–28 mgkg−1) and/or methotrexate (0.1 mgkg−1) treatments on dipeptidyl peptidase IV (DPPIV) and prolyl oligopeptidase (POP) activities and on algesic response in two distinct status of murine macrophages (Mφs) was undertaken. In resident Mφs, DPPIV and POP were affected by neither individual nor combined treatments. In thioglycolate-elicited Mφs, methotrexate increased DPPIV (99–110%) and POP (60%), while cyclosporine inhibited POP (21%). Combined treatment with both drugs promoted a rise (51–84%) of both enzyme activities. Only cyclosporine decreased (42%) the tolerance to algesic stimulus. Methotrexate was revealed to exert prevalent action over that of cyclosporine on proinflammatory Mφ POP. The opposite effects of methotrexate and cyclosporine on POP activity might influence the availability of the nociceptive mediators bradykinin and substance P in proinflammatory Mφs. The exacerbated response to thermally induced algesia observed in cyclosporine-treated animals could be related to upregulation of those mediators.

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Influence of interleukin-1β on bradykinin-induced responses in guinea pig peritoneal macrophages

Abstract: The most likely explanation for the cytokine effects is an influence on the level of the receptor-effector coupling downstream of the agonist binding.

Cited by 5 publications

References 20 publications

The Effects of Systemic Infusion of Bradykinin on Experimental Peritoneal Fibrosis

The Effects of Systemic Infusion of Bradykinin on Experimental Peritoneal Fibrosis

Roles of Immune Cells in Hereditary Angioedema

Methotrexate and Cyclosporine Treatments Modify the Activities of Dipeptidyl Peptidase IV and Prolyl Oligopeptidase in Murine Macrophages

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