Adjuvant effect of zymosan after pulmonary treatment in a mouse ovalbumin allergy model

Young, Shih‐Houng; Wolfarth, Michael G.; Roberts, Jenny R.; Kashon, Michael L.; Antonini, James M.

doi:10.3109/01902148.2012.749960

Cited by 10 publications

(8 citation statements)

References 39 publications

(46 reference statements)

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“…Our results demonstrating the 1,3-␤-glucan-mediated modulation of OVA-induced allergy are partly in contrast to studies performed by Inoue et al (26) using soluble ␤-glucan and Young et al (60) using zymosan during sensitization but not during challenge. Those studies demonstrated exacerbated eosinophilic airway inflammation with mucous cell metaplasia in mice and elevated expression of Th2 cytokines, chemokines, and IgE, which are associated with an allergic response.…”

Section: Discussioncontrasting

confidence: 99%

Protective effects of surfactant protein D treatment in 1,3-β-glucan-modulated allergic inflammation

Fakih

Pilecki

Schlosser

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Surfactant protein D (SP-D) is a pulmonary collectin important in lung immunity. SP-D-deficient mice (Sftpd(-/-)) are reported to be susceptible to ovalbumin (OVA)- and fungal allergen-induced pulmonary inflammation, while treatment with exogenous SP-D has therapeutic effects in such disease models. β-Glucans are a diverse group of polysaccharides previously suggested to serve as fungal ligands for SP-D. We set out to investigate if SP-D could interact with 1,3-β-glucan and attenuate allergic pulmonary inflammation in the presence of 1,3-β-glucan. Allergic airway disease was induced in Sftpd(-/-) and Sftpd(+/+) mice by OVA sensitization and subsequent challenge with OVA, 1,3-β-glucan, or OVA/1,3-β-glucan together. Mice in the combined treatment group were further treated with a high dose of recombinant fragment of human SP-D (rfhSP-D). We demonstrated direct interaction between SP-D and 1,3-β-glucan. OVA-induced mucous cell metaplasia was increased in Sftpd(-/-) mice, supporting previously reported protective effects of endogenous SP-D in allergy. OVA-induced parenchymal CCL11 levels and eosinophilic infiltration in bronchoalveolar lavage were unaffected by 1,3-β-glucan, but were reversed with rfhSP-D treatment. 1,3-β-Glucan treatment did, however, induce pulmonary neutrophilic infiltration and increased TNF-α levels in bronchoalveolar lavage, independently of OVA-induced allergy. This infiltration was also reversed by treatment with rfhSP-D. 1,3-β-Glucan reduced OVA-induced mucous cell metaplasia, T helper 2 cytokines, and IFN-γ production. rfhSP-D treatment further reduced mucous metaplasia and T helper 2 cytokine secretion to background levels. In summary, rfhSP-D treatment resulted in attenuation of both allergic inflammation and 1,3-β-glucan-mediated neutrophilic inflammation. Our data suggest that treatment with high-dose SP-D protects from mold-induced exacerbations of allergic asthma.

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Section: Discussioncontrasting

confidence: 99%

Protective effects of surfactant protein D treatment in 1,3-β-glucan-modulated allergic inflammation

Fakih

Pilecki

Schlosser

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…To determine whether Th17 cells are resistant to glucocorticoid suppression in vivo and whether BCL-2 levels are different among lung Th subsets, we adopted a murine severe asthma model (27–29). After two sensitizations with OVA using zymosan and Pam3CSK4 as adjuvants and repeated OVA challenges, a predominant Th17/neutrophilic inflammation was observed (Fig.…”

Section: Resultsmentioning

confidence: 99%

BCL-2 protects human and mouse Th17 cells from glucocorticoid-induced apoptosis

Banuelos

Shin

Cao

et al. 2016

Allergy

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Background Glucocorticoid resistance has been associated with Th17-driven inflammation, the mechanisms of which are not clear. We determined whether human and mouse Th17 cells are resistant to glucocorticoid-induced apoptosis. Methods Freshly isolated human blood Th17 cells and in vitro differentiated Th17 cells from IL-17F red fluorescent protein reporter mice were treated with dexamethasone, a potent glucocorticoid. Apoptosis was measured using annexin V and DAPI staining. Screening of apoptosis genes was performed using the apoptosis PCR array. Levels of molecules involved in apoptosis were measured using quantitative RT-PCR, flow cytometry, and Western blotting. Knockdown of BCL-2 in murine Th17 cells was performed via retroviral transduction. Cytokines were measured using ELISA. A murine Th17-driven severe asthma model was examined for Th17 glucocorticoid sensitivity in vivo. Results Human and mouse Th17 cells and mouse Th2 cells were resistant to glucocorticoid-induced apoptosis. Th17 cells had glucocorticoid receptors levels comparable to those in other T effectors cells. Th17 cells had high levels of BCL-2, knockdown of which sensitized Th17 cells to dexamethasone-induced apoptosis. Production of IL-22, but not IL-17A and IL-17F, was suppressed by glucocorticoids. STAT3 phosphorylation in Th17 cells was insensitive to glucocorticoid inhibition. Lung Th17 cells in the murine severe asthma model were enhanced, rather than suppressed, by glucocorticoids. Conclusion Th17 cells are resistant to glucocorticoid-induced apoptosis and cytokine suppression, at least in part due to high levels of BCL-2. These findings support a role of Th17 cells in glucocorticoid-resistant inflammatory conditions such as certain endotypes of asthma.

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“…Hence, administration of β‐glucan by the oral route or by intraperitoneal injection inhibits the activity of Th2 cells and eosinophil inflammation in an allergic airways disease model mouse (Kawashima et al, ; Wu et al, ) and exerts a possible anti‐allergic effect in patients with allergic diseases (Jesenak, Hrubisko, Majtan, Rennerova, & Banovcin, ; Yamada, Hamuro, Hatanaka, Hamabata, & Kinoshita, ). However, airways exposure to β‐glucan enhances airways allergic responses and stimulates Th2 activity (Inoue et al, ; Young, Wolfarth, Roberts, Kashon, & Antonini, ).…”

Section: Discussionmentioning

confidence: 99%

Effects of co‐exposure of lipopolysaccharide and β‐glucan (Zymosan A) in exacerbating murine allergic asthma associated with Asian sand dust

Sadakane

Ichinose

Nishikawa

2018

J of Applied Toxicology

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During the 2000s, Asian sand dust (ASD) was implicated in the increasing prevalence of respiratory disorders, including asthma. We previously demonstrated that a fungus from ASD aerosol exacerbated ovalbumin (OVA)‐induced airways inflammation. Exposure to heat‐inactivated ASD (H‐ASD) and either Zymosan A (ZymA, containing β‐glucan) or lipopolysaccharide (LPS) exacerbated allergic airways inflammation in a mouse model, but the effects of co‐exposure of LPS and β‐glucan are unclear. We investigated the effects of co‐exposure of LPS and ZymA in OVA‐induced allergic airways inflammation with ASD using BALB/c mice. Exposure to OVA + LPS enhanced the recruitment of inflammatory cells to the lungs, particularly neutrophils; exposure to OVA + LPS + H‐ASD potentiated this effect. Exposure to OVA + ZymA + H‐ASD stimulated the recruitment of inflammatory cells to the lungs, particularly eosinophils, and serum levels of OVA‐specific IgE and IgG1 antibodies, whereas exposure to OVA + ZymA did not affect most indicators of lung inflammation. Although exposure to OVA + LPS + ZymA + H‐ASD affected a few allergic parameters additively or synergistically, most allergic parameters in this group indicated the same level of exposure to OVA + LPS + H‐ASD or OVA + ZymA + H‐ASD. These results suggest that LPS and ZymA play different roles in allergic airways inflammation with ASD; LPS mainly enhances neutrophil recruitment through H‐ASD, and ZymA enhances eosinophil recruitment through H‐ASD.

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Adjuvant effect of zymosan after pulmonary treatment in a mouse ovalbumin allergy model

Cited by 10 publications

References 39 publications

Protective effects of surfactant protein D treatment in 1,3-β-glucan-modulated allergic inflammation

Protective effects of surfactant protein D treatment in 1,3-β-glucan-modulated allergic inflammation

BCL-2 protects human and mouse Th17 cells from glucocorticoid-induced apoptosis

Effects of co‐exposure of lipopolysaccharide and β‐glucan (Zymosan A) in exacerbating murine allergic asthma associated with Asian sand dust

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