<b>Avian Inflammatory Macrophage Function:</b> Shifts in Arachidonic Acid Metabolism, Respiratory Burst, and Cell-Surface Phenotype During the Response to Sephadex

Golemboski, Karen A.; Whelan, Jay; Shaw, Stephen B.; Kinsella, John E.; Dietert, R. R.

doi:10.1002/jlb.48.6.495

Cited by 30 publications

(9 citation statements)

References 27 publications

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“…AA infusions trigger rapid increases the PVR and PAP without affecting the cardiac output (Wideman et al, 2005a), and the TxA 2 mimetic U44069 is an extremely potent vasoconstrictor in broilers (Wideman et al, 1999(Wideman et al, , 2005aChapman and Wideman, 2006b). Activated chicken macrophages transiently increase their production of TxA 2 (Golemboski et al, 1990). We reasoned that a pharmacologic blockade of COX-1 and COX-2 sufficient to eliminate the PH caused by an i.v.…”

Section: Introductionmentioning

confidence: 98%

Broiler pulmonary hypertensive responses during lipopolysaccharide-induced tolerance and cyclooxygenase inhibition

2009

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Bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary hypertension (PH) characterized by an increase in pulmonary arterial pressure (PAP) that reaches a peak value within 20 to 25 min and then gradually subsides within 60 min. As the PAP subsides PH cannot be reinitiated, signifying the onset of a period of tolerance (refractoriness) to repeated LPS exposure. The present study was conducted to determine the duration of this tolerance, and to evaluate key mediators thought to contribute to LPS-mediated PH in broilers. Tolerance was shown to persist for 4 to 5 d after the initial exposure to LPS. In tolerant broilers supramaximal i.v. injections of LPS did not reinitiate PH, nor was a significant modulatory role for nitric oxide demonstrated. The pulmonary vasculature of tolerant broilers remains responsive to the thromboxane A(2) (TxA(2)) mimetic U44069, 5-hydroxytryptamine (5-HT, serotonin), and constitutive nitric oxide. Meclofenamate successfully blocked the conversion of arachidonic acid to vasoconstrictive eicosanoids such as TxA(2); nevertheless, meclofenamate failed to inhibit PH in response to LPS. Therefore, TxA(2) does not appear to be the primary vasoconstrictor involved in the PH response to LPS and neither does 5-HT. Broilers emerging from tolerance 5 d after the initial exposure to LPS exhibited interindividual variation in their PH responsiveness to a second LPS injection, ranging from zero response (individuals that remain fully tolerant) to large increases in PAP (post-tolerant individuals). Tolerance might be an important compensatory or protective mechanism for broilers whose pulmonary vascular capacity is marginally adequate under optimal conditions, and whose respiratory systems are chronically challenged with LPS in commercial production facilities. The key vasoconstrictors responsible for the PH elicited by LPS remain to be determined.

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Section: Introductionmentioning

confidence: 98%

Broiler pulmonary hypertensive responses during lipopolysaccharide-induced tolerance and cyclooxygenase inhibition

2009

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“…Monocytes-macrophages kill internalized pathogens mainly by secreting either reactive ROI (primarily H 2 O 2 and O 2 ; Golemboski et al, 1990) and RNI (derived from NO; Sung et al, 1991;Qureshi et al, 1993), both of which play important roles in resisting Salmonella infection (Raupach and Kaufmann, 2001;Withanage et al, 2005). To understand the mechanism of differences in killing ability of monocytes-macrophages to Salmonella Pullorum induced by methyltestosterone, ROI and RNI output was measured, and the results suggested that only ROI contributed to the differences.…”

Section: Discussionmentioning

confidence: 99%

Effects of methyltestosterone on immunity against Salmonella Pullorum in dwarf chicks

Li¹,

Zhang²,

Zuo

et al. 2009

Poultry Science

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This study was conducted to determine effects of methyltestosterone on innate immunity and adaptive immunity against Salmonella Pullorum in dwarf chicks. In vivo experiment, comparisons of pathological sections, viable counts of bacteria, specific antibody levels, and subsets of T lymphocytes were set forth between chicks with or without 10(-7) M methyltestosterone treatment (2 d of age through 21 d of age) and challenged with 5 x 10(8) virulent Salmonella Pullorum (7 d of age), and in vitro experiment, phagocytic and killing abilities, reactive oxygen intermediate production, and reactive nitrogen intermediate production of monocytes-macrophages treated with high (10(-8) M/10(6) cell) or physiological (10(-14) M/10(6) cell) concentration of methyltestosterone were examined after Salmonella Pullorum infection. The results showed that (1) in vivo, administration of methyltestosterone enhanced susceptibility to Salmonella Pullorum infection and depressed cellular immunity against Salmonella Pullorum, whereas it had no effect on humoral immunity in dwarf chicks; (2) in vitro, at high concentration, methyltestosterone reduced (P < 0.05) monocytes-macrophages mediated reactive oxygen intermediate-dependent killing of Salmonella Pullorum, whereas low concentration of methyltestosterone enhanced (P < 0.05) reactive oxygen intermediate-dependent killing of Salmonella Pullorum in male dwarf chicks but not in females; and (3) although challenged with Salmonella Pullorum, phagocytic ability and monocytes-macrophages mediated reactive nitrogen intermediate-dependent killing were not affected by methyltestosterone in vitro. The results indicated that methyltestosterone affected the immune response to Salmonella Pullorum in dwarf chicks by changing monocytes-macrophages mediated reactive oxygen intermediate-dependent killing and cellular immunity, and the effects were dose-dependent; furthermore, the former 2 pathways played important roles in preventing Salmonella Pullorum infection in dwarf chicks, although the mechanism needs further study.

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“…Previously, we found that active monocytes surround, adhere, and clump on the positively charged beads in vitro [18,29], but not on the neutral or negatively charged beads. The beads may activate macrophages [18,30] and activated tissue macrophages release growth factors and active cytokines into the wound, providing the primary stimulus for the cascade of cell proliferation and matrix deposition that occur during wound healing [2]. Preliminary studies suggested an increase of TGF-␤1 mRNA in the wounds treated with positively charged beads compared to controls at day 7 postwounding.…”

Section: Discussionmentioning

confidence: 99%

Effects of Electrically Charged Particles in Enhancement of Rat Wound Healing

Wu¹,

Mockros²,

Casperson³

et al. 1999

Journal of Surgical Research

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Avian Inflammatory Macrophage Function: Shifts in Arachidonic Acid Metabolism, Respiratory Burst, and Cell-Surface Phenotype During the Response to Sephadex

Cited by 30 publications

References 27 publications

Broiler pulmonary hypertensive responses during lipopolysaccharide-induced tolerance and cyclooxygenase inhibition

Broiler pulmonary hypertensive responses during lipopolysaccharide-induced tolerance and cyclooxygenase inhibition

Effects of methyltestosterone on immunity against Salmonella Pullorum in dwarf chicks

Effects of Electrically Charged Particles in Enhancement of Rat Wound Healing

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