Airway Hyperresponsiveness is Associated with Inflammatory Cell Infiltration in Allergic Brown-Norway Rats

Elwood, Wayne; Barnes, Peter J.; Chung, Fan

doi:10.1159/000236340

Cited by 58 publications

(30 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present authors wanted to assess the involvement of another Th2 marker, development of airway eosinophilia after allergen challenge. Possible attenuation of airway eosinophilia might have clinical importance, since some previous studies have found that airway eosinophilia is closely related to increased bronchial hyperreactivity [26], although this is not a constant finding [27]. However, infiltration of eosinophils into the airways 24 h after aerosol challenge with TMA-RSA was not attenuated in the group made tolerant to OvA in the present study.…”

Section: Discussioncontrasting

confidence: 52%

Bystander suppression of occupational hapten sensitization in rats made tolerant to ovalbumin

Pullerits¹,

Lundin²,

Cui³

et al. 1998

Eur Respir J

View full text Add to dashboard Cite

Feeding a soluble antigen to an animal is known to cause a state of unresponsiveness against this antigen. If this antigen is given together with another antigen during the sensitization procedure, impairment of the response to the new antigen can also be seen, a phenomenon referred to as bystander suppression. The induction of tolerance against ovalbumin (OvA) and the effect of bystander suppression on the response to the hapten trimellitic anhydride (TMA), a cause of occupational asthma, were studied in Brown-Norway rats. Rats were fed either OvA-containing pellets or standard diet for 16 days before sensitization with the mixture of TMA and OvA. The animals were followed for 6 weeks after sensitization. Animals made tolerant to OvA showed a significantly suppressed delayed-type hypersensitivity (DTH) reaction against both OvA and TMA compared with the nontolerized control group at 5 weeks after sensitization, implying bystander suppression. By contrast, immunoglobulin (Ig)E and IgG antibody levels were suppressed only against OvA, whereas anti-TMA antibody levels were not affected. Airway eosinophilia after a single aerosol challenge at 6 weeks after sensitization using TMA conjugated to rat serum albumin, correlated with IgE anti-TMA levels in the group made tolerant to OvA and was not affected by OvA ingestion. In conclusion, suppressive factors released in ovalbumin-tolerant rats when they are challenged with ovalbumin, can suppress the response to trimellitic anhydride and this suppression is more pronounced for T-helper1-type responses.

show abstract

Section: Discussioncontrasting

confidence: 52%

Bystander suppression of occupational hapten sensitization in rats made tolerant to ovalbumin

Pullerits¹,

Lundin²,

Cui³

et al. 1998

Eur Respir J

View full text Add to dashboard Cite

show abstract

“…These animals develop significant airway hyper-responsiveness to inhaled methacholine in response to OVA challenge. Hyper-responsiveness has been associated with increased BAL-derived CD4 + T cell numbers [27], increased inflammatory-cell influx [28], and increased Eo-associated IL-5 levels in BALF [29]. ICAM-1 is important in generation of hyper-responsiveness, which can be attenuated by treatment with anti-ICAM-1 antibody [30].…”

Section: Discussionmentioning

confidence: 99%

Frontline: Inhibition of allergen‐induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro‐endocrine pathway

et al. 2004

View full text Add to dashboard Cite

Interactions between the neuro-endocrine system and immune system help maintain health. One interaction involves the superior cervical ganglia (SCG), which regulate the prohormone submandibular rat 1 (SMR1) produced by the submandibular gland (SMG). A peptide derived from SMR1, feG, has anti-inflammatory activity, and modification to D-isomer feG enhances bioactivity. We tested feG as a therapeutic agent for airways inflammation, using rats sensitized by OVA or Nippostrongylus brasiliensis (Nb). Treatment with feG but not fdG downregulated OVA-challenge-induced increases in bronchoalveolar lavage (BAL)-derived macrophages, eosinophils and PMN (neutrophils) by 44%, 69% and 67%, respectively, at 24 h. We found that feG also reduced ICAM-1 on BAL-derived macrophages and eosinophils by 27% and 65%, and L-selectin on PMN by 55% following OVA challenge. Furthermore, feG but not fdG reduced the OVA-induced TNF increase in BAL fluid. We showed that feG also down-regulated both hyper-responsiveness to methacholine (by 27%) and microgranulomata formation in the lung parenchyma. In Nb-challenged rats, feG treatment inhibited ex vivo allergen-induced contraction of tracheal smooth muscle by up to 73%. In conclusion, feG, which is a mimetic of a peptide derived from a rat salivary gland prohormone, has antiinflammatory properties in allergic airways inflammation in Brown-Norway rats. The role of the SCG-SMG neuro-endocrine pathway in allergic asthma and other inflammatory diseases requires additional study.

show abstract

“…The aim of the present study is to further clarify the role of MIF in asthma using rats. The study will demonstrate that anti-MIF Ab inhibits ovalbumin (OA)-induced airway inflammation as well as airway hyperresponsiveness in Brown Norway rats, which have been used as a model of atopic asthma [15][16][17].…”

mentioning

confidence: 99%

Role of macrophage migration inhibitory factor in ovalbumin-induced airway inflammation in rats

Kobayashi

Nasuhara

Kamachi

et al. 2006

European Respiratory Journal

View full text Add to dashboard Cite

Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that reportedly counteracts the anti-inflammatory effect of endogenous glucocorticoids. There have only been a few reports that demonstrate a potential link between MIF and bronchial asthma. In an attempt to further clarify the precise role of MIF in asthma, the present authors examined the effect of anti-MIF antibody (Ab) on airway inflammation and airway hyperresponsiveness in an ovalbumin-immunised rat asthma model.Actively immunised Brown Norway rats received ovalbumin inhalation with or without treatment of anti-MIF Ab. The levels of MIF in bronchoalveolar lavage fluid were significantly elevated after the ovalbumin challenge.An immunohistochemical study revealed positive immunostaining for MIF in bronchial epithelium, even in nonsensitised rats, and the MIF staining in bronchial epithelium was enhanced after the ovalbumin challenge. Anti-MIF Ab significantly decreased the number of total cells, neutrophils and eosinophils in the bronchoalveolar lavage fluid of the ovalbumin-challenged rats, and also attenuated the ovalbumin-induced airway hyperresponsiveness to ovalbumin and methacholine. However, anti-MIF Ab did not affect the level of serum ovalbumin-specific IgE, suggesting that anti-MIF Ab did not suppress immunisation itself.The results indicate that macrophage migration inhibitory factor plays a crucial role in airway inflammation and airway hyperresponsiveness in asthma.

show abstract

Airway Hyperresponsiveness is Associated with Inflammatory Cell Infiltration in Allergic Brown-Norway Rats

Cited by 58 publications

References 11 publications

Bystander suppression of occupational hapten sensitization in rats made tolerant to ovalbumin

Bystander suppression of occupational hapten sensitization in rats made tolerant to ovalbumin

Frontline: Inhibition of allergen‐induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro‐endocrine pathway

Role of macrophage migration inhibitory factor in ovalbumin-induced airway inflammation in rats

Contact Info

Product

Resources

About