Obesity impairs resistance to Leishmania major infection in C57BL/6 mice

Autor: Leda Quercia Vieira, Leonardo Gomes Vaz, Lícia Torres, Nivea Carolina Paiva, Franciele Carolina Silva, Tatiani Uceli Maioli, Graziele Ribeiro Goes, Cláudia Martins Carneiro, Felipe Caixeta, Sara Cândida Barbosa, Ana Maria Caetano Faria, Matheus B. H. Carneiro, Vinicius Dantas Martins
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Physiology
RC955-962
Otology
Ear Infections
Pathology and Laboratory Medicine
White Blood Cells
0302 clinical medicine
Risk Factors
Animal Cells
Immune Physiology
Arctic medicine. Tropical medicine
Medicine and Health Sciences
Leishmania major
Immune Response
Lymph node
Mice
Knockout

Innate Immune System
biology
Interleukin-17
Ear
Infectious Diseases
medicine.anatomical_structure
Physiological Parameters
Cytokines
Female
Cellular Types
Anatomy
medicine.symptom
Public aspects of medicine
RA1-1270
Research Article
Immune Cells
Immunology
030231 tropical medicine
Ear infection
Leishmaniasis
Cutaneous

Context (language use)
Inflammation
Lymphatic System
Lesion
Interferon-gamma
03 medical and health sciences
Signs and Symptoms
Immune system
Diagnostic Medicine
Immunity
Parasitic Diseases
medicine
Animals
Obesity
Nutrition
Blood Cells
business.industry
Macrophages
Body Weight
Public Health
Environmental and Occupational Health

Biology and Life Sciences
Cell Biology
Molecular Development
biology.organism_classification
Diet
Mice
Inbred C57BL

030104 developmental biology
Otorhinolaryngology
Immune System
Macrophages
Peritoneal

Lymph Nodes
business
Developmental Biology
Zdroj: Repositório Institucional da UFOP
Universidade Federal de Ouro Preto (UFOP)
instacron:UFOP
PLoS Neglected Tropical Diseases, Vol 14, Iss 1, p e0006596 (2020)
PLoS Neglected Tropical Diseases
Popis: An association between increased susceptibility to infectious diseases and obesity has been described as a result of impaired immunity in obese individuals. It is not clear whether a similar linkage can be drawn between obesity and parasitic diseases. To evaluate the effect of obesity in the immune response to cutaneous Leishmania major infection, we studied the ability of C57BL/6 mice fed a hypercaloric diet (HSB) to control leishmaniasis. Mice with diet-induced obesity presented thicker lesions with higher parasite burden and a more intense inflammatory infiltrate in the infected ear after infection with L. major. There was no difference between control and obese mice in IFN-gamma or IL-4 production by auricular draining lymph node cells, but obese mice produced higher levels of IgG1 and IL-17. Peritoneal macrophages from obese mice were less efficient to kill L. major when infected in vitro than macrophages from control mice. In vitro stimulation of macrophages with IL-17 decreased their capacity to kill the parasite. Moreover, macrophages from obese mice presented higher arginase activity. To confirm the role of IL-17 in the context of obesity and infection, we studied lesion development in obese IL-17R-/- mice infected with L. major and found no difference in skin lesions and the leukocyte accumulation in the draining lymph node is redcuced in knockout mice compared between obese and lean animals. Our results indicate that diet-induced obesity impairs resistance to L. major in C57BL/6 mice and that IL-17 is involved in lesion development.
Author summary Obesity is a serious and increasing public health problem, and also induces a spectrum of metabolic disorders. Some diseases are known to be more severe in the presence of obesity. However, the interactions of obesity with the immune response to infectious agents have not been fully explored. In this study, we investigated the response of obese mice to infection with Leishmania major. C57BL/6 mice were fed a hypercaloric diet (HSB) and infected afterward with L. major. In obese mice, lesions were ticker and more ulcerative, and cells from draining lymph nodes produced more IL-17 when compared with cells from lean mice fed a control diet. Macrophages from obese and lean mice were infected in vitro and stimulated with IL-17 to test the role of this cytokine in effect produced by obesity. Macrophages from obese mice were more infected by L. major than the macrophages from control mice and the number of parasites was increased by treatment with IL-17. IL-17R deficient mice treated with hypercaloric diet showed no difference in lesion size when compared to mice fed control diet. Our findings suggest that diet-induced obesity decrease the resistance to L. major infection of C57BL/6 mice and the IL-17 cytokine may be involved in the lesion formation.
Databáze: OpenAIRE