Cathelicidin LL-37 restoring glucocorticoid function in smoking and lipopolysaccharide-induced airway inflammation in rats

Weng, Jian-Zhen; Wang, Yan; Sun, Tieying

doi:10.1097/cm9.0000000000000107

Cited by 11 publications

(10 citation statements)

References 48 publications

(53 reference statements)

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“…Three papers (n = 3/34, 9%) evaluated the interplay between cathelicidin and commonly used COPD and asthma drugs: corticosteroids [ 54 , 55 , 56 ]. Van der Berge et al found no difference in CAMP/LL-37 gene expression between budesonide and fluticasone propionate treatment [ 51 ].…”

Section: Resultsmentioning

confidence: 99%

A Scoping Analysis of Cathelicidin in Response to Organic Dust Exposure and Related Chronic Lung Illnesses

Golec

Lemieszek

Dutkiewicz

et al. 2022

IJMS

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Over two billion people worldwide are exposed to organic dust, which can cause respiratory disorders. The discovery of the cathelicidin peptide provides novel insights into the lung’s response to organic dust; however, its role in the lung’s response to organic dust exposure and chronic lung diseases remains limited. We conducted a scoping review to map the current evidence on the role of cathelicidin LL-37/CRAMP in response to organic dust exposure and related chronic lung diseases: hypersensitivity pneumonitis (HP), chronic obstructive pulmonary disease (COPD) and asthma. We included a total of n = 53 peer-reviewed articles in this review, following the process of (i) a preliminary screening; (ii) a systematic MEDLINE/PubMed database search; (iii) title, abstract and full-text screening; (iv) data extraction and charting. Cathelicidin levels were shown to be altered in all clinical settings investigated; its pleiotropic function was confirmed. It was found that cathelicidin contributes to maintaining homeostasis and participates in lung injury response and repair, in addition to exerting a positive effect against microbial load and infections. In addition, LL-37 was found to sustain continuous inflammation, increase mucus formation and inhibit microorganisms and corticosteroids. In addition, studies investigated cathelicidin as a treatment modality, such as cathelicidin inhalation in experimental HP, which had positive effects. However, the primary focus of the included articles was on LL-37’s antibacterial effect, leading to the conclusion that the beneficial LL-37 activity has not been adequately examined and that further research is required.

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Section: Resultsmentioning

confidence: 99%

A Scoping Analysis of Cathelicidin in Response to Organic Dust Exposure and Related Chronic Lung Illnesses

Golec

Lemieszek

Dutkiewicz

et al. 2022

IJMS

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“…Non-typeable Haemophilus influenzae exacerbates COPD by upregulating PI3K signalling [123][124][125]. It appears that bacterial lipopolysaccharide plays an important role by inducing ROS and a cascade of PI3K signalling in the lung [126][127][128][129]. In addition to bacteria, certain fungi exacerbate the COPD phenotype.…”

Section: Involvement Of Mirnas Targeting Pi3k Signalling In Copd Path...mentioning

confidence: 99%

PI3K signalling in chronic obstructive pulmonary disease and opportunities for therapy

Moradi

Jarrahi

Ahmadi

et al. 2021

The Journal of Pathology

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Chronic obstructive pulmonary disease (COPD) is a chronic lung disease characterised by airway inflammation and progressive obstruction of the lung airflow. Current pharmacological treatments include bronchodilators, alone or in combination with steroids, or other anti-inflammatory agents, which have only partially contributed to the inhibition of disease progression and mortality. Therefore, further research unravelling the underlying mechanisms is necessary to develop new anti-COPD drugs with both lower toxicity and higher efficacy. Extrinsic signalling pathways play crucial roles in COPD development and exacerbations. In particular, phosphoinositide 3-kinase (PI3K) signalling has recently been shown to be a major driver of the COPD phenotype. Therefore, several small-molecule inhibitors have been identified to block the hyperactivation of this signalling pathway in COPD patients, many of them showing promising outcomes in both preclinical animal models of COPD and human clinical trials. In this review, we discuss the critically important roles played by hyperactivated PI3K signalling in the pathogenesis of COPD. We also critically review current therapeutics based on PI3K inhibition, and provide suggestions focusing on PI3K signalling for the further improvement of the COPD phenotype.

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“…They exposed the whole rats to SCS (tar content 13 mg, and the nicotine content 0.8 mg) for 28 days in a custom-built fumigation chamber of 72L, with an intratracheal injection of LPS on the 1 st and 14 th day. They found increased levels of 8-iso-PGF2α, interleukin-8 (IL-8), and TNF-α in BALF and serum, while a decreased expression level of HDAC2 (histone deacetylase subtype plays a major role in preventing pathogenesis by inhibiting the expression of an inflammatory gene), and increased levels of PI3K, and p-AKT (oxidative stress activates this pathway which ultimately causes phosphorylation and inactivation of HDAC2) in lung tissue [36,37]. Male, Dunkin Hartley out-bred guinea pigs (350-400g) were used in a study for the induction of COPD using 200µl LPS intranasal instillation (5mg/ml in sterile saline).…”

Section: Laboratory Animal Models For Inducing Copd Using Different Ways Of Cs Exposurementioning

confidence: 99%

“…But due to short modelling time, partial COPD characteristics were established. [36,37] Mainstream CS and LPS Rat 24 cigarettes per day 1 h twice a day, 7 days a week, CS (6 week), LPS+CS (4week), CS+LPS (6 week).…”

Section: Use Of Mainstream Cs (Mcs) With Lps For Inducing Copdmentioning

confidence: 99%

“…The airway inflammation, emphysema, and mucous plugging in small bronchioles were more severe in the animals of CS + LPS group as compared to that in CS and LPS + CS groups. [37,38] Mice Mainstream CS at 250 μg/L wet total particulate matter (WTPM) for 5 h, 0.5 μg LPS/L for 1 h/day, twice per week, Smoke group (250 μg/L,WTPM), LPS group (0.5μgLPS/L), Smoke + LPS group (250μg/L,WTPM+0.5 μg LPS/L).…”

Section: Use Of Mainstream Cs (Mcs) With Lps For Inducing Copdmentioning

confidence: 99%

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Cigarette smoke exposure induced animal models of COPD – procedural variations and apparatus

Urmila¹,

Rai²,

Siddiqui³

et al. 2021

J Pre Clin Clin Res.

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Introduction and objective. Chronic obstructive pulmonary disease (COPD) is a progressive disorder that makes breathing difficult, characterized by chronic bronchitis, mucus hypersecretion, airway remodelling, and emphysema. Although caused by various factors, the leading cause is active or passive cigarette smoking (CS) is. The treatment available provides symptomatic relief and is associated with serious adverse effects, such as cardiovascular events and pneumonia; hence, there is an unmet need for research on drug treatment for COPD. This literature review provides an update on the various animal models of COPD that have been developed by the exposure of CS alone, or in combination with other inducing agents. Abbreviated description of the state of knowledge. The combination of SCS/MCS with LPS should be preferred to a single smoke component to induce COPD. It was observed that mouse models are extensively used, C57B1/6 and BALB/c females are more vulnerable to COPD, whereas, in rat models, male SD rats are mostly used. Guinea pigs, due to their anatomical similarity, are found to be a better model that can be used to develop COPD. Conclusions. Suitable animal models and validated apparatus are crucial for successful COPD animal model development.Conventionally authenticated research-grade cigarettes should be used for effortless distribution of a specific concentration of total suspended particles (TSP) or total particulate matter (TPM), including nicotine and carbon monoxide. There is also a need to focus on the various types of apparatus to be used for COPD induction in murine models considering optimum exposure, reliability as well as the sturdiness of the apparatus which would provide better execution of the protocol with minimum harm to the experimenter.

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Cathelicidin LL-37 restoring glucocorticoid function in smoking and lipopolysaccharide-induced airway inflammation in rats

Cited by 11 publications

References 48 publications

A Scoping Analysis of Cathelicidin in Response to Organic Dust Exposure and Related Chronic Lung Illnesses

A Scoping Analysis of Cathelicidin in Response to Organic Dust Exposure and Related Chronic Lung Illnesses

PI3K signalling in chronic obstructive pulmonary disease and opportunities for therapy

Cigarette smoke exposure induced animal models of COPD – procedural variations and apparatus

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