Radiodetoxified Endotoxin—Induced Tolerance Alters Monocyte but Not Neutrophil CD11b and CD18 Expression in Response to Lipopolysaccharide

Connall, Timothy; Zhang, Jing; Vaziri, N. D.; Schwartz, Robert J.; Kaupke, Charles J.; Oveisi, Fariba; Wilson, Samuel E.

doi:10.1001/archsurg.1994.01420350051005

Cited by 11 publications

(6 citation statements)

References 33 publications

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“…The observed LPS-induced decline in CD18 MFI was unexpected, but the interesting findings by Wong et al allow us to raise the hypothesis that our findings reflect an adequate immune response to acute LPS-induced inflammation with a profitable downregulation of CD18 and a subsequent attenuated inflammatory response. Findings similar to ours have been described in vivo on neutrophils in LPS-challenged rodents [20], in which sham treatment (saline, anaesthesia) per se decreased MFI CD11a ⁄ CD18 at 6 h, and LPS contributed with a further decline at 1 and 6 h. CD18 was downregulated by LPS in monocytes in a murine study [28]. In contrast, Rezaie-Majd et al [18] found upregulation of CD18 in stimulated PBMC, and the discrepancy between their and our results could be explained by the use of TNF-a, and not LPS, as stimulus.…”

Section: Discussionsupporting

confidence: 88%

“…allow us to raise the hypothesis that our findings reflect an adequate immune response to acute LPS‐induced inflammation with a profitable downregulation of CD18 and a subsequent attenuated inflammatory response. Findings similar to ours have been described in vivo on neutrophils in LPS‐challenged rodents [20], in which sham treatment (saline, anaesthesia) per se decreased MFI CD11a/CD18 at 6 h, and LPS contributed with a further decline at 1 and 6 h. CD18 was downregulated by LPS in monocytes in a murine study [28]. In contrast, Rezaie‐Majd et al.…”

Section: Discussionsupporting

confidence: 85%

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Dynamic Expression of the Signal Regulatory Protein α and CD18 on Porcine PBMC During Acute Endotoxaemia

et al. 2008

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Endotoxaemia elicits a massive inflammatory insult affecting the β2 integrin CD18. Being an adhesion molecule, CD18 is pivotal in inflammation and, moreover, exiting data suggest that CD18 is a lipopolysaccharide (LPS) receptor. Early LPS‐induced inflammation is regulated by the signal regulatory protein (SIRPα), which is identical to the porcine panmyelocytic marker swine CD workshop 3 (SWC3), and LPS‐induced downregulation of SIRPα has been described in vitro. The dynamic SIRPα/SWC3 and CD18 expression on peripheral blood mononuclear cells (PBMC) in vivo during LPS‐induced inflammation is the focus of this study. Pigs were randomized into LPS (n = 12) or control (n = 6) groups. At start 0 min, LPS infusion was stepwise (2.5–15 μg/kg/h, 30 min) followed by maintenance infusion (2.5 μg/kg/h, 330 min). PBMC were isolated at 0, 60, 240 and 360 min, and two‐colour flow cytometry was performed using monoclonal antibodies identifying SWC3 and CD18. Viability was tested using 7‐amino‐actinomycin D. LPS dramatically changed the relative distribution of circulating myeloid cells. At 60 min monocytes disappeared. This was followed by reappearance of a distinct population with low CD18 and SIRPα/SWC3 expression. Cell sorting showed that the appearing population comprised band neutrophils and apoptotic/dead cells. The remaining monocytes expressed less CD18 at 360 min than the controls (P = 0.03). The appearance of a distinct cell population comprising apoptotic cells and band neutrophils consistent with LPS‐induced apoptosis, and decreased CD18 expression on monocytes suggests that early CD18 downregulation is profitable for the host in a situation with an intense LPS stimulus.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 85%

Dynamic Expression of the Signal Regulatory Protein α and CD18 on Porcine PBMC During Acute Endotoxaemia

et al. 2008

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“…Pretreatment of macrophages with RD-LPS induces tolerance of the cells towards NO induction by toxic LPS. Second, like LPS, RD-LPS induces CD11b and CD18 integrin expression on PMN [37]. Furthermore, RD-LPS reduces lethality in mice after induction of bacterial peritonitis [37].…”

Section: Induction Of Tlr-4 Expressionmentioning

confidence: 95%

“…Furthermore, RD-LPS reduces lethality in mice after induction of bacterial peritonitis [37]. And third, RD-LPS increases the production of white blood cells in healthy animals [37], which might be an extra benefit because immediately after infection, a systemic leukopenia is established [93].…”

Section: Induction Of Tlr-4 Expressionmentioning

confidence: 99%

The toll-like receptor-4 (TLR-4) pathway and its possible role in the pathogenesis ofEscherichia colimastitis in dairy cattle

et al. 2007

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-Mastitis is one of the most costly production diseases in the dairy industry that is caused by a wide array of microorganisms. In this review, we focus on the Gram-negative Escherichia coli infections that often occur at periods when the innate immune defence mechanisms are impaired (i.e., parturition through the first 60 days of lactation). There is substantial evidence demonstrating that at these periods, the expected influx of polymorphonuclear neutrophil leukocytes (PMN) into the mammary gland is delayed during inflammation after intramammary infection with E. coli. Here, we provide some hypotheses on the potential mechanisms of action on how the disease may develop under circumstances of immunosuppression, and describe the potential involvement of the toll-like receptor-4 signal transduction pathway in the pathogenesis of E. coli mastitis. In addition, some ideas are proposed to help prevent E. coli mastitis and potentially other diseases caused by Gram-negative infections in general.

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“…Thus, we suggest that gamma-ray irradiation modified that part of the LPS molecule complex, possibly in the lipid A moiety [22], which is known to be responsible for toxicity including the enhanced production of above cytokines. However, other parts of the irradiated molecule could activate their specific binding sites, leading to the observed effects of RD-LPS [17,[25][26][27].…”

Section: Discussionmentioning

confidence: 99%

Radiodetoxified Lipopolysaccharide Fails to Activate the Hypophyseal- Pituitary-Adrenal Axis in the Rat

Barna

Bertók

Koenig

et al. 2000

Neuroimmunomodulation

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Lipopolysaccharide (LPS) is known to raise the concentration of the circulating stress hormones such as ACTH, corticosterone and β-endorphin. This effect of endotoxin is mediated by different immune system-released hormone-like factors (e.g. interleukins, tumor necrosis factor etc.). Gamma-ray irradiation of LPS alters its biological properties and results in a radiodetoxified LPS preparation with numerous beneficial effects and decreased toxicity. In this study we compared the neuroendocrine effects of a commercial LPS and our native and radiodetoxified LPS preparations in rats. Plasma ACTH, corticosterone and β-endorphin levels were measured by specific radioimmunoassays 120 min after intraperitoneal LPS administration. Control animals were injected with saline. Results show a dramatic increase in all hormones after administration of commercial and our native LPS preparation. Hormone levels in saline-injected controls and radiodetoxified LPS-treated rats did not rise significantly. These results suggest that radio-detoxification disintegrated that part of the LPS molecule complex which is responsible for toxicity including an enhanced production of cytokines, which trigger the hypothalamo-pituitary-adrenal axis.

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Radiodetoxified Endotoxin—Induced Tolerance Alters Monocyte but Not Neutrophil CD11b and CD18 Expression in Response to Lipopolysaccharide

Cited by 11 publications

References 33 publications

Dynamic Expression of the Signal Regulatory Protein α and CD18 on Porcine PBMC During Acute Endotoxaemia

Dynamic Expression of the Signal Regulatory Protein α and CD18 on Porcine PBMC During Acute Endotoxaemia

The toll-like receptor-4 (TLR-4) pathway and its possible role in the pathogenesis ofEscherichia colimastitis in dairy cattle

Radiodetoxified Lipopolysaccharide Fails to Activate the Hypophyseal- Pituitary-Adrenal Axis in the Rat

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