scholarly journals EFFECT OF 12-WEEK LOW-INTENSITY EXERCISE ON INTERLEUKIN-2, INTERFERON-GAMMA AND INTERLEUKIN-4 CYTOKINE PRODUCTION IN RAT SPLEENS

2018 ◽  
Vol 14 (3) ◽  
pp. e14-e19
Author(s):  
Eun-Ju Choi ◽  
Chang-Jin Lee ◽  
Hyo-Hyun Park ◽  
Wi-Young So
Keyword(s):  
Interferon Gamma ◽  
Cytokine Production ◽  
Interleukin 2 ◽  
Male Rats ◽  
Interleukin 4 ◽  
Control Group ◽  
T Helper ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Helper Type

Background and Objective High-intensity exercise has been linked to immunity; however, the relationship between low-intensity exercise and the immune system is unclear. In this study, the effects of exercise on cytokine production in T helper 1 (interleukin-2 [IL-2] and interferon-gamma [INF-g]) and T helper 2 cells (interleukin-4 [IL-4]) in spleens were investigated. Material and Methods Sprague–Dawley male rats were divided into a control group (CON, n = 10) and a low-intensity exercise group (EX, n = 10). EX rats were trained on a treadmill (8 m/min, 50 min/day, 5 times over 12 weeks). Spleen tissues were analyzed by hematoxylin-eosin staining and real-time PCR to quantify IL-4, INF-γ, and IL-2 expression. Results IL-4 expression was significantly higher in the EX group than in the CON group (p < 0.05). However, IL-2 and INF-γ expression did not differ between groups (p > 0.05). Conclusion These results suggest that exercise in rats enhances immune function by regulating cytokine production in T helper type 2 (IL-4) cells, but not in T helper type 1 (IL-2 and IFN-g) cells of the activated spleen.

scholarly journals CD28-induced costimulation of T helper type 2 cells mediated by induction of responsiveness to interleukin 4.

1993 ◽  
Vol 178 (5) ◽  
pp. 1645-1653 ◽  
Author(s):  
J G McArthur ◽  
D H Raulet
Keyword(s):  
Interleukin 2 ◽  
Interleukin 4 ◽  
Th2 Cells ◽  
T Helper ◽  
Autocrine Growth ◽  
Th Cells ◽  
Antigen Presenting ◽  
Helper Type

Type 1 and type 2 cloned T helper (Th) cells are believed to require different antigen-presenting cell (APC)-derived costimuli for proliferation. In the case of Th1-cloned T cells, CD28 signaling costimulates production of autocrine interleukin 2 (IL-2). Th2 cells produce their autocrine growth factor, IL-4, without costimulation, but require APC-derived costimuli, or IL-1, to respond to IL-4. Here we demonstrate that engagement of CD28 on Th2 cells with anti-CD28 antibody or with APC-associated B7 costimulates Th2 responsiveness to IL-4 but does not affect IL-4 or IL-2 production by Th2 cells. Costimulation of Th2 cells via CD28 appears to involve the induction of IL-1 production by Th2 cells, which acts in an autocrine fashion to induce IL-4 responsiveness. These results suggest that CD28-induced costimulation plays an important role in responses mediated by both types of Th cells.

scholarly journals Priming for T helper type 2 differentiation by interleukin 2–mediated induction of interleukin 4 receptor α-chain expression

2008 ◽  
Vol 9 (11) ◽  
pp. 1288-1296 ◽  
Author(s):  
Wei Liao ◽  
Dustin E Schones ◽  
Jangsuk Oh ◽  
Yongzhi Cui ◽  
Kairong Cui ◽  
...  
Keyword(s):  
Interleukin 2 ◽  
Interleukin 4 ◽  
T Helper ◽  
Α Chain ◽  
Interleukin 4 Receptor ◽  
Helper Type

scholarly journals Induction of T Helper Type 1 Responses by a Polysaccharide Deacetylase from Cryptococcus neoformans

2003 ◽  
Vol 71 (9) ◽  
pp. 5412-5417 ◽  
Author(s):  
Carmelo Biondo ◽  
Concetta Beninati ◽  
Mauro Bombaci ◽  
Luciano Messina ◽  
Giuseppe Mancuso ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cryptococcus Neoformans ◽  
Interleukin 2 ◽  
Gamma Interferon ◽  
Interleukin 4 ◽  
T Helper ◽  
Spleen Cells ◽  
Induce Cell Proliferation ◽  
Helper Type

ABSTRACT A 25-kDa cryptococcal deacetylase (d25) was found here to induce cell proliferation, as well as secretion of interleukin 2 and gamma interferon, but not interleukin 4, in spleen cells from d25-immunized or Cryptococcus neoformans-infected mice. The gamma interferon, but not the interleukin 2, response was required for the protective activities of d25 immunization in a murine cryptococcosis model.

scholarly journals Interleukin 4 and T helper type 2 cells are required for development of experimental onchocercal keratitis (river blindness).

1995 ◽  
Vol 182 (4) ◽  
pp. 931-940 ◽  
Author(s):  
E Pearlman ◽  
J H Lass ◽  
D S Bardenstein ◽  
M Kopf ◽  
F E Hazlett ◽  
...  
Keyword(s):  
T Cell ◽  
Interferon Gamma ◽  
Nude Mice ◽  
Mononuclear Cells ◽  
Corneal Stroma ◽  
Interleukin 4 ◽  
T Helper ◽  
Stromal Keratitis ◽  
Helper Type

Inflammation of the corneal stroma (stromal keratitis) is a serious complication of infection with the nematode parasite Onchocerca volvulus. Because stromal keratitis is believed to be immunologically mediated in humans, we used a murine model to examine the role of T cells and T helper cell cytokines in the immunopathogenesis of these eye lesions. BALB/c mice immunized subcutaneously and injected intrastromally with soluble O. volvulus antigens (OvAg) developed pronounced corneal opacification and neovascularization. The corneal stroma was edematous and contained numerous eosinophils and mononuclear cells. Stromal keratitis in immunized mice was determined to be T cell dependent based on the following observations: (a) T cell-deficient nude mice immunized and injected intrastromally with OvAg fail to develop corneal pathology; and (b) adoptive transfer of spleen cells from OvAg-immunized BALB/c mice to naive nude mice before intrastromal injection of OvAg results in development of keratitis. OvAg-stimulated lymph node and spleen cell cytokine production was dependent on CD4 cells and included interleukin (IL)-4 and IL-5, but not interferon gamma, indicating a predominant T helper type 2 cell-like response. Inflamed corneas from immunized BALB/c mice and from reconstituted nude mice had greatly elevated CD4 and IL-4 gene expression compared with interferon gamma. Mice in which the IL-4 gene was disrupted failed to develop corneal disease, demonstrating that IL-4 is essential in the immunopathogenesis of O. volvulus-mediated stromal keratitis.

scholarly journals Dysregulation of interleukin 4, interleukin 5, and interferon gamma gene expression in steroid-resistant asthma.

1995 ◽  
Vol 181 (1) ◽  
pp. 33-40 ◽  
Author(s):  
D Y Leung ◽  
R J Martin ◽  
S J Szefler ◽  
E R Sher ◽  
S Ying ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Affinity ◽  
Interferon Gamma ◽  
Messenger Rna ◽  
Oral Prednisone ◽  
Interleukin 2 ◽  
Interleukin 4 ◽  
Cytokine Gene Expression ◽  
Ifn Gamma ◽  
Steroid Resistant

In steroid-resistant (SR) asthma, there is a lack of clinical responsiveness to oral prednisone. Previous studies indicate that this may be explained by the effect of the combination of interleukin 2 (IL-2) and IL-4 on glucocorticoid receptor binding affinity. By contrast, steroid-sensitive (SS) asthmatics respond well to glucocorticoids, and this is accompanied by a decrease in the numbers of bronchoalveolar lavage (BAL) messenger RNA+ (mRNA+) cells expressing IL-4 and IL-5, and an increase in interferon gamma (IFN-gamma) transcripts. In the present study, we hypothesized that SR asthma is associated with alterations in T helper types 1/2 (Th2/Th1)-type cytokine gene expression. BAL was performed in six SR asthmatics and six SS asthmatics, before and after a 1-wk course of 40 mg daily prednisone. mRNA+ cells for IL-2, IL-4, IL-5, and IFN-gamma was measured by in situ hybridization using 35S-labeled RNA probes. Before prednisone therapy, there were significantly greater numbers of BAL cells (per 1,000) expressing IL-2 mRNA (p &lt; 0.01) and IL-4 mRNA (p &lt; 0.05) in SR asthmatics as compared with SS asthmatics, but no differences between the two groups in the numbers of BAL cells expressing IFN-gamma or IL-5 mRNA expression were observed. After a 1-wk course of prednisone, IL-2 expression was not altered in either group. However, SS asthmatics had a significant decrease in the numbers of BAL cells expressing mRNA for IL-4 (p &lt; 0.01) and IL-5 (p &lt; 0.001), and a rise in the numbers of IFN-gamma mRNA+ cells (p &lt; 0.01). In contrast, after prednisone treatment, SR asthmatics had no significant change in either the number of BAL cells expressing mRNA for IL-4 or IL-5. Of note, there was an unexpected decrease in the numbers of IFN-gamma mRNA+ cells (p = 0.05). Our current findings indicate that SR asthma is associated with a dysregulation of the expression of the genes encoding for Th2/Th1 cytokines in airway cells and is compatible with the concept that a combination of IL-2 and IL-4 induce glucocorticoid (GR) binding affinity and T cell responsiveness to glucocorticoids.

scholarly journals Nintedanib reduces corticosteroid resistance pulmonary fibrosis induced by bleomycin in mice by increasing the expression of β3 & β6 integrins

2021 ◽  
Author(s):  
Doha O Alghamdi ◽  
Hala S Abdel Kawy ◽  
Zuhair A Damanhouri
Keyword(s):  
Pulmonary Fibrosis ◽  
Lung Tumor ◽  
Histopathological Examination ◽  
Interleukin 2 ◽  
Interleukin 4 ◽  
Control Group ◽  
Lung Water ◽  
Necrosis Factor Alpha ◽  
Major Health Problem ◽  
Corticosteroid Resistance

Abstract Background:Corticosteroid resistance pulmonary fibrosis is a major health problem. This study aimed to determine the effectiveness of nintedanib on corticosteroid resistance pulmonary fibrosis induced by bleomycin in mice.Methods:The mice were divided into five groups 12 mice each. control group, BLM group received single dose of bleomycin (BLM), BLM+MP group received BLM and methylprednisolone (MP), BLM+NIN group received BLM and nintedanib(NIN) and BLM + NIN + MP group. The lung tissues were obtained for biochemical analysis, gene expression and histopathological examination on day 7 and day 28.Results:After 7 days, both NIN groups showed a significant decrease in the levels of interleukin-2, interleukin-4, interferon-gamma, lung tumor necrosis factor-alpha, Malondialdehyde and lung water content with a significant increase in the Glutathione level in lung tissues compared to MP group. After 28 days, both NIN groups showed a significant reduction in hydroxyproline, and Trans-forming Growth Factor beta lung tissues contents compared to MP group, and they showed a positive effect on the expression of β 3 &β6 integrins compared to the negative effect of MP group. Histopathologically, both NIN groups showed significant improvement compared to MP group by H&E and Masson’s trichrome stains. Immunohistochemical staining revealed negative BCL-2 expression in the cytoplasm of bronchiolar epithelium in both NIN groups after 7 and 28 days of treatment. Lung tissue morphometric studies showed significant improvement of pathological changes induced by BLM in both NIN groups.Conclusion:Altogether, our data indicates that nintedanib overcame corticosteroid resistance pulmonary fibrosis induced by bleomycin.

scholarly journals Interactions of thymic stromal lymphopoietin with interleukin-4 in adaptive immunity during Aspergillus fumigatus keratitis

2021 ◽  
Vol 14 (10) ◽  
pp. 1473-1483
Author(s):  
Chen Chen ◽  
◽  
Fang Han ◽  
Jia-Yin Wu ◽  
Lin Sun ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Adaptive Immunity ◽  
Post Infection ◽  
Thymic Stromal Lymphopoietin ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
T Helper ◽  
Cytokine Levels ◽  
Pretreated Group ◽  
Helper Type

AIM: To investigate the potential interactions of thymic stromal lymphopoietin (TSLP) with interleukin-4 (IL-4) in adaptive immunity during fungal keratitis (FK). METHODS: An FK mouse model was induced with Aspergillus fumigatus (AF) hyphal infection. Mice were divided into several groups: untreated, phosphate buffer saline (PBS), infected with AF, and pretreated with a scrambled siRNA, a TSLP-specific siRNA (TSLP siRNA), murine recombinant TSLP (rTSLP), immunoglobulin G (IgG), murine recombinant IFN (rIFN-γ), murine recombinant IL-4 (rIL-4), rIL-13, murine recombinant IL-17A (rIL-17A), and murine recombinant IL-17F (rIL-17F) groups. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) or Western blot were performed to determine mRNA and protein levels in the inflamed cornea. Cytokine locations were observed by immunofluoresence staining after AF hyphal infection. RESULTS: Compared to those in the untreated group, TSLP and T helper type 1 (Th1) cytokine levels in the AF group were upregulated at 24h post infection (hpi), and those of T helper type 2 (Th2) and T helper type 17 (Th17) cytokines were increased at 5d post infection (dpi). Th2 cytokine levels were decreased in the TSLP siRNA-pretreated group and increased in the rTSLP-pretreated group compared with the AF group. The TSLP level was increased in the rIL-4-pretreated group, but there were no significant changes among the other groups. Immunofluorescence staining showed cytokine locations after AF hyphal infection. CONCLUSION: TSLP induces a Th2 immune response and promots Th2 T cell differentiation in vivo. IL-4 promotes TSLP secretion. Therefore, TSLP with IL-4 regulates adaptive immunity in FK.

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