Involvement of nitric oxide on the peritoneal neutrophil influx induced by staphylococcal enterotoxin B in mouse

Franco‐Penteado, Carla F.; DeSouza, Ivani A.; Teixeira, Simone Aparecida; Ribeiro-DaSilva, G; Nucci, Gilberto De; Antunes, Edson

doi:10.1016/s0041-0101(01)00095-2

Cited by 19 publications

(15 citation statements)

References 16 publications

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“…In contrast, i.p. injection of SEB into mice resulted in an influx of neutrophils into the peritoneal cavity, consistent with previous reports (20). Under these conditions, neutrophil recruitment into the peritoneal cavity was comparable to that observed following i.v.…”

Section: Tlt2 Expression Is Increased In Response To Inflammationsupporting

confidence: 91%

Trem-Like Transcript 2 Is Expressed on Cells of the Myeloid/Granuloid and B Lymphoid Lineage and Is Up-Regulated in Response to Inflammation

King

Herrin

Justement

2006

The Journal of Immunology

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The triggering receptor expressed on myeloid cells (TREM) gene cluster encodes a group of transmembrane proteins that are emerging as important components in innate and adaptive immunity. In both mice and humans, the TREM gene cluster encodes eight receptors; only four of these, however, are direct homologs: TREM-1, TREM-2, TREM-like transcript 1 (TLT1), and TLT2. Of the transmembrane receptors encoded by the four conserved genes within this cluster, TLT2 has not been studied previously. Data presented in this study demonstrate that TLT2 is expressed early in B cell development in conjunction with B220 and is detected on all developing mouse B cell populations as well as B cells in the periphery. TLT2 expression on B cells in the periphery exhibits a distinct hierarchy with the highest detectable levels observed on B1 B cells in the peritoneum. The overall gradation of TLT2 expression on B cells is: B1 > marginal zone/transitional 2 > transitional 1 > follicular. Additionally, TLT2 expression was observed on mouse neutrophils throughout the body. Although monocytes were not observed to express TLT2, resident peritoneal and lung macrophages do express TLT2, suggesting that it is up-regulated in association with terminal differentiation of monocytes. Finally, both neutrophils and macrophages were observed to up-regulate TLT2 expression in vivo in response to inflammatory stimuli, whereas TLT2 expression on B cells remained unchanged. In conclusion, the data suggest that TLT2 may be involved in the innate immune response based on its expression profile and the fact that it is up-regulated in response to inflammation.

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Section: Tlt2 Expression Is Increased In Response To Inflammationsupporting

confidence: 91%

Trem-Like Transcript 2 Is Expressed on Cells of the Myeloid/Granuloid and B Lymphoid Lineage and Is Up-Regulated in Response to Inflammation

King

Herrin

Justement

2006

The Journal of Immunology

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“…Similar to our observations, there is evidence that the treatment of animals with selective inhibitors of iNOS or cNOS enhances the neutrophil migration to in¯ammatory sites (Ialenti et al, 2000;Paul-Clark et al, 2001;McCartney-Francis et al, 2001); on the other hand, other studies contradict our ®ndings, i.e. animals treated with NOS inhibitors, or iNOS7/7 mice, presented a reduction in neutrophil migration to in¯ammatory sites (Ajuebor et al, 1998;Ialenti et al, 2000;Cuzzocrea et al, 2000;Paul-Clark et al, 2001;Franco-Penteado et al, 2001;McCartney-Francis et al, 2001). It is suggested that the suppressor eect of NOS inhibitors upon neutrophil migration could be a consequence Figure 7 Quanti®cation of neutrophil migration into the peritoneal cavity (A), CFU in the peritoneal exudate (B) and survival of iNOS Knockout mice (C) injected with sub-lethal or lethal inoculums of S. aureus.…”

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confidence: 90%

“…In (D) survival of the animals is expressed as per cent survival and was determined daily for 7 days. of vasoconstriction, leading to a reduction in local blood ow, due to the use of high doses and/or systemic administration of the drugs (Ialenti et al, 2000;Paul-Clark et al, 2001;Franco-Penteado et al, 2001). However, a decrease in blood¯ow in the microcirculation cannot alone explain the reduction in neutrophil migration induced by zymosan and carrageenan observed in iNOS7/7 mice (Ajuebor et al, 1998;Cuzzocrea et al, 2000).…”

mentioning

confidence: 99%

Involvement of NO in the failure of neutrophil migration in sepsis induced by Staphylococcus aureus

Crosara-Alberto

Darini

Inoue

et al. 2002

British J Pharmacology

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Sepsis induced by S. aureus was used to investigate whether neutrophil migration failure to infectious focus correlates with lethality in Gram‐positive bacteria‐induced sepsis in mice. By contrast with the sub‐lethal (SL‐group), the lethal (L‐group) intraperitoneal inoculum of S. aureus caused failure of neutrophil migration (92% reduction), high CFU in the exudate, bacteremia and impairment of in vitro neutrophil chemotactic activity. Pre‐treatments of L‐group with adequate doses of aminoguanidine prevented the neutrophil migration failure and improved the survival of the animals (pre‐treated: 43%; untreated: 0% survival). Thus, the impairment of neutrophil migration in the L‐group appears to be mediated by nitric oxide (NO). The injection of S. aureus SL‐inoculum in iNOS deficient (−/−) or aminoguanidine‐treated wild‐type mice (pre‐ and post‐treatment), which did not present neutrophil migration failure, paradoxically caused severe peritonitis and high mortality. This fact is explainable by the lack of NO dependent microbicidal activity in migrated neutrophils. In conclusion, although the NO microbicidal mechanism is active in neutrophils, the failure of their migration to the infectious focus may be responsible for the severity and outcome of sepsis. British Journal of Pharmacology (2002) 136, 645–658; doi:10.1038/sj.bjp.0704734

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“…Although known to be less potent than SEA, SEB provoked marked accumulation of predominately neutrophils in the present study, which exhibited kinetics similar to those reported for SEA-induced leukocyte recruitment (37). Previous investigations have shown that neutrophil recruitment upon challenge with SEB is regulated by migration inhibitory factor and nitric oxide (3,12). Here we show for the first time that MIP-2 and KC are key mediators of SEB-induced neutrophil accumulation in vivo, which suggests that CXC chemokines constitute an important component in superantigen-triggered acute inflammation.…”

Section: Fig 4 Time-dependent Leukocyte Response To Seb Animals Resupporting

confidence: 61%

Staphylococcal Enterotoxin B-Induced Acute Inflammation Is Inhibited by Dexamethasone: Important Role of CXC Chemokines KC and Macrophage Inflammatory Protein 2

Schramm

Thorlacius

2003

Infect Immun

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This study was conducted to examine the anti-inflammatory mechanisms of dexamethasone during leukocyte recruitment and expression of the CXC chemokines macrophage inflammatory protein 2 (MIP-2) (CXCL2) and cytokine-induced neutrophil chemoattractant (KC) (CXCL1) in staphylococcal enterotoxin B (SEB)-induced acute inflammation. To do this, SEB was injected into murine air pouches with or without dexamethasone pretreatment for 2 h. SEB induced infiltration of leukocytes in a dose-and time-dependent manner, with the maximal response observed after 4 h of treatment with 10 g of SEB. The recruited leukocytes comprised more than 77% neutrophils. Moreover, SEB challenge (10 g) provoked time-dependent secretion of CXC chemokines, which peaked after 1 h. Local administration of antibodies against MIP-2 and KC significantly reduced SEB-triggered neutrophil accumulation by 38 and 59%, respectively. Dexamethasone (10 mg kg ؊1 ) significantly decreased neutrophil recruitment by 82% and reduced secretion of MIP-2 and KC by 89 and 85%, respectively, in response to SEB challenge. Our data demonstrate that dexamethasone potently inhibits neutrophil recruitment in SEB-induced inflammation. Moreover, we provide evidence that MIP-2 and KC are key mediators in the neutrophil response to SEB. Furthermore, our findings demonstrate that dexamethasone attenuates SEB-induced expression of MIP-2 and KC. Thus, this study elucidates important signaling pathways of SEB-induced neutrophil recruitment and anti-inflammatory mechanisms of action of dexamethasone.

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Involvement of nitric oxide on the peritoneal neutrophil influx induced by staphylococcal enterotoxin B in mouse

Cited by 19 publications

References 16 publications

Trem-Like Transcript 2 Is Expressed on Cells of the Myeloid/Granuloid and B Lymphoid Lineage and Is Up-Regulated in Response to Inflammation

Trem-Like Transcript 2 Is Expressed on Cells of the Myeloid/Granuloid and B Lymphoid Lineage and Is Up-Regulated in Response to Inflammation

Involvement of NO in the failure of neutrophil migration in sepsis induced by Staphylococcus aureus

Staphylococcal Enterotoxin B-Induced Acute Inflammation Is Inhibited by Dexamethasone: Important Role of CXC Chemokines KC and Macrophage Inflammatory Protein 2

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