Oral recombinant human or mouse lactoferrin reduces<i>Mycobacterium tuberculosis</i>TDM induced granulomatous lung pathology

Hwang, Shen An; Kruzel, Marian L.; Actor, Jeffrey K.

doi:10.1139/bcb-2016-0061

Cited by 17 publications

(11 citation statements)

References 40 publications

(49 reference statements)

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“…Particularly, it has been observed that mice treated with LF manifest an increase in the proportion of IL-12/IL-10, which results in increased Th1 cells, with a protective role against Mtb ( 100 , 101 ). The anti-inflammatory properties of human and mouse LF were also corroborated in another Mtb mouse infected model ( 102 ). In addition, other studies clearly demonstrated the immunomodulatory role of LF, improving BCG-vaccine efficacy when used as adjuvant ( 147 , 148 ).…”

Section: Human Endogenous Amps Involved In the Fight Against Tb Infecmentioning

confidence: 69%

Host Antimicrobial Peptides: The Promise of New Treatment Strategies against Tuberculosis

Arranz-Trullén

Pulido

et al. 2017

Front. Immunol.

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Tuberculosis (TB) continues to be a devastating infectious disease and remerges as a global health emergency due to an alarming rise of antimicrobial resistance to its treatment. Despite of the serious effort that has been applied to develop effective antitubercular chemotherapies, the potential of antimicrobial peptides (AMPs) remains underexploited. A large amount of literature is now accessible on the AMP mechanisms of action against a diversity of pathogens; nevertheless, research on their activity on mycobacteria is still scarce. In particular, there is an urgent need to integrate all available interdisciplinary strategies to eradicate extensively drug-resistant Mycobacterium tuberculosis strains. In this context, we should not underestimate our endogenous antimicrobial proteins and peptides as ancient players of the human host defense system. We are confident that novel antibiotics based on human AMPs displaying a rapid and multifaceted mechanism, with reduced toxicity, should significantly contribute to reverse the tide of antimycobacterial drug resistance. In this review, we have provided an up to date perspective of the current research on AMPs to be applied in the fight against TB. A better understanding on the mechanisms of action of human endogenous peptides should ensure the basis for the best guided design of novel antitubercular chemotherapeutics.

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Section: Human Endogenous Amps Involved In the Fight Against Tb Infecmentioning

confidence: 69%

Host Antimicrobial Peptides: The Promise of New Treatment Strategies against Tuberculosis

Arranz-Trullén

Pulido

et al. 2017

Front. Immunol.

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“…General lung inflammation was assessed as lung weight index (LWI) at 7 days post IV TDM challenge, reflecting peak granulomatous response to TDM 12 [ Figure 1]. As previously reported, TDM-IV Acute treatment increased LWI significantly, at both low (10 μg/mouse) 12 and mid-range (25 μg/mouse) 19 doses, with increased LWI presenting at the higher level. C57BL/6 mice given administered light mineral oil alone (no TDM) did not exhibit changes to LWI (not shown).…”

Section: Comparison Of Tdm Induced Pathology: Hypercoagulation Vs Acumentioning

confidence: 83%

Mycobacterial trehalose 6,6′-dimycolate induced vascular occlusion is accompanied by subendothelial inflammation

2019

Self Cite

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Mycobacterium tuberculosis (MTB) is a pathogen that infects and kills millions yearly. The mycobacterium's cell wall glycolipid trehalose 6,6'-dimycolate (TDM) has been used historically to model MTB induced inflammation and granuloma formation. Alterations to the model can significantly influence the induced pathology. One such method incorporates intraperitoneal preexposure, after which the intravenous injection of TDM generates pathological damage effectively mimicking the hypercoagulation, thrombus formation, and tissue remodeling apparent in lungs of infected individuals. The purpose of these experiments is to examine the histological inflammation involved in the TDM mouse model that induces development of the hemorrhagic response. TDM induced lungs of C57BL/6 mice to undergo granulomatous inflammation. Further histological examination of the peak response demonstrated tissue remodeling consistent with hypercoagulation. The observed vascular occlusion indicates that obstruction likely occurs due to subendothelial localized activity leading to restriction of blood vessel lumens. Trichrome staining revealed that associated damage in the hypercoagulation model is consistent with intra endothelial cell accumulation of innate cells, bordered by collagen deposition in the underlying parenchyma. Overall, the hypercoagulation model represents a comparative pathological instrument for understanding mechanisms underlying development of hemorrhage and vascular occlusion seen during MTB infection.

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“…Meanwhile, to alleviate symptoms of SARI, we suppose some drugs that are effective in treating TDMinduced pneumonia considering the antigen structure similarity:radix sophorae [34]; lactoferrin [35].…”

Section: Changing Of Expression Profile Of C-type Lecin Family Indicamentioning

confidence: 99%

Activating organ’s immunizing power against COVID–19–learning from SARS

Wang

Xia²

2020

Preprint

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Background Coronaviruses cause respiratory diseases in many animals, including humans.Spike protein is an important component of coronavirus structure and the formation of ACE2 (angiotensin converting enzyme 2)-spike complex mediates virus entry to host cells.C-type lectin family are widely distribute on the surface of human cells and have been shown to activate the immune system. In this article, we first illustrate why we can "learn from SARS" with phylogenetic analysis. Then, we use SARS spike protein structure, to inferring our molecular docking experiment, revealing the potential capacity of C-type lectin to directly interact with spike protein obstructs the formation of spike-ACE2 complex. Considering the expression profile of C-type lectin family changing significantly during infection, we predict certain members of this kind of protein as potential therapeutic target and verify their assumed function by inferring an C-type lectindependent CD4/CD28 T cell survival molecular network with endogenous molecular network theory (EMT) and comparing the predicted expression trend corresponding to each molecular with experiment data. Methods Alignments are inferred by MAFFT V7 ( G-ins-i, Blosom). Maximum likelihood analyses and bootstrap test carried out by RAXML V8.2 ML+BP online platform. Protein structure is predicted by SWISSMODELLING online platform. Molecular docking experiment is carried out by Z-dock Version 3.0.2. C-type lectin-dependent CD4/CD28 T cell Network is inferred by EMT theory.Result Our molecular docking experiment revealing the potential capacity of C-type lectin to directly interact with spike protein obstructs the formation of spike-ACE2 complex.Based on the expression profile of C-type lectin family during infection, we predicting certain member of this kind of protein as potential therapeutic target such as Clec7a, Clec12a and Clec11a, corresponding immune cell types such as CD4/CD28 T Yi Wang conceived the project, designed the experiment and wrote the manuscript.Chuanxin Xia wrote the manuscript. All authors read and approved the final manuscript. AcknowledgementThanks for my sister's kindly help.Hoping this work can inspiring fellow scientists for related experiment design and improving people's confidence in overcoming SARI.

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Oral recombinant human or mouse lactoferrin reducesMycobacterium tuberculosisTDM induced granulomatous lung pathology

Cited by 17 publications

References 40 publications

Host Antimicrobial Peptides: The Promise of New Treatment Strategies against Tuberculosis

Host Antimicrobial Peptides: The Promise of New Treatment Strategies against Tuberculosis

Mycobacterial trehalose 6,6′-dimycolate induced vascular occlusion is accompanied by subendothelial inflammation

Activating organ’s immunizing power against COVID–19–learning from SARS

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