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Diffuse Lung Disease |

Chitin and β-Glucan Reduce a LPS-Induced Secretion of Inflammatory Cytokines “In Vitro” FREE TO VIEW

Marjeta Tercelj, PhD; Barbara Salobir, PhD; Sanja Stopinsek, PhD; Sasa Simcic, PhD; Alojz Ihan, PhD; Ragnar Rylander, PhD
Author and Funding Information

University Medical Clinical Centre, Ljubljana, Slovenia


Chest. 2014;145(3_MeetingAbstracts):248A. doi:10.1378/chest.1823612
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Abstract

SESSION TITLE: ILD Posters

SESSION TYPE: Poster Presentations

PRESENTED ON: Saturday, March 22, 2014 at 01:15 PM - 02:15 PM

PURPOSE: A previous study demonstrated that inflammatory cytokines in the blood of patients with sarcoidosis were related to the pulmonary granuloma infiltration. This study was undertaken to evaluate if agents in the fungal cell wall would influence the cellular cytokine response to an inflammatory challenge "in vitro".

METHODS: Peripheral blood monocyte cells (PBMC) were isolated from patients with sarcoidosis (n=19) and controls (n=18). The cells were exposed to lipopolysaccharide (LPS) alone or in combination with the fungal cell wall agents β-glucan or chitin. The secretion of TNFα, interleukin (IL)-6, IL-10, and IL-12 was measured. Blood samples were taken to determine inflammatory cytokines and a chest x-ray was taken and the degree of granuloma infiltration was scored. Domestic exposure to fungi was determined by measuring the amount of airborne β-N-acetylhexosaminidase (NAHA).

RESULTS: LPS induced a secretion of TNFα, IL-6, IL-10, and IL-12 from PBMC - higher in sarcoidosis. Chitin depressed the secretion of all cytokines, less so in controls. The degree of suppression varied between the cytokines (TNFα 16%, IL-6 59%, IL-10 83%, and IL-12 19%). There were relationships between the x-ray scores and the depression of IL-12 (by chitin p=0.011 and by β-glucan 0.005), and between the domestic exposure to fungi and the chitin depression of IL-6 and IL-10 (p= 0.002 for both). For serum cytokines there were relationships between TNFα and the chitin depression of IL-10 and IL-12 (p=0.045 and 0.015), For sIL-2R and sIL-12 there were relations to the β-glucan depression of TNFα and IL-12 (sIL-2R p=0.002 and 0.001, and sIL-12 p=0.004 and 0.003).

CONCLUSIONS: The results demonstrate that chitin and β-glucan depressed the cellular response to an inflammatory agent. The degree of the depression was related to several clinical variables and to the domestic exposure to fungi. The depression was most pronounced for IL-6 and IL-10. These cytokines have anti-inflammatory effects that prevent the formation of granulomas. The depression of these cytokines by fungal cell wall agents may thus be a mechanism behind the formation of granulomas in sarcoidosis.

CLINICAL IMPLICATIONS: Fungal exposure should be explored in cases of sarcoidosis as this exposure might influence the severity of the disease.

DISCLOSURE: The following authors have nothing to disclose: Marjeta Tercelj, Barbara Salobir, Sanja Stopinsek, Sasa Simcic, Alojz Ihan, Ragnar Rylander

No Product/Research Disclosure Information


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