Inflammation-induced alterations in maternal-fetal Heme Oxygenase (HO) are associated with sustained innate immune cell dysregulation in mouse offspring

Ozen, Maide; Zhao, Hui; Kalish, Flora; Yang, Yang; Jantzie, Lauren L.; Wong, Ronald J.; Stevenson, David K.

doi:10.1371/journal.pone.0252642

Cited by 4 publications

(6 citation statements)

References 53 publications

(112 reference statements)

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“…It has been found that parecoxib can attenuate the hepatic ischemia-reperfusion injury in rats by inhibiting the inflammation and oxidative stress 6 . Heme oxygenase-1 (HO-1) is an inducible heme oxygenase, and its activation is one of the most important cytoprotective mechanisms during cell stress 7 . Parecoxib can induce the HO-1 expression in macrophages and vascular smooth muscle cells through reactive oxygen species (ROS)-dependent pathway 8 .…”

Section: Introductionmentioning

confidence: 99%

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Qin

Jin

et al. 2021

Acta Cir. Bras.

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Purpose: To investigate the protective effect of parecoxib against lung ischemia-reperfusion injury (LIRI) in rats and the mechanism. Methods: Thirty rats were divided into sham-operated, LIRI and LIRI+parecoxib groups. LIRI model (ischemia for 60 min, followed by reperfusion for 120 min) was constructed in LIRI and LIRI+parecoxib groups. In LIRI+parecoxib group, 10 mg/kg parecoxib was given via femoral vein 15 min before ischemia beginning. At the end of the reperfusion, blood gas analysis, lung wet to dry mass ratio measurement, lung tissue biochemical determination and heme oxygenase-1 (HO-1) protein expression determination were performed. Results: Compared with LIRI group, in LIRI+parecoxib group the oxygenation index was significantly increased, the alveolar-arterial oxygen partial pressure difference was significantly decreased, the lung wet to dry mass ratio was significantly decreased, the lung tissue malondialdehyde content was significantly decreased, the lung tissue superoxide dismutase and myeloperoxidase activities were significantly increased, the lung tissue tumor necrosis factor α and interleukin 1β levels were significantly decreased, and the lung tissue HO-1 protein expression level was significantly increased (all P < 0.05). Conclusion: Parecoxib pretreatment can mitigate the LIRI in rats by reducing oxidative stress, inhibiting inflammatory response and upregulating HO-1 expression in lung tissue.

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Section: Introductionmentioning

confidence: 99%

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Qin

Jin

et al. 2021

Acta Cir. Bras.

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“…At P60, brain and peripheral blood mononuclear cells (PBMCs) were collected from adult rats for flow cytometry consistent previous reports (17,(25)(26)(27)(28)(29)(30)(31). Using a Miltenyi adult brain dissociation kit and Miltenyi gentleMACS ™ protocol,…”

Section: Flow Cytometrymentioning

confidence: 97%

“…Using a separate panel, T cells were identified by assessing CD45 + CD3 + cells. CD45 + CD3 + CD4 + were classified as helper T cells and CD45 + CD3 + CD4 + CD25 + as regulatory T cells (Tregs) (22,23,29,30) (Figures 2A-G).…”

Section: Advances In Drug and Alcohol Researchmentioning

confidence: 99%

Methadone alters the peripheral inflammatory and central immune landscape following prenatal exposure in rats

Madurai¹,

Kitase²,

Hamimi

et al. 2022

Adv. Drug Alcohol Res.

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Opioid use during pregnancy continues to rise at alarming rates with a parallel trend in the number of infants and children exposed to opioid medications each year. Prenatal opioid exposure (POE) occurs at a critical timepoint in neurodevelopment disrupting intricate pathways essential for neural-immune maturation with the potential for devastating long-term consequences. Understanding the mechanisms underlying injury associated with POE is essential to address long-term outcomes and identify diagnostic and therapeutic biomarkers in this vulnerable patient population. Using an established preclinical model of POE, we investigated changes in cerebral and peripheral inflammation and peripheral blood mononuclear cell (PBMC) activity. We hypothesized that neuroinflammation, as defined by changes in specific cerebral immune cell populations, would exist in adult rats following POE concomitant with sustained peripheral immune hyperreactivity (SPIHR). Our data demonstrated alterations in cerebral immune cells at postnatal day 60 (P60) typified by increased regulatory T cells (p < 0.01) and neutrophils (p < 0.05) in rats with POE compared to controls. Evaluation of serum revealed increased levels of IL-6 (p < 0.05) and CXCL1 (p < 0.05) at P21 in rats with POE compared to controls with no significant difference in cytokine or chemokine levels between the two groups at P60. Additionally, PBMCs isolated from rats with POE at P21 demonstrated baseline hypersecretion of IL-6 (p < 0.01) and SPIHR with increased levels of TNF-α (p < 0.05) and CXCL1 (p < 0.05) following stimulation with LPS. At P60, however, there was no significant difference found in cytokine or chemokine levels secreted by PBMCs isolated from rats with POE at baseline or with LPS stimulation when compared to controls. Taken together, these data demonstrate cerebral inflammation months after prenatal opioid exposure and long after the resolution of systemic inflammation and SPIHR seen at toddler age equivalent. Chronic alterations in the cerebral immune cell populations secondary to prenatal opioid exposure may underly long-term consequences of developmental brain injury including deficits in cognition and attention. These findings may be invaluable to further investigations of precise biomarkers of injury and targeted therapeutics for this vulnerable population.

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“…HO-1 plays a crucial role in heme degradation and cellular responses to stress [26]. During pregnancy, HO-1 maintains a balanced immune response and supports healthy placental development [27]. Evidence from a mouse model [27] indicates that it helps protect against oxidative stress and inflammation, which are often elevated in pregnancy-associated conditions.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of plasma proteins in pregnant women exposed toPlasmodium falciparummalaria

Kanoi,

Waweru,

Kobia

et al. 2024

Preprint

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In sub-Saharan Africa, pregnant women are at greater risk of malaria infection than non-pregnant adult women. The infection may lead to pregnancy-associated malaria (PAM) because of the sequestration of Plasmodium falciparum-infected erythrocytes in the placental intervillous space. Although there are several tools for diagnosing malaria infection during pregnancy, including blood smear microscopic examination, rapid diagnostic tests, and PCR, there are no tools for detecting placental infection and, by extension, any dysfunction associated with PAM. Thus, PAM, specifically placental infection, can only be confirmed via postnatal placental histopathology. Therefore, there is an urgent need for specific serum biomarkers of PAM. Here, we used the high throughput proximity extension assay to screen plasma from malaria-exposed pregnant women for differentially expressed proteins that can predict PAM or adverse malaria outcomes. Such biomarkers may also elucidate the pathophysiology of PAM. We observed that the IgG Fc receptor IIb (Uniprot ID P31994) and HO-1 (P09601) are consistently highly expressed in malaria-positive samples compared to samples from malaria-negative pregnant women. On the contrary, NRTN (Q99748) and IL-20 (Q9NYY1) were differentially expressed in the malaria-negative women. IL-20 exhibited the highest discriminatory power (AUC = 0.815), indicating a strong association with malaria status. These proteins should be considered for further evaluation as biomarkers of malaria-induced placental dysfunction in pregnant women.

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Inflammation-induced alterations in maternal-fetal Heme Oxygenase (HO) are associated with sustained innate immune cell dysregulation in mouse offspring

Cited by 4 publications

References 53 publications

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Parecoxib mitigates lung ischemia-reperfusion injury in rats by reducing oxidative stress and inflammation and up-regulating HO-1 expression

Methadone alters the peripheral inflammatory and central immune landscape following prenatal exposure in rats

Differential expression of plasma proteins in pregnant women exposed toPlasmodium falciparummalaria

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