TY  - JOUR
AU  - Popović, Dušanka
AU  - Kulaš, Jelena
AU  - Tucović, Dina
AU  - Popov Aleksandrov, Aleksandra
AU  - Malešević, Anastasija
AU  - Glamočlija, Jasmina
AU  - Brdarić, Emilija
AU  - Soković Bajić, Svetlana
AU  - Golić, Nataša
AU  - Mirkov, Ivana
AU  - Tolinački, Maja
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6084
AB  - While the effect of gut microbiota and/or inflammation on a distant body site, including the lungs (gut–lung axis), has been well characterized, data about the influence of lung microbiota and lung inflammation on gut homeostasis (lung–gut axis) are scarce. Using a well-characterized model of pulmonary infection with the fungus Aspergillus fumigatus, we investigated alterations in the lung and gut microbiota by next-generation sequencing of the V3–V4 regions of total bacterial DNA. Pulmonary inflammation due to the fungus A. fumigatus caused bacterial dysbiosis in both lungs and gut, but with different characteristics. While increased alpha diversity and unchanged bacterial composition were noted in the lungs, dysbiosis in the gut was characterized by decreased alpha diversity indices and modified bacterial composition. The altered homeostasis in the lungs allows the immigration of new bacterial species of which 41.8% were found in the feces, indicating that some degree of bacterial migration from the gut to the lungs occurs. On the contrary, the dysbiosis occurring in the gut during pulmonary infection was a consequence of the local activity of the immune system. In addition, the alteration of gut microbiota in response to pulmonary infection depends on the bacterial composition before infection, as no changes in gut bacterial microbiota were detected in a rat strain with diverse gut bacteria. The data presented support the existence of the lung–gut axis and provide additional insight into this mechanism.
PB  - American Society for Microbiology
T2  - Microbiology Spectrum
T1  - Gut microbial dysbiosis occurring during pulmonary fungal infection in rats is linked to inflammation and depends on healthy microbiota composition
IS  - 5
VL  - 11
DO  - 10.1128/spectrum.01990-23
SP  - e0199023
ER  - 

@article{
author = "Popović, Dušanka and Kulaš, Jelena and Tucović, Dina and Popov Aleksandrov, Aleksandra and Malešević, Anastasija and Glamočlija, Jasmina and Brdarić, Emilija and Soković Bajić, Svetlana and Golić, Nataša and Mirkov, Ivana and Tolinački, Maja",
year = "2023",
abstract = "While the effect of gut microbiota and/or inflammation on a distant body site, including the lungs (gut–lung axis), has been well characterized, data about the influence of lung microbiota and lung inflammation on gut homeostasis (lung–gut axis) are scarce. Using a well-characterized model of pulmonary infection with the fungus Aspergillus fumigatus, we investigated alterations in the lung and gut microbiota by next-generation sequencing of the V3–V4 regions of total bacterial DNA. Pulmonary inflammation due to the fungus A. fumigatus caused bacterial dysbiosis in both lungs and gut, but with different characteristics. While increased alpha diversity and unchanged bacterial composition were noted in the lungs, dysbiosis in the gut was characterized by decreased alpha diversity indices and modified bacterial composition. The altered homeostasis in the lungs allows the immigration of new bacterial species of which 41.8% were found in the feces, indicating that some degree of bacterial migration from the gut to the lungs occurs. On the contrary, the dysbiosis occurring in the gut during pulmonary infection was a consequence of the local activity of the immune system. In addition, the alteration of gut microbiota in response to pulmonary infection depends on the bacterial composition before infection, as no changes in gut bacterial microbiota were detected in a rat strain with diverse gut bacteria. The data presented support the existence of the lung–gut axis and provide additional insight into this mechanism.",
publisher = "American Society for Microbiology",
journal = "Microbiology Spectrum",
title = "Gut microbial dysbiosis occurring during pulmonary fungal infection in rats is linked to inflammation and depends on healthy microbiota composition",
number = "5",
volume = "11",
doi = "10.1128/spectrum.01990-23",
pages = "e0199023"
}

Popović, D., Kulaš, J., Tucović, D., Popov Aleksandrov, A., Malešević, A., Glamočlija, J., Brdarić, E., Soković Bajić, S., Golić, N., Mirkov, I.,& Tolinački, M.. (2023). Gut microbial dysbiosis occurring during pulmonary fungal infection in rats is linked to inflammation and depends on healthy microbiota composition. in Microbiology Spectrum
American Society for Microbiology., 11(5), e0199023.
https://doi.org/10.1128/spectrum.01990-23

Popović D, Kulaš J, Tucović D, Popov Aleksandrov A, Malešević A, Glamočlija J, Brdarić E, Soković Bajić S, Golić N, Mirkov I, Tolinački M. Gut microbial dysbiosis occurring during pulmonary fungal infection in rats is linked to inflammation and depends on healthy microbiota composition. in Microbiology Spectrum. 2023;11(5):e0199023.
doi:10.1128/spectrum.01990-23 .

Popović, Dušanka, Kulaš, Jelena, Tucović, Dina, Popov Aleksandrov, Aleksandra, Malešević, Anastasija, Glamočlija, Jasmina, Brdarić, Emilija, Soković Bajić, Svetlana, Golić, Nataša, Mirkov, Ivana, Tolinački, Maja, "Gut microbial dysbiosis occurring during pulmonary fungal infection in rats is linked to inflammation and depends on healthy microbiota composition" in Microbiology Spectrum, 11, no. 5 (2023):e0199023,
https://doi.org/10.1128/spectrum.01990-23 . .

TY  - JOUR
AU  - Ninkov, Marina
AU  - Popov Aleksandrov, Aleksandra
AU  - Mirkov, Ivana
AU  - Demenesku, Jelena
AU  - Tucović, Dina
AU  - Jovanović Stojanov, Sofija
AU  - Golic, Natasa
AU  - Tolinacki, Maja
AU  - Kataranovski, Dragan
AU  - Brceski, Ilija
AU  - Kataranovski, Milena
PY  - 2016
UR  - https://www.sciencedirect.com/science/article/pii/S0278691516302423?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3378
AB  - Influence of genetic background on toxicity of oral cadmium (Cd) administration (30 days, in drinking
water; 5 ppm and 50 ppm of cadmium) was examined in Albino Oxford (AO) and Dark Agouti (DA) rats.
Similar cadmium deposition was noted in gut and draining mesenteric lymph nodes (MLN) of both
strains but intensity and/or the pattern of responses to cadmium in these tissues differ. Less intense
intestinal damage and leukocyte infiltration was observed in gut of cadmium-exposed AO rats. While
gut-associated lymph node cells of DA rats responded to cadmium with an increase of cell proliferation,
oxidative activity, IFN-g, IL-17 production and expression, no changes of these activities of MLN cells of
cadmium-treated AO rats were observed. Spleen, which accumulated cadmium comparable to MLN,
responded to metal by drop in cell viability and by reduced responsiveness of proliferation and cytokine
production to stimulation in DA rats solely, which suggest tissue dependence of cadmium effects. More
pronounced cadmium effects on MLN and spleen cells of DA rats (which accumulated similar cadmium
doses as AO rats), showed greater susceptibility of this strain to cadmium. The results presented, for the
first time, depict the influence of genetic background to effects of oral cadmium administration.
T2  - Food and Chemical Toxicology
T1  - Strain differences in toxicity of oral cadmium intake in rats
VL  - 96
DO  - 10.1016/j.fct.2016.07.021
SP  - 11
EP  - 23
ER  - 

@article{
author = "Ninkov, Marina and Popov Aleksandrov, Aleksandra and Mirkov, Ivana and Demenesku, Jelena and Tucović, Dina and Jovanović Stojanov, Sofija and Golic, Natasa and Tolinacki, Maja and Kataranovski, Dragan and Brceski, Ilija and Kataranovski, Milena",
year = "2016",
abstract = "Influence of genetic background on toxicity of oral cadmium (Cd) administration (30 days, in drinking
water; 5 ppm and 50 ppm of cadmium) was examined in Albino Oxford (AO) and Dark Agouti (DA) rats.
Similar cadmium deposition was noted in gut and draining mesenteric lymph nodes (MLN) of both
strains but intensity and/or the pattern of responses to cadmium in these tissues differ. Less intense
intestinal damage and leukocyte infiltration was observed in gut of cadmium-exposed AO rats. While
gut-associated lymph node cells of DA rats responded to cadmium with an increase of cell proliferation,
oxidative activity, IFN-g, IL-17 production and expression, no changes of these activities of MLN cells of
cadmium-treated AO rats were observed. Spleen, which accumulated cadmium comparable to MLN,
responded to metal by drop in cell viability and by reduced responsiveness of proliferation and cytokine
production to stimulation in DA rats solely, which suggest tissue dependence of cadmium effects. More
pronounced cadmium effects on MLN and spleen cells of DA rats (which accumulated similar cadmium
doses as AO rats), showed greater susceptibility of this strain to cadmium. The results presented, for the
first time, depict the influence of genetic background to effects of oral cadmium administration.",
journal = "Food and Chemical Toxicology",
title = "Strain differences in toxicity of oral cadmium intake in rats",
volume = "96",
doi = "10.1016/j.fct.2016.07.021",
pages = "11-23"
}

Ninkov, M., Popov Aleksandrov, A., Mirkov, I., Demenesku, J., Tucović, D., Jovanović Stojanov, S., Golic, N., Tolinacki, M., Kataranovski, D., Brceski, I.,& Kataranovski, M.. (2016). Strain differences in toxicity of oral cadmium intake in rats. in Food and Chemical Toxicology, 96, 11-23.
https://doi.org/10.1016/j.fct.2016.07.021

Ninkov M, Popov Aleksandrov A, Mirkov I, Demenesku J, Tucović D, Jovanović Stojanov S, Golic N, Tolinacki M, Kataranovski D, Brceski I, Kataranovski M. Strain differences in toxicity of oral cadmium intake in rats. in Food and Chemical Toxicology. 2016;96:11-23.
doi:10.1016/j.fct.2016.07.021 .

Ninkov, Marina, Popov Aleksandrov, Aleksandra, Mirkov, Ivana, Demenesku, Jelena, Tucović, Dina, Jovanović Stojanov, Sofija, Golic, Natasa, Tolinacki, Maja, Kataranovski, Dragan, Brceski, Ilija, Kataranovski, Milena, "Strain differences in toxicity of oral cadmium intake in rats" in Food and Chemical Toxicology, 96 (2016):11-23,
https://doi.org/10.1016/j.fct.2016.07.021 . .