CXC Chemokines CXCL1, CXCL9, CXCL10 and CXCL12 are Variably Expressed in Patients with Sickle Cell Disease and Carriers: Are They Predictive Tools for Disease Complications?

Ostadebrahimi, Hamid; Jamali, Zahra; Nazari, Mahmood; Bahri, Mina; Farahmandnia, Zahra; Khandany, Behjat Kalantary; Taheri, Mohsen; Khorramdelazad, Hossein; Hakimizadeh, Elham; Zaker, Farhad; Rezaeian, Mohsen; Hassanshahi, Gholamhossein

doi:10.7754/clin.lab.2013.121237

Cited by 7 publications

(4 citation statements)

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“…In a previous report from our group, TNF and IL6 were shown to be increased in SCA, both in steady state and in crisis patients, while TGFB was shown to be decreased in crisis patients, as compared to steady‐ state patients and healthy controls (Carvalho et al., ). IL6, TGF‐beta (Keikhaei et al., ), and CXCL12 (Ostadebrahimi et al., ) levels have been previously shown to be increased in SCA crisis and steady state, as compared to healthy controls, although without statistical significance and not exclusively elevated in one of the two conditions evaluated, as in our data. VEGF levels were already shown not to differ between steady‐state and crisis patients in general, but some VEGF gene polymorphisms were correlated with crisis and VEGF plasma levels (Al‐Habboubi et al., ).…”

Section: Discussionsupporting

confidence: 72%

“…Total CD36 + reticulocytes have been shown to increase during the crisis state (Sawadogo et al., ). CXCL10 levels have been shown to be increased in crisis, although not significantly (Ostadebrahimi et al., ). The differential expression of IL‐15 was described in groups of SCA patients with variable serum levels of C‐reactive protein (van Beers et al., ).…”

Section: Discussionmentioning

confidence: 99%

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Differential gene expression analysis of sickle cell anemia in steady and crisis state

Zanette

Santiago

Leite

et al. 2019

Annals of Human Genetics

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Sickle cell anemia is one of the most prevalent genetic diseases worldwide, showing great clinical heterogeneity. This study compared the gene expression patterns between sickle cell anemia pediatric patients in steady state and in crisis state, as compared to age‐paired, healthy individuals. RNA sequencing was performed from these groups of patients/controls using Illumina HiSeq 2500 equipment. The resulting differentially expressed genes were loaded into QIAGEN's ingenuity pathway analysis. The results showed that EIF2 pathway and NRF2‐mediated oxidative stress‐response pathways were more highly activated both in steady state and in crisis patients, as compared to healthy individuals. In addition, we found increased activation of eIF4 and p70S6K signaling pathways in crisis state compared to healthy individuals. The transcription factor GATA‐1 was found exclusively in steady state while SPI was found exclusively in crisis state. IL6 and VEGFA were found only in crisis state, while IL‐1B was found exclusively in steady state. The regulator effects analysis revealed IgG1 as an upstream regulator in steady state compared to healthy individuals, resulting in invasion of prostate cancer cell lines as the disease/function outcome. For crisis‐state patients versus healthy individuals, two networks of regulator effects revealed STAT1, CD40LG, TGM2, IRF7, IRF4, and IRF1 acting as upstream regulators, resulting in disease/function outcomes, including engulfment of cells and aggregation of blood cells and inflammation of joints. Our results indicated genes and pathways that can provide clues on the molecular events involved in the severity of sickle cell disease.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Differential gene expression analysis of sickle cell anemia in steady and crisis state

Zanette

Santiago

Leite

et al. 2019

Annals of Human Genetics

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“…Despite high morbidity rates, surprisingly little is known about the mechanisms underlying the generation and maintenance of chronic pain in this disease. It is known, however, that both SCD patients and transgenic animal models exist in a persistent pro-inflammatory state; chemokines including CXCL1 [43], CXCL8 (interleukin 8, IL8) [38], CXCL9, CXCL10 [56], CXCL12 [43], and CX3CL1 (fractalkine) [54] are significantly elevated in the serum of SCD patients or mouse models. The focus of these studies was CCL2, a chemokine that has previously been shown to sensitize primary sensory afferents in neuropathic pain models [30].…”

Section: Discussionmentioning

confidence: 99%

Chemokine (c-c motif) receptor 2 mediates mechanical and cold hypersensitivity in sickle cell disease mice

Sadler

Zappia

O’Hara

et al. 2018

Pain

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Approximately one-third of individuals with sickle cell disease (SCD) develop chronic pain. This debilitating pain is inadequately treated because the underlying mechanisms driving the pain are poorly understood. In addition to persistent pain, patients with SCD are also in a tonically proinflammatory state. Previous studies have revealed that there are elevated plasma levels of many inflammatory mediators including chemokine (c-c motif) ligand 2 (CCL2) in individuals with SCD. Using a transgenic mouse model of SCD, we investigated the contributions of CCL2 signaling to SCD-related pain. Inhibition of chemokine receptor 2 (CCR2), but not CCR4, alleviated the behavioral mechanical and cold hypersensitivity in SCD. Furthermore, acute CCR2 blockade reversed both the behavioral and the in vitro responsiveness of sensory neurons to an agonist of TRPV1, a neuronal ion channel previously implicated in SCD pain. These results provide insight into the immune-mediated regulation of hypersensitivity in SCD and could inform future development of analgesics or therapeutic measures to prevent chronic pain.

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“…More than 50 chemokines and 20 chemokine receptors have been recognized to date [29]. Multiple members of CXC chemokines have been confirmed to be involved in inflammatory conditions such as type-1 diabetes [30], Behcet's syndrome, diabetes mellitus [31], osteoporosis [32], preterm delivery [33], cancer [34], systemic lupus erythematosus (SLE) and tick-borne encephalitis. However, a clear relationship between chemokines and CAD needs to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

et al. 2021

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Coronary artery disease (CAD) and coronary heart disease (CHD) constitute two of the leading causes of death in Europe, USA and the rest of the world. According to the latest reports of the Iranian National Health Ministry, CAD is the main cause of death in Iranian patients with an age over 35 years despite a significant reduction in mortality due to early interventional treatments in the context of an acute coronary syndrome (ACS). Inflammation plays a fundamental role in coronary atherogenesis, atherosclerotic plaque formation, acute coronary thrombosis and CAD establishment. Chemokines are well-recognized mediators of inflammation involved in several bio-functions such as leucocyte migration in response to inflammatory signals and oxidative vascular injury. Different chemokines serve as chemo-attractants for a wide variety of cell types including immune cells. CXC motif chemokine ligand 10 (CXCL10), also known as interferon gamma-induced protein 10 (IP-10/CXLC10), is a chemokine with inflammatory features whereas CXC chemokine receptor 3 (CXCR3) serves as a shared receptor for CXCL9, 10 and 11. These chemokines mediate immune responses through the activation and recruitment of leukocytes, eosinophils, monocytes and natural killer (NK) cells. CXCL10, interleukin (IL-15) and interferon (IFN-g) are increased after a COVID-19 vaccination with a BNT162b2 mRNA (Pfizer/BioNTech) vaccine and are enriched by tumor necrosis factor alpha (TNF-α) and IL-6 after the second vaccination. The aim of the present study is the presentation of the elucidation of the crucial role of CXCL10 in the patho-physiology and pathogenesis of CAD and in identifying markers associated with the vaccination resulting in antibody development.

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CXC Chemokines CXCL1, CXCL9, CXCL10 and CXCL12 are Variably Expressed in Patients with Sickle Cell Disease and Carriers: Are They Predictive Tools for Disease Complications?

Cited by 7 publications

References 0 publications

Differential gene expression analysis of sickle cell anemia in steady and crisis state

Differential gene expression analysis of sickle cell anemia in steady and crisis state

Chemokine (c-c motif) receptor 2 mediates mechanical and cold hypersensitivity in sickle cell disease mice

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review

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