scholarly journals Murine eosinophil development and allergic lung eosinophilia are largely dependent on the signaling adaptor GRB2

2018 ◽  
Vol 48 (11) ◽  
pp. 1786-1795 ◽  
Author(s):  
Ralf Willebrand ◽  
Axel Dietschmann ◽  
Lars Nitschke ◽  
Sven Krappmann ◽  
David Voehringer
Keyword(s):  
Lung Eosinophilia

Induction of lung eosinophilia and neutrophilia in guinea pigs following injection of Sephadex beads

Inflammation ◽  
1993 ◽  
Vol 17 (5) ◽  
pp. 537-550 ◽  
Author(s):  
K. Maghni ◽  
F. Blanchette ◽  
P. Sirois
Keyword(s):  
Guinea Pigs ◽  
Lung Eosinophilia

scholarly journals Prior Exposure to Live Mycobacterium bovis BCG Decreases Cryptococcus neoformans-Induced Lung Eosinophilia in a Gamma Interferon-Dependent Manner

2003 ◽  
Vol 71 (6) ◽  
pp. 3384-3391 ◽  
Author(s):  
Gerhard Walzl ◽  
Ian R. Humphreys ◽  
Ben G. Marshall ◽  
Lorna Edwards ◽  
Peter J. M. Openshaw ◽  
...  
Keyword(s):  
Cryptococcus Neoformans ◽  
Mycobacterium Bovis ◽  
Mycobacterial Infection ◽  
Gamma Interferon ◽  
Delayed Type Hypersensitivity ◽  
Infection Model ◽  
Dependent Manner ◽  
Interleukin 5 ◽  
Lung Eosinophilia ◽  
Mycobacterial Antigens

ABSTRACT Some common childhood infections appear to prevent the development of atopy and asthma. In some Mycobacterium bovis BCG-vaccinated populations, strong delayed-type hypersensitivity responses to mycobacterial antigens are associated with a reduced risk of atopy. Although BCG exposure decreases allergen-induced lung eosinophilia in animal models, little attention has been given to the effect of immunity to BCG on responses against live pathogens. We used the murine Cryptococcus neoformans infection model to investigate whether prior BCG infection can alter such responses. The present study shows that persistent pulmonary BCG infection of C57BL/6 mice induced an increase in gamma interferon, a reduction in interleukin-5, and a decrease in lung eosinophilia during subsequent Cryptococcus infection. This effect was long lasting, depended on the presence of live bacteria, and required persistence of mycobacterial infection in the lung. Reduction of eosinophilia was less prominent after infection with a mutant BCG strain (ΔhspR), which was rapidly cleared from the lungs. These observations have important implications for the development of vaccines designed to prevent Th2-mediated disease and indicate that prior lung BCG vaccination can alter the pattern of subsequent host inflammation.

Preclinical Safety and Pharmacology of an Anti-Human Interleukin-13 Monoclonal Antibody in Normal Macaques and in Macaques with Allergic Asthma

2008 ◽  
Vol 27 (5) ◽  
pp. 351-358 ◽  
Author(s):  
Pauline L. Martin ◽  
Dusti Fisher ◽  
William Glass ◽  
Karyn O’Neil ◽  
Anuk Das ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Allergic Asthma ◽  
Immunoglobulin E ◽  
Cynomolgus Macaque ◽  
Lavage Fluid ◽  
Antigen Challenge ◽  
Interleukin 13 ◽  
Lung Eosinophilia

Interleukin-13 (IL-13) plays a central role in chronic airway diseases, including asthma. These studies were conducted to evaluate the safety of administration of a human anti-IL-13 monoclonal antibody (mAb) to normal macaques and in macaques with allergic asthma. In addition, serum and bronchioalveolar lavage fluid were collected from allergic cynomolgus macaques in order to identify potential surrogate markers of IL-13 pharmacology that could be useful for subsequent clinical trials. In vitro studies demonstrated that the anti-IL-13 mAb inhibited the pharmacological actions of both human and cynomolgus macaque IL-13. Allergic macaques were treated systemically with 10 mg/kg anti-IL-13 mAb 1 day prior to inhaled Ascaris suum antigen challenge. Normal macaques were dosed intravenously with anti-IL-13 once per week for 3 weeks at doses of 10 or 50 mg/kg. Treatment of macaques with the anti-IL-13 mAb was not associated with any toxicologically significant findings. A slight treatment-related but nonadverse decrease in platelet counts was observed in both the normal and allergic macaques. In allergic macaques, the anti-IL-13 mAb treatment did not affect lung function, lung eosinophilia, or serum or BAL immunoglobulin E (IgE) concentrations but did produce a reduction in BAL and serum eotaxin concentrations ( p < .05) at 6 h post antigen challenge. This study shows that administration of an anti-IL-13 mAb was well tolerated in both normal and allergic asthmatic macaques and that serum eotaxin concentrations may be a useful early in vivo marker for evaluating IL-13 inhibition in patients with asthma.

scholarly journals Eosinophil-derived IL-13 promotes emphysema

2019 ◽  
Vol 53 (5) ◽  
pp. 1801291 ◽  
Author(s):  
Alfred D. Doyle ◽  
Manali Mukherjee ◽  
William E. LeSuer ◽  
Tyler B. Bittner ◽  
Saif M. Pasha ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Responses ◽  
Pulmonary Inflammation ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Chronic Type ◽  
Obstructive Pulmonary Disease ◽  
Lung Eosinophilia

The inflammatory responses in chronic airway diseases leading to emphysema are not fully defined. We hypothesised that lung eosinophilia contributes to airspace enlargement in a mouse model and to emphysema in patients with chronic obstructive pulmonary disease (COPD).A transgenic mouse model of chronic type 2 pulmonary inflammation (I5/hE2) was used to examine eosinophil-dependent mechanisms leading to airspace enlargement. Human sputum samples were collected for translational studies examining eosinophilia and matrix metalloprotease (MMP)-12 levels in patients with chronic airways disease.Airspace enlargement was identified in I5/hE2 mice and was dependent on eosinophils. Examination of I5/hE2 bronchoalveolar lavage identified elevated MMP-12, a mediator of emphysema. We showed, in vitro, that eosinophil-derived interleukin (IL)-13 promoted alveolar macrophage MMP-12 production. Airspace enlargement in I5/hE2 mice was dependent on MMP-12 and eosinophil-derived IL-4/13. Consistent with this, MMP-12 was elevated in patients with sputum eosinophilia and computed tomography evidence of emphysema, and also negatively correlated with forced expiratory volume in 1 s.A mouse model of chronic type 2 pulmonary inflammation exhibited airspace enlargement dependent on MMP-12 and eosinophil-derived IL-4/13. In chronic airways disease patients, lung eosinophilia was associated with elevated MMP-12 levels, which was a predictor of emphysema. These findings suggest an underappreciated mechanism by which eosinophils contribute to the pathologies associated with asthma and COPD.

scholarly journals Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Yahao Ren ◽  
Takamichi Ichinose ◽  
Miao He ◽  
Seiichi Youshida ◽  
Masataka Nishikawa ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Immune Cell ◽  
Adaptor Protein ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Pathological Changes ◽  
Th2 Response ◽  
Lung Eosinophilia ◽  
High Concentrations

Abstract Background Lipopolysaccharide (LPS) often presents in high concentrations in particulate matter (PM), few studies have reported the enhancing effects of both LPS and PM on airway inflammation in mice and the role of toll-like receptors (TLRs) in this process. Asian sand dust (ASD) is observed most frequently during the spring. This study aimed to clarify the role of TLRs in murine lung eosinophilia exacerbated by ASD and LPS. Methods The effects of LPS and ASD co-treatment on ovalbumin (OVA)-induced lung eosinophilia were investigated using wild-type (WT), TLR2−/−, TLR4−/−, and adaptor protein myeloid differentiation factor 88 (MyD88)−/− BALB/c mice. ASD was heated (H-ASD) to remove the toxic organic substances. WT, TLR2−/−, TLR4−/− and MyD88−/− BALB/c mice were intratracheally instilled with four different combinations of LPS, H-ASD and OVA treatment. Subsequently, the pathological changes in lungs, immune cell profiles in bronchoalveolar lavage fluid (BALF), inflammatory cytokines/chemokines levels in BALF and OVA-specific immunoglobulin (Ig) in serum were analyzed. Results In WT mice, H-ASD + LPS exacerbated OVA-induced lung eosinophilia. This combination of treatments increased the proportion of eosinophils and the levels of IL-5, IL-13, eotaxin in BALF, as well as the production of OVA-specific IgE and IgG1 in serum compared to OVA treatment alone. Although these effects were stronger in TLR2−/− mice than in TLR4−/− mice, the expression levels of IL-5, IL-13, eotaxin were somewhat increased in TLR4−/− mice treated with OVA + H-ASD + LPS. In MyD88−/− mice, this pro-inflammatory mediator-induced airway inflammation was considerably weak and the pathological changes in lungs were negligible. Conclusions These results suggest that LPS and H-ASD activate OVA-induced Th2 response in mice, and exacerbate lung eosinophilia via TLR4/MyD88, TLR4/TRIF and other TLR4-independent pathways.

scholarly journals The effects of several drugs on airway hyperresponsiveness and lung eosinophilia induced by Sephadex particles

1992 ◽  
Vol 58 ◽  
pp. 204
Author(s):  
Masayuki Asano ◽  
Noriaki Inamura ◽  
Kunio Nakahara ◽  
Akira Nagayoshi ◽  
Toyokazu Isono ◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
Lung Eosinophilia

Airborne Asian sand dust enhances murine lung eosinophilia

2010 ◽  
Vol 22 (12) ◽  
pp. 1012-1025 ◽  
Author(s):  
Miao He ◽  
Takamichi Ichinose ◽  
Seiichi Yoshida ◽  
Masataka Nishikawa ◽  
Ikuko Mori ◽  
...  
Keyword(s):  
Murine Lung ◽  
Lung Eosinophilia ◽  
Asian Sand Dust ◽  
Sand Dust

Dexamethasone reduces lung eosinophilia, and VCAM-1 and ICAM-1 expression induced by Sephadex beads in rats

2003 ◽  
Vol 468 (1) ◽  
pp. 59-66 ◽  
Author(s):  
Akemi Ito ◽  
Mio Miyake ◽  
Masashi Morishita ◽  
Komei Ito ◽  
Shinpei Torii ◽  
...  
Keyword(s):  
Lung Eosinophilia

A novel model of antigen-induced lung eosinophilia in brown-noway rats: effect of methylprednisolone

1990 ◽  
Vol 183 (4) ◽  
pp. 1191-1192 ◽  
Author(s):  
I.M. Richards ◽  
S.K. Shields ◽  
R.L. Griffin ◽  
C.J. Dunn
Keyword(s):  
Lung Eosinophilia ◽  
Novel Model
Sign in / Sign up

Export Citation Format

Share Document