Lipocalin2 protects against airway inflammation and hyperresponsiveness in a murine model of allergic airway disease

Dittrich, A.-M.; Krokowski, M.; Meyer, Hellmuth-Alexander; Quarcoo, David; Avagyan, A.; Ahrens, Birgit; Kube, SM; Witzenrath, Martin; Loddenkemper, Christoph; Cowland, Jack B.; Hamelmann, Eckard

doi:10.1111/j.1365-2222.2010.03508.x

Cited by 34 publications

(23 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Lcn2, which is a small protein of 25 kD, is a transporter with several functions, including regulation of immune responses, cell growth and differentiation, transportation of iron, and synthesis of prostaglandin (Flower et al, 2000;Grzyb et al, 2006). Recent studies have shown that Lcn2 is up-regulated following allergen sensitization and airway challenges in lung tissues and have protective functions in allergic airway disease (Dittrich et al, 2010). Serpina3n is a member of a multigene family of serpins, which are the largest family of protease inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Identification of new altered genes in rat cochleae with noise-induced hearing loss

Han

Hong

Zhong

et al. 2012

Gene

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Identification of new altered genes in rat cochleae with noise-induced hearing loss

Han

Hong

Zhong

et al. 2012

Gene

View full text Add to dashboard Cite

“…ITIH1 was reported previously to possess anti-inflammatory activity through the inhibition of complement proteins (30). Lipocalin-2, a molecule involved in antimicrobial defense (28), protects against airway inflammation in a mouse model of allergic asthma (23). In addition, the tumor necrosis factor receptor superfamily 9 protein (Tnfrsf9) was shown previously to push the balance between Th17 cells and Tregs in favor of Treg generation (40).…”

Section: Resultsmentioning

confidence: 99%

Pertussis Toxin Exacerbates and Prolongs Airway Inflammatory Responses during Bordetella pertussis Infection

2012

View full text Add to dashboard Cite

Throughout infection, pathogenic bacteria induce dramatic changes in host transcriptional repertoires. An understanding of how bacterial factors influence host reprogramming will provide insight into disease pathogenesis. In the human respiratory pathogen Bordetella pertussis, the causative agent of whooping cough, pertussis toxin (PT) is a key virulence factor that promotes colonization, suppresses innate immune responses during early infection, and causes systemic disease symptoms. To determine the full extent of PT-associated gene regulation in the airways through the peak of infection, we measured global transcriptional profiles in the lungs of BALB/c mice infected with wild-type (WT) or PT-deficient (⌬PT) B. pertussis. ⌬PT bacteria were inoculated at a dose equivalent to the WT dose and at a high dose (⌬PT high ) to distinguish effects caused by higher bacterial loads achieved in WT infection from effects associated with PT. The results demonstrated that PT was associated with a significant upregulation of immune and inflammatory response genes as well as several other genes implicated in airway pathology. In contrast to the early, transient responses observed for ⌬PT high infection, WT infection induced a prolonged expression of inflammatory genes and increased the extent and duration of lung histopathology. In addition, the administration of purified PT to ⌬PT high -infected mice 1 day after bacterial inoculation exacerbated and prolonged inflammatory responses and airway pathology. These data indicate that PT not only is associated with exacerbated host airway responses during peak B. pertussis infection but also may inhibit host mechanisms of attenuating and resolving inflammation in the airways, suggesting possible links between PT and pertussis disease symptoms.

show abstract

“…Other studies revealed that Lcn2 also binds other types of siderophores, such as bacillibactin ( B. anthracis ) (157) and carboxy-mycobactin (mycobacteria) (158). Lcn2 is one of the most commonly studied novel biomarkers (159) and has emerged as a promising biomarker for different pulmonary diseases (97), kidney injury (160–163), liver failure (164), and tumorigenesis (144). Thus, the clinical relevance of Lcns is rapidly increasing even though the exact mechanisms behind their functions remain to be elucidated.…”

Section: Antimicrobial Peptidesmentioning

confidence: 99%

Antimicrobial Activity of Mesenchymal Stem Cells: Current Status and New Perspectives of Antimicrobial Peptide-Based Therapies

2017

View full text Add to dashboard Cite

While mesenchymal stem cells (MSCs)-based therapy appears to be promising, there are concerns regarding possible side effects related to the unwanted suppression of antimicrobial immunity leading to an increased risk of infection. Conversely, recent data show that MSCs exert strong antimicrobial effects through indirect and direct mechanisms, partially mediated by the secretion of antimicrobial peptides and proteins (AMPs). In fact, MSCs have been reported to increase bacterial clearance in preclinical models of sepsis, acute respiratory distress syndrome, and cystic fibrosis-related infections. This article reviews the current evidence regarding the direct antimicrobial effector function of MSCs, focusing mainly on the role of MSCs-derived AMPs. The strategies that might modulate the expression and secretion of these AMPs, leading to enhanced antimicrobial effect, are highlighted. Furthermore, studies evaluating the presence of AMPs in the cargo of extracellular vesicles (EVs) are underlined as perspective opportunities to develop new drug delivery tools. The antimicrobial potential of MSCs-derived EVs can also be heightened through cell conditioning and/or drug loading. Finally, improving the pharmacokinetics and delivery, in addition to deciphering the multi-target drug status of AMPs, should synergistically lead to key advances against infections caused by drug-resistant strains.

show abstract

Lipocalin2 protects against airway inflammation and hyperresponsiveness in a murine model of allergic airway disease

Abstract: These data indicate a protective role for Lcn2 in allergic airway disease, suggesting a pro-apoptotic effect as the underlying mechanism.

Cited by 34 publications

References 28 publications

Identification of new altered genes in rat cochleae with noise-induced hearing loss

Identification of new altered genes in rat cochleae with noise-induced hearing loss

Pertussis Toxin Exacerbates and Prolongs Airway Inflammatory Responses during Bordetella pertussis Infection

Antimicrobial Activity of Mesenchymal Stem Cells: Current Status and New Perspectives of Antimicrobial Peptide-Based Therapies

Contact Info

Product

Resources

About