Tregcells may regulate interlukin-17 production by modulating TH1 responses in 1,3-β-glucan-induced lung inflammation in mice

Chen, Ying; Liu, Fangwei; Wu, Dong; Song, Laiyu; Li, Cuiying; Wen, Tao; Yu, Yong; Dai, Wujing; Chen, Jie

doi:10.3109/1547691x.2012.711784

Cited by 3 publications

(4 citation statements)

References 43 publications

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“…LPS and 1,3-b-glucan have been established to induce increased levels of these cytokines (Chen et al, 2013;Joh et al, 2012;Ribeiro et al, 2011). Therefore, we speculate that microbial ligands adsorbed to PM2.5rd cause, at least partially, neutrophilic lung inflammation.…”

Section: Discussionmentioning

confidence: 94%

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

Ichinose

Ren

et al. 2015

Inhalation Toxicology

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PM2.5 can exacerbate asthma. Organic substances adsorbed on PM2.5-rich dust (PM2.5rd) were inactivated by heating at 360 °C. To characterize the role of organic substances, the effects of PM2.5rd and heated PM2.5-rich dust (H-PM2.5 rd) on allergic lung inflammation were investigated. BALB/c mice were intratracheally administered PM2.5rd or H-PM2.5rd with or without ovalbumin (OVA) four times at 2-week intervals. PM2.5rd, but not H-PM2.5rd, caused neutrophilic alveolitis and bronchitis. In the presence of OVA, PM2.5rd caused severe eosinophil infiltration and goblet cells proliferation in airways, along with a marked induction of the Th2 cytokines interleukin (IL)-4 and IL-13, and the eosinophil-related cytokine IL-5 in bronchoalveolar lavage fluid (BALF). OVA + H-PM2.5rd caused a weaker response. PM2.5rd showed adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production, but H-PM2.5rd showed minimal effects. These findings suggested that PM2.5rd-bound substances might aggravate lung eosinophilia. To clarify the roles of TLR2, TLR4, and MyD88 on cytokine production in PM2.5rd, murine bone marrow-derived macrophages (BMDMs) from wild-type (WT), TLR2(-/-), TLR4(-/-), and MyD88(-/-) BALB/c mice were stimulated with dust. Cytokine production was low or undetectable in TLR4(-/-) cells, but occurred from TLR2(-/-) cells, and production by MyD88(-/-) cells was higher than by TLR4(-/-) cells. These results suggest that TLR4 and TLR2 ligands (LPS and β-glucan, respectively) mainly contributed to cytokines production induced by PM2.5rd. In addition to chemical substances, PM2.5-bound microbial substances might act in inflammatory and allergic lung diseases.

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Section: Discussionmentioning

confidence: 94%

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

Ichinose

Ren

et al. 2015

Inhalation Toxicology

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“…Previous studies already demonstrated that Treg could obviously regulate 1,3-β-glucan-induced lung inflammation (9, 10). Similarly, as a regulatory immune cell subset, whether the regulation of B10 was associated with Treg?…”

Section: Discussionmentioning

confidence: 96%

“…Patients with hypersensitivity pneumonitis exhibit high percentage of lymphocytes in peripheral blood, which indicates a crucial role of lymphocytes in the development of hypersensitivity pneumonitis (8). We have previously showed that multiple CD4 + T lymphocyte responses dominated in different stages after 1,3-β-glucan exposure, including T helper (Th)1, Th2, Th17, and regulatory T cell (Treg) (9, 10). Exogenous 1,3-β-glucan induces numerous kinds of inflammatory cytokines and chemokine through NF-kB and NLRP3 signal pathways (11, 12).…”

Section: Introductionmentioning

confidence: 99%

IL-10-Producing B Cells Regulate T Helper Cell Immune Responses during 1,3-β-Glucan-Induced Lung Inflammation

Liu

Dai

et al. 2017

Front. Immunol.

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With the rapid development of industry and farm, fungi contamination widely exists in occupational environment. Inhalation of fungi-contaminated organic dust results in hypersensitivity pneumonitis. 1,3-β-Glucan is a major cell wall component of fungus and is considered as a biomarker of fungi exposure. Current studies showed that 1,3-β-glucan exposure induced lung inflammation, which involved uncontrolled T helper (Th) cell immune responses, such as Th1, Th2, Th17, and regulatory T cell (Treg). A recently identified IL-10-producing B cells (B10) was reported in regulating immune homeostasis. However, its regulatory role in hypersensitivity pneumonitis is still subject to debate. In our study, we comprehensively investigated the role of B10 and the relationship between B10 and Treg in 1,3-β-glucan-induced lung inflammation. Mice with insufficient B10 exhibited more inflammatory cells accumulation and severer pathological inflammatory changes. Insufficient B10 led to increasing Th1, Th2, and Th17 responses and restricted Treg function. Depletion of Treg before the onset of inflammation could suppress B10. Whereas, Treg depletion only at the late stage of inflammation failed to affect B10. Our study demonstrated that insufficient B10 aggravated the lung inflammation mediated by dynamic shifts in Th immune responses after 1,3-β-glucan exposure. The regulatory function of B10 on Th immune responses might be associated with Treg and IL-10. Treg could only interact with B10 at an early stage.

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“…The immunomodulatory activity of β-glucans from S. cerevisiae has been described in several clinical trials, but also adequately characterized in preclinical papers and in vitro investigations where the capacity of pure 1,3-1,6-β-glucans at concentration ≥ 10 µg/mL in increasing Th1, Th2 and Treg response in different immunocompetent cell lines [38,39] emerged.…”

Section: Discussionmentioning

confidence: 99%

Investigation on the Efficacy of Two Food Supplements Containing a Fixed Combination of Selected Probiotics and β-Glucans or Elderberry Extract for the Immune System: Modulation on Cytokines Expression in Human THP-1 and PBMC

Cappellucci,

Baini,

Miraldi

et al. 2024

Foods

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Several herbal and other natural products are used as ingredients in food supplements to strengthen immunity even if, very often, marketed products are proposed without a clear rationale or experimental evidence. In this study, we aimed to investigate the effect on human monocytes (THP-1) and on ex vivo human peripheral blood mononuclear cells (PBMC) of two formulations, one containing Bifidobacterium animalis subsp. lactis Bl-04® with β-glucans (for adults) and one containing Lactobacillus rhamnosus CRL1505 with elderberry extract (for children). We compared formulations with single ingredients, with bacterial lipopolysaccharide (LPS) and the drug pidotimod; cytokines expression level was evaluated testing different concentrations of samples at two exposure times. As expected, LPS caused a non-specific huge upregulation of cytokines expression both in THP-1 and in PBMC, whereas pidotimod mainly upregulated IL-2 in PBMC and IL-8 in THP-1. The two formulations showed a difference between a pro-inflammatory stimulus such as LPS, and also from an immunostimulant drug, such as pidotimod, as they mainly upregulated the expression of IL-6 and IL-10 in PBMC but not in THP-1, in a concentration-dependent mode. Probiotics were shown to play a major role, but β-glucans and elderberry extract exerted a synergistic activity. This work demonstrated that combining selected probiotics with other natural products having immunomodulatory properties is an interesting strategy to develop innovative formulations in the sector of food supplements.

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T_regcells may regulate interlukin-17 production by modulating T_H1 responses in 1,3-β-glucan-induced lung inflammation in mice

Cited by 3 publications

References 43 publications

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

PM2.5-rich dust collected from the air in Fukuoka, Kyushu, Japan, can exacerbate murine lung eosinophilia

IL-10-Producing B Cells Regulate T Helper Cell Immune Responses during 1,3-β-Glucan-Induced Lung Inflammation

Investigation on the Efficacy of Two Food Supplements Containing a Fixed Combination of Selected Probiotics and β-Glucans or Elderberry Extract for the Immune System: Modulation on Cytokines Expression in Human THP-1 and PBMC

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