scholarly journals A Human Lung-Associated Streptomyces sp. TR1341 Produces Various Secondary Metabolites Responsible for Virulence, Cytotoxicity and Modulation of Immune Response

Author(s):  
Andrej Herbrík ◽  
Erika Corretto ◽  
Alica Chroňáková ◽  
Helena Langhansová ◽  
Petra Petrásková ◽  
...  
2020 ◽  
Vol 10 ◽  
Author(s):  
Andrej Herbrík ◽  
Erika Corretto ◽  
Alica Chroňáková ◽  
Helena Langhansová ◽  
Petra Petrásková ◽  
...  

2021 ◽  
Vol 9 (8) ◽  
pp. 1547
Author(s):  
Erika Corretto ◽  
Ana Catalina Lara ◽  
Lucie Kotrbová ◽  
František Lorenc ◽  
Kateřina Petříčková ◽  
...  

Streptomyces sp. TR1341 was isolated from the sputum of a man with a history of lung and kidney tuberculosis, recurrent respiratory infections, and COPD. It produces secondary metabolites associated with cytotoxicity and immune response modulation. In this study, we complement our previous results by identifying the genetic features associated with the production of these secondary metabolites and other characteristics that could benefit the strain during its colonization of human tissues (virulence factors, modification of the host immune response, or the production of siderophores). We performed a comparative phylogenetic analysis to identify the genetic features that are shared by environmental isolates and human respiratory pathogens. The results showed a high genomic similarity of Streptomyces sp. TR1341 to the plant-associated Streptomyces sp. endophyte_N2, inferring a soil origin of the strain. Putative virulence genes, such as mammalian cell entry (mce) genes were not detected in the TR1341’s genome. The presence of a type VII secretion system, distinct from the ones found in Mycobacterium species, suggests a different colonization strategy than the one used by other actinomycete lung pathogens. We identified a higher diversity of genes related to iron acquisition and demonstrated that the strain produces ferrioxamine B in vitro. These results indicate that TR1341 may have an advantage in colonizing environments that are low in iron, such as human tissue.


2021 ◽  
Vol 15 (3) ◽  
pp. 039901
Author(s):  
Ecem Saygili ◽  
Ece Yildiz-Ozturk ◽  
Macauley J. Green ◽  
Amir M. Ghaemmaghami ◽  
Ozlem Yesil-Celiktas

Author(s):  
Courtney Tindle ◽  
MacKenzie Fuller ◽  
Ayden Fonseca ◽  
Sahar Taheri ◽  
Stella-Rita Ibeawuchi ◽  
...  

SummarySARS-CoV-2, the virus responsible for COVID-19, causes widespread damage in the lungs in the setting of an overzealous immune response whose origin remains unclear. We present a scalable, propagable, personalized, cost-effective adult stem cell-derived human lung organoid model that is complete with both proximal and distal airway epithelia. Monolayers derived from adult lung organoids (ALOs), primary airway cells, or hiPSC-derived alveolar type-II (AT2) pneumocytes were infected with SARS-CoV-2 to create in vitro lung models of COVID-19. Infected ALO-monolayers best recapitulated the transcriptomic signatures in diverse cohorts of COVID-19 patient-derived respiratory samples. The airway (proximal) cells were critical for sustained viral infection, whereas distal alveolar differentiation (AT2→AT1) was critical for mounting the overzealous host immune response in fatal disease; ALO monolayers with well-mixed proximodistal airway components recapitulated both. Findings validate a human lung model of COVID-19, which can be immediately utilized to investigate COVID-19 pathogenesis and vet new therapies and vaccines.GRAPHIC ABSTRACTHIGHLIGHTSHuman lung organoids with mixed proximodistal epithelia are createdProximal airway cells are critical for viral infectivityDistal alveolar cells are important for emulating host responseBoth are required for the overzealous response in severe COVID-19IN BRIEFAn integrated stem cell-based disease modeling and computational approach demonstrate how both proximal airway epithelium is critical for SARS-CoV-2 infectivity, but distal differentiation of alveolar pneumocytes is critical for simulating the overzealous host response in fatal COVID-19.


1977 ◽  
Vol 5 (2) ◽  
pp. 67-73 ◽  
Author(s):  
Tukaram V. Darnule ◽  
Vinay Likhite ◽  
Gerard M. Turino ◽  
Ines Mandl

2019 ◽  
Vol 8 (23) ◽  
Author(s):  
Wilbert Serrano ◽  
Raul M. Olaechea ◽  
Joachim Wink ◽  
Michael W. Friedrich

A new strain of Streptomyces sp., strain RFCAC02, was isolated from the gut of the Pacific chub mackerel Scomber japonicus peruanus. This strain produces a variety of secondary metabolites.


Biomaterials ◽  
2020 ◽  
Vol 230 ◽  
pp. 119599 ◽  
Author(s):  
Huu Thuy Trang Duong ◽  
Thavasyappan Thambi ◽  
Yue Yin ◽  
Seong Han Kim ◽  
Thanh Loc Nguyen ◽  
...  

2007 ◽  
Vol 75 (8) ◽  
pp. 3729-3738 ◽  
Author(s):  
Kaushik Chakrabarty ◽  
Wenxin Wu ◽  
J. Leland Booth ◽  
Elizabeth S. Duggan ◽  
Nancy N. Nagle ◽  
...  

ABSTRACT Bacillus anthracis, the causative agent of inhalational anthrax, enters a host through the pulmonary system before dissemination. We have previously shown that human alveolar macrophages participate in the initial innate immune response to B. anthracis spores through cell signal-mediated cytokine release. We proposed that the lung epithelia also participate in the innate immune response to this pathogen, and we have developed a human lung slice model to study this process. Exposure of our model to B. anthracis (Sterne) spores rapidly activated the mitogen-activated protein kinase signaling pathways ERK, p38, and JNK. In addition, an RNase protection assay showed induction of mRNA of several cytokines and chemokines. This finding was reflected at the translational level by protein peak increases of 3-, 25-, 9-, 34-, and 5-fold for interleukin-6 (IL-6), tumor necrosis factor alpha, IL-8, macrophage inflammatory protein 1α/β, and monocyte chemoattractant protein 1, respectively, as determined by an enzyme-linked immunosorbent assay. Inhibition of individual pathways by UO126, SP600125, and SB0203580 decreased induction of chemokines and cytokines by spores, but this depended on the pathways inhibited and the cytokines and chemokines induced. Combining all three inhibitors reduced induction of all cytokines and chemokines tested to background levels. An immunohistochemistry analysis of IL-6 and IL-8 revealed that alveolar epithelial cells and macrophages and a few interstitial cells are the source of the cytokines and chemokines. Taken together, these data showed the activation of the pulmonary epithelium in response to B. anthracis spore exposure. Thus, the lung epithelia actively participate in the innate immune response to B. anthracis infection through cell signal-mediated elaboration of cytokines and chemokines.


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