Intravenous Immunoglobulin G Attenuates Pulmonary Hypertension but Induces Local Neutrophil Influx in Meconium Aspiration in Piglets

Holopainen, Riikka; Soukka, Hanna; Halkola, Lauri; Kääpä, Pietari

doi:10.1159/000083371

Cited by 3 publications

(2 citation statements)

References 55 publications

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“…Although IgG pretreatment diminished pulmonary hypertension response and improved oxygenation, the intrapulmonary shunt fraction, systemic hemodynamics, or lung tissue changes were comparable, and neutrophil influx into the lungs was even higher than in non-treated group [176].…”

Section: Immunoglobulin Gmentioning

confidence: 84%

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Mokrá¹,

Mokrý

2007

CPR

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Pathophysiology of meconium aspiration syndrome (MAS) is complex and interactions between individual pathomechanisms are still not completely understood. As recently shown, inflammation plays a significant role in the pathogenesis of MAS. Activated cells release and stimulate production of a wide variety of mediators, including cytokines, enzymes, reactive species, and other biologically active substances in meconium-injured lungs. Anti-inflammatory drugs acting on different levels of inflammatory cascade may in combination with other treatment (exogenous surfactant, inhaled NO, liquid ventilation) improve the clinical status of newborns with MAS. For example, corticosteroids modulate activity of phospholipase A 2 and induced NO synthase, influence migration and activation of leukocytes, and reduce lung edema. Cyclooxygenase inhibitors modulate production of thromboxane and prostaglandins. Phosphodiesterase inhibitors have vasodilating, bronchodilating and anti-inflammatory effects. Antioxidants diminish formation of reactive species. However, there are many other drugs., e.g. anti-cytokine antibodies, inhibitors of complement, inhibitors of angiotensinconverting enzyme, anticoagulants, inhibitors of proteolytic enzymes, calcium-channel blockers etc. that may be beneficial in MAS. Nevertheless, further testing is necessary until the novel approaches may be recommended. In this article, authors reviewed main factors participating in meconium-induced inflammation and pointed out some targets for its pharmacological modulation.

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Section: Immunoglobulin Gmentioning

confidence: 84%

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Mokrá¹,

Mokrý

2007

CPR

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“…Myeloperoxidase activity is usually used as an important indicator of neutrophil accumulation. 22 The chemotaxis is related to the presence of powerful chemotactic role of IL-8. In a study by Ruiz et al 23 addition of polyclonal immunoglobulin G (IgG) activated the mononuclear cells to express IL-8 cytokine production, which could promote intrapulmonary accumulation and infiltration of neutrophils.…”

Section: Neutrophil Influxmentioning

confidence: 99%

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

Vidyasagar

Zagariya

2008

J Perinatol

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To review current literature related to cellular mechanisms of meconiuminduced lung injury (MILI). Review of published experimental in vitro and in vivo MAS studies using human and animal lung cells. We found that meconium induces expression of cytokines and angiotensin II (ANG II)-induced apoptotic process in the lung cells. We postulate that inflammatory cytokines induce ANG II expression, which causes apoptotic cell death after binding to its AT1 receptors. We also demonstrated expression of serpins associated with meconium instillation into the lungs. Serpins are proteins that inhibit cellular proteases and elastases. Expression of serpins may be an attempt to recover lung from these injurious effects. In summary our studies show that whereas meconium induces inflammatory cytokines and subsequent cell apoptosis, the lung cells also try to protect themselves by inducing serpins. The balance of these interactions will determine the residual damage. We believe these new findings are very important in understanding of MILI.

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An Unsettled Promise: The Newborn Piglet Model of Neonatal Acute Respiratory Distress Syndrome (NARDS). Physiologic Data and Systematic Review

2019

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Despite great advances in mechanical ventilation and surfactant administration for the newborn infant with life-threatening respiratory failure no specific therapies are currently established to tackle major pro-inflammatory pathways. The susceptibility of the newborn infant with neonatal acute respiratory distress syndrome (NARDS) to exogenous surfactant is linked with a suppression of most of the immunologic responses by the innate immune system, however, additional corticosteroids applied in any severe pediatric lung disease with inflammatory background do not reduce morbidity or mortality and may even cause harm. Thus, the neonatal piglet model of acute lung injury serves as an excellent model to study respiratory failure and is the preferred animal model for reasons of availability, body size, similarities of porcine and human lung, robustness, and costs. In addition, similarities to the human toll-like receptor 4, the existence of intraalveolar macrophages, the sensitivity to lipopolysaccharide, and the production of nitric oxide make the piglet indispensable in anti-inflammatory research. Here we present the physiologic and immunologic data of newborn piglets from three trials involving acute lung injury secondary to repeated airway lavage (and others), mechanical ventilation, and a specific anti-inflammatory intervention via the intratracheal route using surfactant as a carrier substance. The physiologic data from many organ systems of the newborn piglet—but with preference on the lung—are presented here differentiating between baseline data from the uninjured piglet, the impact of acute lung injury on various parameters (24 h), and the follow up data after 72 h of mechanical ventilation. Data from the control group and the intervention groups are listed separately or combined. A systematic review of the newborn piglet meconium aspiration model and the repeated airway lavage model is finally presented. While many studies assessed lung injury scores, leukocyte infiltration, and protein/cytokine concentrations in bronchoalveolar fluid, a systematic approach to tackle major upstream pro-inflammatory pathways of the innate immune system is still in the fledgling stages. For the sake of newborn infants with life-threatening NARDS the newborn piglet model still is an unsettled promise offering many options to conquer neonatal physiology/immunology and to establish potent treatment modalities.

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Intravenous Immunoglobulin G Attenuates Pulmonary Hypertension but Induces Local Neutrophil Influx in Meconium Aspiration in Piglets

Cited by 3 publications

References 55 publications

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis

An Unsettled Promise: The Newborn Piglet Model of Neonatal Acute Respiratory Distress Syndrome (NARDS). Physiologic Data and Systematic Review

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