Adipose Tissue: A Safe Haven for Parasites?

Tanowitz, Herbert B.; Scherer, Philipp E.; Mota, Maria M.; Figueiredo, Luísa M.

doi:10.1016/j.pt.2016.11.008

Cited by 73 publications

(71 citation statements)

References 59 publications

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“…There is a gap in the understanding of how obesity affects the course of intracellular infections, including parasite infections. In accordance with the negative association between obesity and infectious diseases already described (23,35,36), our study showed that obese mice had higher parasite burden than control mice, failing to control parasite growth. In addition, lesions in obese mice were larger and more ulcerative than the ones observed in the control group.…”

Section: Discussionsupporting

confidence: 92%

Obesity impairs resistance toLeishmania majorinfection in C57BL/6 mice

Maioli

Silva

Martins

et al. 2018

Preprint

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23An association between increased susceptibility to infectious diseases and obesity has been 24 described as a result of impaired immunity in obese individuals. It is not clear whether a similar 25 linkage can be drawn between obesity and parasitic diseases. To evaluate the effect of obesity 26 in the immune response to cutaneous L. major infection, we studied the ability of C57BL/6 mice 27 submitted to a high fat and sugar diet to control leishmaniasis. Mice with diet-induced obesity 28 presented thicker lesions with higher parasite burden and more inflammatory infiltrate in the 29 infected ear when infected with L. major. We observe no difference in IFN-γ or IL-4 production 30 by draining lymph node cells between control and obese mice, but obese mice presented 31 higher production of IgG1 and IL-17. A higher percentage of in vitro-infected peritoneal 32 macrophages was found when these cells were obtained from obese mice when compared to 33 lean mice. In vitro stimulation of macrophages with IL-17 decreased the capacity of cells from 34 control mice to kill the parasite. Moreover, macrophages from obese mice presented higher 35 arginase activity. Together our results indicate that diet-induced obesity impairs resistance to L. 36 major in C57BL/6 mice without affecting the development of Th1 response. 37 38 39 4 40 Author Summary 41The obesity is a public health problem and it is reaching extraordinary numbers in the world 42 and others diseases are being involved and aggravated as consequence of obesity. What we 43 know is that some diseases are more severe in obese people than in normal people. We did not 44 know how obesity changes the profile of immune response to infectious agents, leading to the 45 more severe diseases. That`s why we decided to investigate how obese mice lead with 46 Leishmania major infection. Leishmaniasis is a protozoa parasite infection considered a 47 neglected disease. To try our hypothesis we gave a hipercaloric diet to induce obesity in 48 C57BL/6 mice. After that, we injected L. major in the mice ear and followed the lesion for 8 49 weeks. We observed a ticker lesion and the cells from draining lymph node from obese mice 50 produced more IL-17 than cells from normal mice. We also infected in vitro, macrophages from 51 obese mice and stimulated the cells with IL-17, and we observed that the macrophages from 52 obese mice are more infected by the L. major and it is worst in the presence of IL-17. Our 53 results suggest that diet induced obesity decrease the resistance to infection. 54 55 157 20 °C. 158 159 Histology

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Section: Discussionsupporting

confidence: 92%

Obesity impairs resistance toLeishmania majorinfection in C57BL/6 mice

Maioli

Silva

Martins

et al. 2018

Preprint

View full text Add to dashboard Cite

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“…Parasites such as Trypanosoma cruzi , Trypanosoma brucei , and Plasmodium spp. infiltrate adipose tissue and reside in extracellular spaces or directly infect adipocytes of humans or mice, which have been excellently reviewed [5, 6]. A number of studies have described infection of human and murine adipocytes by bacteria including Mycobacterium tuberculosis , Enterococcus faecalis , Staphylococcus aureus, and Rickettsia prowazekii [7–12].…”

Section: Adipose Tissue: a Reservoir For Diverse Microbesmentioning

confidence: 99%

HIV Persistence in Adipose Tissue Reservoirs

Couturier

Lewis

2018

Curr HIV/AIDS Rep

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Memory CD4 T cells and macrophages, the major host cells for HIV, accumulate in adipose tissue during HIV/SIV infection of humans and rhesus macaques. Whereas HIV and SIV proviral DNA is detectable in CD4 T cells of multiple fat depots in virtually all infected humans and monkeys examined, viral RNA is less frequently detected, and infected macrophages may be less prevalent in adipose tissue. However, based on viral outgrowth assays, adipose-resident CD4 T cells are latently infected with virus that is replication-competent and infectious. Additionally, adipocytes interact with CD4 T cells and macrophages to promote immune cell activation and inflammation which may be supportive for HIV persistence. Antiviral effector cells, such as CD8 T cells and NK/NKT cells, are abundant in adipose tissue during HIV/SIV infection and typically exceed CD4 T cells, whereas B cells are largely absent from adipose tissue of humans and monkeys. Additionally, CD8 T cells in adipose tissue of HIV patients are activated and have a late differentiated phenotype, with unique TCR clonotypes of less diversity relative to blood CD8 T cells. With respect to the distribution of antiretroviral drugs in adipose tissue, data is limited, but there may be class-specific penetration of fat depots. The trafficking of infected immune cells within adipose tissues is a common event during HIV/SIV infection of humans and monkeys, but the virus may be mostly transcriptionally dormant. Viral replication may occur less in adipose tissue compared to other major reservoirs, such as lymphoid tissue, but replication competence and infectiousness of adipose latent virus are comparable to other tissues. Due to the ubiquitous nature of adipose tissue, inflammatory interactions among adipocytes and CD4 T cells and macrophages, and selective distribution of antiretroviral drugs, the sequestration of infected immune cells within fat depots likely represents a major challenge for cure efforts.

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“…Tryponosoma cruzi also infects adipocytes (specialised cells of adipose tissue) and is capable of consuming stored lipids 48 . It is unclear how T. brucei , an extracellular parasite, accesses lipids that are stored inside adipocytes, which constitute the largest storage of lipids in a mammalian host.…”

Section: Metabolic Adaptations During the Trypanosoma Brucei Lifementioning

confidence: 99%

Metabolic reprogramming during the Trypanosoma brucei life cycle

et al. 2017

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Cellular metabolic activity is a highly complex, dynamic, regulated process that is influenced by numerous factors, including extracellular environmental signals, nutrient availability and the physiological and developmental status of the cell. The causative agent of sleeping sickness, Trypanosoma brucei, is an exclusively extracellular protozoan parasite that encounters very different extracellular environments during its life cycle within the mammalian host and tsetse fly insect vector. In order to meet these challenges, there are significant alterations in the major energetic and metabolic pathways of these highly adaptable parasites. This review highlights some of these metabolic changes in this early divergent eukaryotic model organism.

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Adipose Tissue: A Safe Haven for Parasites?

Cited by 73 publications

References 59 publications

Obesity impairs resistance toLeishmania majorinfection in C57BL/6 mice

Obesity impairs resistance toLeishmania majorinfection in C57BL/6 mice

HIV Persistence in Adipose Tissue Reservoirs

Metabolic reprogramming during the Trypanosoma brucei life cycle

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