Clinical events and their relation to the tumor necrosis factor-alpha and interleukin-10 genotypes in Sickle-Cell-Anemia patients

Cavalcante, Jânio Emanuel Andrade; Machado, Rosângela Pinheiro Gonçalves; Laurentino, Marilia Rocha; Santos, Talyta Ellen de Jesus dos; Bandeira, Izabel Cristina Justino; Filho, Pedro Aurio Maia; Figueiredo, Monalisa Feliciano; Martins, Alice Maria Costa; Lemes, Romélia Pinheiro Gonçalves

doi:10.1016/j.hemonc.2015.11.002

Cited by 13 publications

(8 citation statements)

References 26 publications

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“…The finding of proinflammatory cytokines, particularly IL-1 and CRP, being higher at baseline (0-h) and at each time-point in SCA compared with the wild-type patients with HbAA is consistent with previous reports showing significant elevations of various proinflammatory cytokines among patients with SCA in their steady state. 7,8,13–18 Most of these studies also report no significant difference in the levels of the anti-inflammatory cytokines among these patients, similar to our findings. Other studies have shown that the altered cytokine levels correlate with altered hematological and clinical parameters.…”

Section: Discussionsupporting

confidence: 91%

“…4–6 In the setting of acute cholecystitis, a proinflammatory cytokine cascade may be seen of magnitude beyond that of wild-type (hemoglobin AA [HbAA]) patients. 7,8 The influence of this heightened inflammatory response on surgical outcomes in patients with SCA with acute cholecystitis has not been fully explored. Studies have profiled changes in cytokine of wild-type patients after laparoscopy, but this has not been well studied in patients with SCA (hemoglobin SS [HbSS]).…”

Section: Introductionmentioning

confidence: 99%

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The Inflammatory Response to Surgery in Sickle Cell Disease Patients Undergoing Cholecystectomy

Adisa

Adedeji

Bolarinwa

et al. 2019

JSLS

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Background and Objectives: Patients with sickle cell anemia (SCA) may have elevated inflammatory markers in health, and this may be heightened after open operations. The inflammatory response of patients with SCA after minimally invasive surgeries has not been fully explored. Patients and Methods: Consecutive patients with SCA and with hemoglobin AA (HbAA) undergoing laparoscopic cholecystectomy for acute cholecystitis were recruited into the study. Blood samples were taken before induction of anesthesia (0-h); at 4, 12, 24, and 48 h; and on postoperative day 7. Samples were analyzed for serum C-reactive protein and interleukin (IL)-1 through IL-18. Results: Twenty-three patients, including 9 with SCA and 14 with HbAA, were recruited with 4 cases performed by open laparotomy. At 0-h, proinflammatory IL-1 levels (6.1 versus 4.8) and C-reactive protein levels (32.5 versus 26.6) were higher in patients with hemoglobin SS (HbSS) than in patients with HbAA, respectively. Over time, inflammatory markers were generally higher at each time-point for patients with HbSS compared with patients with HbAA for both proinflammatory and anti-inflammatory cytokines, rising immediately after surgery and up to 48 hours, then returning to baseline by postoperative day 7. There was a higher mean IL-1 level across all time-points in the HbSS group than in the HbAA group ( P = .04). Conclusion: This exploratory study found an enhanced inflammatory response to cholecystectomy in patients with SCA compared with patients with HbAA. Minimally invasive surgical strategies for this patient group may help to mediate this response.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

The Inflammatory Response to Surgery in Sickle Cell Disease Patients Undergoing Cholecystectomy

Adisa

Adedeji

Bolarinwa

et al. 2019

JSLS

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“…Pathare et al [71] and Raghupathy et al [90] demonstrated significantly higher levels of IL-4 in SCA patients at steady state like our results. Taylor et al [91] also demonstrated higher levels of IL-4 and IL-10 in SCA patients at steady state, even though Cavalcante et al [92] did not show significantly different serum levels of IL-10 between steady state SCA patients and control subjects. Musa et al [14] demonstrated higher levels of IL-4 in SCA patients in vasoocclusive crises than in steady state and control subjects; however, their levels of IL-10 were higher in SCA patients at steady state than in crises and control individuals corroborating our results.…”

Section: Discussionmentioning

confidence: 99%

Sickle Cell Anemia Patients Display an Intricate Cellular and Serum Biomarker Network Highlighted by TCD4+CD69+ Lymphocytes, IL-17/MIP-1β, IL-12/VEGF, and IL-10/IP-10 Axis

Garcia

Júnior

Soares

et al. 2020

Journal of Immunology Research

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Background. Sickle cell anemia (SCA) is associated with a chronic proinflammatory state characterized by elevated leukocyte count, mortality from severe recurrent infections, and subsequent vasoocclusive complications with leukocyte adhesion to the endothelium and increased plasma levels of inflammatory cytokines. The immune system has a close connection with morbidity in SCA, but further studies are needed to uncover the involvement of innate and adaptive immunities in modulating the SCA physiopathology. We performed measurements of the frequency of innate and adaptive immunity cells, cytokines, chemokines, and growth factors and immunophenotyping of Toll-like receptor and adhesion molecule expression in the blood of SCA patients and healthy donors to evaluate the different profiles of these biomarkers, the relationship among them, and their correlation to laboratory records and death risk. Material and Methods. Immunophenotyping of cells, Toll-like receptors, and adhesion molecules were performed from peripheral blood samples of SCA patients and healthy donors by flow cytometry and cytokine/chemokine/growth factor measurement by the Luminex technique performed from the serum of the same subjects. Results. Cells of adaptive immunity such as IL-12, IL-17, and IL-10 cytokines; IL-8, IP-10, MIP-1α, MIP-1β, and RANTES chemokines; and VEGF, FGF-basic, and GM-CSF growth factors were higher in SCA patients than healthy donors regardless of any laboratorial and clinical condition. However, high death risk appears to have relevant biomarkers. Conclusion. In the SCA pathophysiology at steady state, there is a broad immunological biomarker crosstalk highlighted by TCD4+CD69+ lymphocytes, IL-12 and IL-17 inflammatory and IL-10 regulatory cytokines, MIP-1α, MIP-1β, and IP-10 chemokines, and VEGF growth factor. High expression of TLR2 in monocytes and VLA-4 in TCD8+ lymphocytes and high levels of MIP-1β and RANTES appear to be relevant in high death risk conditions. The high reticulocytosis and high death risk conditions present common correlations, and there seems to be a balance by the Th2 profile.

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“…TNF-α activates endothelial cells and neutrophils ( 34 ). In the non-malaria conditions, TNF-α was significantly elevated in HbSS- compared to HbAA- ( Supplement Figure 1 ).…”

Section: Discussionmentioning

confidence: 99%

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

et al. 2020

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In 2018, 228 million cases and 405,000 malaria-associated deaths were reported worldwide with a majority being in Africa. A wide range of factors, including parasitemia, host immunity, inflammatory responses to infection, and host hemoglobin genotype, mediate the severity of malaria. Among the hemoglobinopathies, hemoglobin S (HbS) is caused by a single amino acid substitution of Glutamic Acid replaced by Valine at the sixth position of the beta-globin chain (E6V). Hemoglobin C (HbC) on the other hand, involves a single amino acid substitution of Glutamic Acid by a Lysine (E6K), which has received the most attention. These substitutions alter the stability of Hb leading to wide-ranging hematological disorders. The homozygous state of hemoglobin S (HbSS) results in sickle cell anemia (SCA) whereas the heterozygous state (HbAS) results in sickle cell trait (SCT). Both mutations are reported to mediate the reduction in the severity and fatality of Plasmodium falciparum malaria. The mechanism underlying this protection is poorly understood. Since both malaria and sickle cell disease (SCD) are associated with the destruction of erythrocytes and widespread systemic inflammation, identifying which inflammatory factor(s) mediate susceptibility of individuals with different hemoglobin genotypes to Plasmodium infection could result in the discovery of new predictive markers and interventions against malaria or SCD severity. We hypothesized that hemoglobin genotypes modulate the inflammatory response to Plasmodium infection. We conducted a cross-sectional study in Ghana, West Africa, between 2014 and 2019 to ascertain the relationships between blood inflammatory cytokines, Plasmodium infection, and hemoglobin genotype. A total of 923 volunteers were enrolled in the study. A total of 74, age and sex-matched subjects were identified with various genotypes including HbAS, HbAC, HbSS, HbSC, HbCC, or HbAA. Complete blood counts and serum inflammatory cytokine expression levels were assessed. The results indicate that differential expression of CXCL10, TNF-α, CCL2, IL-8, and IL-6 were tightly linked to hemoglobin genotype and severity of Plasmodium infection and that these cytokine levels may be predictive for susceptibility to severe malaria or SCD severity.

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Clinical events and their relation to the tumor necrosis factor-alpha and interleukin-10 genotypes in Sickle-Cell-Anemia patients

Abstract: The patients presented prevalence of TNF-alpha and IL-10 low-profile producer. The cytokine serum levels presented an association with the presence of polytransfusion and ACS in SCA patients.

Cited by 13 publications

References 26 publications

The Inflammatory Response to Surgery in Sickle Cell Disease Patients Undergoing Cholecystectomy

The Inflammatory Response to Surgery in Sickle Cell Disease Patients Undergoing Cholecystectomy

Sickle Cell Anemia Patients Display an Intricate Cellular and Serum Biomarker Network Highlighted by TCD4+CD69+ Lymphocytes, IL-17/MIP-1β, IL-12/VEGF, and IL-10/IP-10 Axis

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

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