Kinetics and mode of peptide delivery via the respiratory mucosa determine the outcome of activation versus TH2 immunity in allergic inflammation of the airways

Hall, Gillian; Lund, L.; Lamb, Jonathan R.; Jarman, Edward J.

doi:10.1067/mai.2002.129800

Cited by 23 publications

(16 citation statements)

References 36 publications

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“…[17] Hall et al reported that chitosan could prevent the induction of Th2-mediated pulmonary inflammation after sensitization and challenge of the airways with allergen. [31] We also suggested previously that WSC has antiinflammatory effects and inhibits the production of TNF-a and IL-6 in human astrocytoma cells activated by amyloid b peptide and IL-1b. [19] Activated mast cell-derived pro-inflammatory cytokines are important pathologic factors of progression of allergic inflammation.…”

Section: Mast Cells Function As An Important Component Of the Allergimentioning

confidence: 77%

Inhibitory Effect of Water‐Soluble Chitosan on TNF‐α and IL‐8 Secretion from HMC‐1 Cells

Kim

You²,

You³

et al. 2004

Immunopharmacology and Immunotoxicology

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Mast cells are known to play an active role as effector cells in allergic inflammation and in diverse immunological and pathological processes. Activated mast cell-derived pro-inflammatory cytokines are important pathologic factors of progression of allergic inflammation. In this study, we investigated whether pro-inflammatory cytokines (TNF-alpha and IL-8) can be induced by calcium stimulation in HMC-1 cells, and high molecular weight water-soluble chitosan (WSC) can inhibit the production of these cytokines. We provided evidence that the secretion of TNF-alpha and IL-8 from HMC-1 cells was induced by Ca2+-ionophore A23187 or Ca2+-ATPase inhibitor TSG. Treatment of WSC (10 microg/ml) prior to stimulation with calcium agonists significantly blocked the secretion of TNF-alpha by 65.1% for A23187 and 87.7% for TSG. IL-8 secretion in response to A23187 or TSG was inhibited by 49.2% for A23187 and 34.1% for TSG, respectively, compared to absence of WSC. These results suggest that WSC has potential regulatory effects on allergic inflammatory diseases by down-modulating Ca2+-induced mast cell activation.

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Section: Mast Cells Function As An Important Component Of the Allergimentioning

confidence: 77%

Inhibitory Effect of Water‐Soluble Chitosan on TNF‐α and IL‐8 Secretion from HMC‐1 Cells

Kim

You²,

You³

et al. 2004

Immunopharmacology and Immunotoxicology

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“…Compounds with modulatory properties might influence the tolerance induction in the mucosa [29]. For instance, the delivery of soluble peptides adsorbed to chitosan increases antigen release and maintains a sustained production of IL-10, facilitating tolerance induction [30]. Although the tolerance of SCII is characterized poorly, our data indicated the enhanced secretion of IL-10 upon the SCII feeding, suggesting that SCII might induce active cellular suppression.…”

Section: Discussionmentioning

confidence: 94%

Oral Administration of Shark Type II Collagen Suppresses Complete Freund’s Adjuvant-Induced Rheumatoid Arthritis in Rats

et al. 2012

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Objective: Shark type II collagen (SCII) is extracted as a glycoprotein from the cartilage of blue shark (Prionace glauca). We aim to confirm the effects of oral tolerance of SCII on inflammatory and immune responses to the ankle joint of rheumatoid-arthritis rats induced by Complete Freund’s Adjuvant (CFA). Materials and Methods: The onset of rheumatoid arthritis (RA) was observed 14 ± x days after injection of CFA. Rats in the control group were treated with acetic acid by oral administration (0.05 mmol kg−1d−1, days 14–28), while rats in experimental groups were treated by oral administration with SCII (1 or 3 mg kg−1d−1, days 14–28), Tripterygium wilfordii polyglycosidium (TWP) (10 mg kg−1d−1, days 14–28), and bovine type II collagen from US (US-CII) (1 mg kg−1d−1, days 14–28), respectively. The severity of arthritis was evaluated by the articular swelling. The immunological indexes observed included delayed type hypersensitivity (DTH) reaction, the level of interleukins 10 (IL-10) in rat blood serum and morphological characterization. Mixed lymphocyte culture (MLC) was performed to investigate the relationship between T cell apoptosis and specific immune tolerance induced by SCII. Results: Treatment with SCII for 2 weeks significantly attenuated the acute inflammation. The rats orally administrated with SCII at the level of 3 mg kg−1d−1 (SCII 3) and US-CII had decreased DTH reaction compared with rats in control group. Rats treated with SCII 3 had the highest level of IL-10 with 102 pg/mL. SCII with concentration of 10 μg/L could help to significantly enhance level of Fas/Apo-1 in T cell in vitro. The result of histological staining indicated that the recovery of the articular membranes of ankle joint in SCII 3 group was greatly enhanced. Conclusions: Our results suggest that appropriate dose of SCII can not only ameliorate symptoms but also modify the disease process of Complete-Freunds-Adjuvant-induced arthritis. Oral administration of SCII might be a potential candidate as a novel drug for further investigation.

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“…Chitosan's ability to modulate oral immunity is particular. At the same dose evaluated in this work, it reduces the enzymatic degradation of several proteins including CII [21,45], recruits immature dendritic cells at the inductive sites [22], promotes the expression of TGF‐β and IL‐4 mRNAs [21] and stimulates the release of IL‐10 [21,22,46]. Compounds with modulatory properties might influence the tolerance induction in the mucosa [47].…”

Section: Discussionmentioning

confidence: 99%

The biocompatible polysaccharide chitosan enhances the oral tolerance to type II collagen

Porporatto

Canali

Bianco

et al. 2008

Clinical and Experimental Immunology

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SummaryChitosan is a mucoadhesive polysaccharide that promotes the transmucosal absorption of peptides and proteins. At mucosal sites chitosan exhibits immunomodulatory activities and stimulates the release of regulatory cytokines. Herein we evaluated the effect of the co-administration of chitosan in the tolerance to type II collagen (CII) using an experimental model of arthritis. Rats were fed diluent (acetic acid), 1 mg CII, 1 mg chitosan or 1 mg CII + 1 mg chitosan during 5 days before immunization with CII in Freund's complete adjuvant. Systemic effects were evaluated in draining lymph nodes after antigenic challenge or during the clinical evolution of arthritis. Specific antibodies, proliferation against CII and the production of interferon (IFN)-g and interleukin-10 were assessed. Clinical signs were observed 13-15 days after primary immunization. The CII : chitosan group presented the lowest incidence and developed moderate arthritis, with reduced levels of immunoglobulin (Ig)G2a anti-CII, a limited proliferation in draining lymph nodes and a lower release of IFN-g after restimulation with CII. Our results demonstrate that chitosan enhances the tolerance to an articular antigen with a decrease in the inflammatory responses and, as a consequence, an improvement in clinical signs.

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Kinetics and mode of peptide delivery via the respiratory mucosa determine the outcome of activation versus TH2 immunity in allergic inflammation of the airways

Cited by 23 publications

References 36 publications

Inhibitory Effect of Water‐Soluble Chitosan on TNF‐α and IL‐8 Secretion from HMC‐1 Cells

Inhibitory Effect of Water‐Soluble Chitosan on TNF‐α and IL‐8 Secretion from HMC‐1 Cells

Oral Administration of Shark Type II Collagen Suppresses Complete Freund’s Adjuvant-Induced Rheumatoid Arthritis in Rats

The biocompatible polysaccharide chitosan enhances the oral tolerance to type II collagen

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