Dataset Information

Transgenic sickle cell mouse plasma and brain

ABSTRACT: Sickle cell disease (SCD) is a genetic disorder caused by a mutation in the beta hemoglobin gene, resulting in red blood cell distortion, hemolysis, and severe pain episodes. Chronic pain in SCD is believed to be largely driven by neuroinflammation and central sensitization, yet the exact neurobiological mechanisms remain unclear. Hemorphins, opioid peptides derived from beta-hemoglobin, may bridge this gap by influencing opioid signaling pathways that could alleviate the pain experienced in SCD. In this study, we investigated the levels of hemorphins in both plasma and brain tissues of transgenic SCD mice using liquid chromatography-mass spectrometry (LC-MS).

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain, Blood Plasma

SUBMITTER: Yanqi Tan

LAB HEAD: Jonathan V. Sweedler

PROVIDER: PXD056826 | Pride | 2025-11-25

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	2024_SCD_Pep_A1_Slot1-19_1_4062.d.zip	Other
	2024_SCD_Pep_A2_Slot1-20_1_4064.d.zip	Other
	2024_SCD_Pep_A3_Slot1-21_1_4073.d.zip	Other
	2024_SCD_Pep_A4_Slot1-22_1_4076.d.zip	Other
	2024_SCD_Pep_A5_Slot1-23_1_4083.d.zip	Other

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Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.

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Transgenic sickle cell mouse plasma and brain

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