scholarly journals Dexamethasone Alters Tracheal Aspirate T-Cell Cytokine Production in Ventilated Preterm Infants

Children ◽  
2021 ◽  
Vol 8 (10) ◽  
pp. 879
Author(s):  
Siamak M. Yazdi ◽  
Ekta U. Patel ◽  
Colby D. Richardson ◽  
K. Thomas Hardy ◽  
John E. Baatz ◽  
...  
Keyword(s):  
T Cell ◽  
Preterm Infants ◽  
Cytokine Production ◽  
Tracheal Aspirate ◽  
Cell Phenotype ◽  
Dexamethasone Treatment ◽  
Term Infants ◽  
Mechanically Ventilated ◽  
Cytokine Profiles ◽  
Cell Cytokine Production

Postnatal corticosteroids improve respiratory status and facilitate respiratory support weaning in preterm infants with bronchopulmonary dysplasia (BPD). Older literature describes characteristic cytokine profiles in tracheal aspirates (TA) of BPD patients which are altered with corticosteroids. Corticosteroids also influence peripheral blood T-cell presence. However, little is known regarding TA T-cell phenotype and cytokine production before or after exogenous corticosteroids. We hypothesized that postnatal dexamethasone alters the TA T-cell cytokine profiles of preterm infants. TA samples were collected from 14 infants born from 23 0/7 to 28 6/7 weeks who were mechanically ventilated for at least 14 days. Samples were collected up to 72 h before a ten-day dexamethasone course and again 1 to 3 calendar days after dexamethasone initiation. The primary outcome was change in T cell populations present in TA and their intracellular cytokine profile after dexamethasone treatment, ascertained via flow cytometry. Following dexamethasone treatment, there were significant decreases in respiratory severity score (RSS), percent CD4+IL-6+ cells, CD8+IL-6+ cells, CXCR3+IL-6+ cells, and CXCR3+IL-2+ cells and total intracellular IFN-γ in TA. RSS significantly correlated with TA percent CD4+IL-6+ cells. To our knowledge, this is the first study demonstrating that dexamethasone reduced T-cell IL-6 and this reduction was associated with improved RSS in pre-term infants with evolving BPD.

Dexamethasone Alters Tracheal Aspirate T-Cell Phenotype in Ventilated Preterm Infants

2019 ◽  
Author(s):  
E. Patel ◽  
C.D. Richardson ◽  
S.Z. Yazdi ◽  
K.T. Hardy ◽  
J.E. Baatz ◽  
...  
Keyword(s):  
T Cell ◽  
Preterm Infants ◽  
Tracheal Aspirate ◽  
Cell Phenotype

scholarly journals Associations between Monocyte and T Cell Cytokine Profiles in Autism Spectrum Disorders: Effects of Dysregulated Innate Immune Responses on Adaptive Responses to Recall Antigens in a Subset of ASD Children

2019 ◽  
Vol 20 (19) ◽  
pp. 4731 ◽  
Author(s):  
Harumi Jyonouchi ◽  
Lee Geng
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Cytokine Production ◽  
Autism Spectrum ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Tlr Agonists ◽  
Cytokine Profiles ◽  
Spectrum Disorders ◽  
Cell Cytokine Production

Changes in monocyte cytokine production with toll like receptor (TLR) agonists in subjects with autism spectrum disorders (ASD) were best reflected by the IL-1β/IL-10 ratios in our previous research. The IL-1β/IL-10 based subgrouping (low, normal, and high) of ASD samples revealed marked differences in microRNA expression, and mitochondrial respiration. However, it is unknown whether the IL-1β/IL-10 ratio based subgrouping is associated with changes in T cell cytokine profiles or monocyte cytokine profiles with non-TLR agonists. In ASD (n = 152) and non-ASD (n = 41) subjects, cytokine production by peripheral blood monocytes (PBMo) with TLR agonists and β-glucan, an inflammasome agonist, and T cell cytokine production by peripheral blood mononuclear cells (PBMCs) with recall antigens (Ags) (food and candida Ags) were concurrently measured. Changes in monocyte cytokine profiles were observed with β-glucan in the IL-1β/IL-10 ratio based ASD subgroups, along with changes in T cell cytokine production and ASD subgroup-specific correlations between T cell and monocyte cytokine production. Non-ASD controls revealed considerably less of such correlations. Altered innate immune responses in a subset of ASD children are not restricted to TLR pathways and correlated with changes in T cell cytokine production. Altered trained immunity may play a role in the above described changes.

Modulation of T cell cytokine production by miR-144* with elevated expression in patients with pulmonary tuberculosis

2011 ◽  
Vol 48 (9-10) ◽  
pp. 1084-1090 ◽  
Author(s):  
Yanhua Liu ◽  
Xinjing Wang ◽  
Jing Jiang ◽  
Zhihong Cao ◽  
Bingfen Yang ◽  
...  
Keyword(s):  
T Cell ◽  
Pulmonary Tuberculosis ◽  
Cytokine Production ◽  
Elevated Expression ◽  
Cell Cytokine Production

The Role of Accessory Cell Products in the Regulation of T Cell Cytokine Production

1996 ◽  
pp. 305-308 ◽  
Author(s):  
M. L. Kapsenberg ◽  
C. M. U. Hilkens ◽  
T. C. T. M. Pouw van der Kraan ◽  
E. A. Wierenga ◽  
A. Snijders
Keyword(s):  
T Cell ◽  
Cytokine Production ◽  
Accessory Cell ◽  
Cell Cytokine Production

scholarly journals T Cell Tolerance Induced by Cross-Reactive TCR Ligands Can Be Broken by Superagonist Resulting in Anti-Inflammatory T Cell Cytokine Production

2005 ◽  
Vol 175 (3) ◽  
pp. 1491-1497 ◽  
Author(s):  
Zsolt Illés ◽  
Hanspeter Waldner ◽  
Jayagopala Reddy ◽  
Estelle Bettelli ◽  
Lindsay B. Nicholson ◽  
...  
Keyword(s):  
T Cell ◽  
Cytokine Production ◽  
T Cell Tolerance ◽  
Cell Tolerance ◽  
Anti Inflammatory ◽  
Cell Cytokine Production

Salutary effects of 17β-estradiol on T-cell signaling and cytokine production after trauma-hemorrhage are mediated primarily via estrogen receptor-α

2007 ◽  
Vol 292 (6) ◽  
pp. C2103-C2111 ◽  
Author(s):  
Takao Suzuki ◽  
Tomoharu Shimizu ◽  
Huang-Ping Yu ◽  
Ya-Ching Hsieh ◽  
Mashkoor A. Choudhry ◽  
...  
Keyword(s):  
T Cells ◽  
Estrogen Receptor ◽  
T Cell ◽  
Signaling Pathways ◽  
Cytokine Production ◽  
Estrogen Receptor Α ◽  
Male Rats ◽  
17Β Estradiol ◽  
Ifn Γ ◽  
Cell Cytokine Production

Although 17β-estradiol (E2) administration following trauma-hemorrhage prevents the suppression in splenocyte cytokine production, it remains unknown whether the salutary effects of 17β-estradiol are mediated via estrogen receptor (ER)-α or ER-β. Moreover, it is unknown which signaling pathways are involved in 17β-estradiol's salutary effects. Utilizing an ER-α- or ER-β-specific agonist, we examined the role of ER-α and ER-β in E2-mediated restoration of T-cell cytokine production following trauma-hemorrhage. Moreover, since MAPK, NF-κB, and activator protein (AP)-1 are known to regulate T-cell cytokine production, we also examined the activation of MAPK, NF-κB, and AP-1. Male rats underwent trauma-hemorrhage (mean arterial pressure 40 mmHg for 90 min) and fluid resuscitation. ER-α agonist propyl pyrazole triol (PPT; 5 μg/kg), ER-β agonist diarylpropionitrile (DPN; 5 μg/kg), 17β-estradiol (50 μg/kg), or vehicle (10% DMSO) was injected subcutaneously during resuscitation. Twenty-four hours thereafter, splenic T cells were isolated, and their IL-2 and IFN-γ production and MAPK, NF-κB, and AP-1 activation were measured. T-cell IL-2 and IFN-γ production was decreased following trauma-hemorrhage, and this was accompanied with a decrease in T-cell MAPK, NF-κB, and AP-1 activation. PPT or 17β-estradiol administration following trauma-hemorrhage normalized those parameters, while DPN administration had no effect. Since PPT, but not DPN, administration following trauma-hemorrhage was as effective as 17β-estradiol in preventing the T-cell suppression, it appears that ER-α plays a predominant role in mediating the salutary effects of 17β-estradiol on T cells following trauma-hemorrhage, and that such effects are likely mediated via normalization of MAPK, NF-κB, and AP-1 signaling pathways.

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