Methamphetamine administration modifies leukocyte proliferation and cytokine production in murine tissues

Peerzada, Habibullah; Gandhi, Jay A.; Guimarães, Allan J.; Nosanchuk, Joshua D.; Martinez, Luis R.

doi:10.1016/j.imbio.2013.02.001

Cited by 43 publications

(58 citation statements)

References 19 publications

(25 reference statements)

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“…Terfenadine (an antiallergy drug) causes thymocyte death through a mitochondrial pathway and results in a remarkable increase in DNA fragmentation and the activation of certain caspases in rats (Enomoto et al 2004;Pozzesi et al 2014). Methamphetamine administration in a rodent model promotes apoptosis through caspase-9 activation and diminishes the thymic cellularity (Fujikawa et al 2007;Peerzada et al 2013;Pozzesi et al 2014). Geldanamycin, a heat shock protein-90 inhibitor, which is usually used as an anti-cancer agent, can target several oncogenic signaling pathways simultaneously (Cortese et al 2013;Fukuyo et al 2010).…”

Section: Role Of Chemotherapy In Atimentioning

confidence: 99%

Acute Thymic Involution and Mechanisms for Recovery

Ansari

Liu

2017

Arch. Immunol. Ther. Exp.

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Section: Role Of Chemotherapy In Atimentioning

confidence: 99%

Acute Thymic Involution and Mechanisms for Recovery

Ansari

Liu

2017

Arch. Immunol. Ther. Exp.

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“…A previous study (3) reported that the widest distribution and the highest uptake of MA in the human body occurred in the lungs, and that this may render the lungs vulnerable to infection, pulmonary hypertension and pulmonary edema (3,4). The long-lasting pulmonary toxic effects of MA have placed an increased burden on healthcare costs (5).…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine protects against methamphetamine-induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats

Wang

Liu

et al. 2016

Molecular Medicine Reports

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Methamphetamine (MA) abuse is a major public health and safety concern throughout the world and a growing burden on healthcare costs. The purpose of the present study was to investigate the protective effect of fluoxetine against MA-induced chronic pulmonary inflammation and to evaluate the potential role of nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidative stress. Wistar rats were divided into control, MA and two fluoxetine-treated groups. Rats in the MA and the two fluoxetine-treated groups were treated daily with intraperitoneal injection of 10 mg/kg MA twice daily. Rats in the two fluoxetine-treated groups were injected intragastrically with fluoxetine (2 and 10 mg/kg) once daily, respectively. After 5 weeks, the rats were euthanized and hematoxylin and eosin staining, immunohistochemistry, western blot analysis and redox assay were performed. It was demonstrated that chronic exposure to MA can induce pulmonary inflammation in rats, with the symptoms of inflammatory cell infiltration, crowded lung parenchyma, thickened septum and a reduced number of alveolar sacs. Fluoxetine attenuated pulmonary inflammation and the expression of interleukin-6 and tumor necrosis factor-α in rat lungs. Fluoxetine inhibited MA-induced increases in the expression levels of serotonin transporter (SERT) and p-p38 mitogen-activated protein kinase (MAPK), and reversed the MA-induced decrease in nuclear Nrf2 and human heme oxygenase-1 in lungs. Fluoxetine at 10 mg/kg significantly reversed the reduced glutathione (GSH) level, the ratio of GSH/oxidized glutathione, and the reactive oxygen species level in rat lungs from the MA group. These findings suggested that fluoxetine, a SERT inhibitor, has a protective effect against MA-induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats.

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“…METH adversely impacts immunological responses, which might contribute to the higher rate and more rapid progression of certain infections in drug abusers. We recently demonstrated that METH administration modifies leukocyte proliferation and cytokine production in diverse murine tissues (7). Also, the highest uptake of the drug occurs in lung, and levels are intermediate in brain (8).…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine Enhances Cryptococcus neoformans Pulmonary Infection and Dissemination to the Brain

Patel

Desai

Frasés

et al. 2013

mBio

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Methamphetamine (METH) is a major addictive drug of abuse in the United States and worldwide, and its use is linked to HIV acquisition. The encapsulated fungus Cryptococcus neoformans is the most common cause of fungal meningitis in patients with AIDS. In addition to functioning as a central nervous system stimulant, METH has diverse effects on host immunity. Using a systemic mouse model of infection and in vitro assays in order to critically assess the impact of METH on C. neoformans pathogenesis, we demonstrate that METH stimulates fungal adhesion, glucuronoxylomannan (GXM) release, and biofilm formation in the lungs. Interestingly, structural analysis of the capsular polysaccharide of METH-exposed cryptococci revealed that METH alters the carbohydrate composition of this virulence factor, an event of adaptation to external stimuli that can be advantageous to the fungus during pathogenesis. Additionally, we show that METH promotes C. neoformans dissemination from the respiratory tract into the brain parenchyma. Our findings provide novel evidence of the impact of METH abuse on host homeostasis and increased permissiveness to opportunistic microorganisms.

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Methamphetamine administration modifies leukocyte proliferation and cytokine production in murine tissues

Cited by 43 publications

References 19 publications

Acute Thymic Involution and Mechanisms for Recovery

Acute Thymic Involution and Mechanisms for Recovery

Fluoxetine protects against methamphetamine-induced lung inflammation by suppressing oxidative stress through the SERT/p38 MAPK/Nrf2 pathway in rats

Methamphetamine Enhances Cryptococcus neoformans Pulmonary Infection and Dissemination to the Brain

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