Advanced search
Start date
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Absence of NOD2 receptor predisposes to intestinal inflammation by a deregulation in the immune response in hosts that are unable to control gut dysbiosis

Full text
de Souza, Patricia Reis [1, 2] ; Guimaraes, Francielle Rodrigues [1, 2] ; Sales-Campos, Helioswilton [1, 3, 2] ; Bonfa, Giuliano [4] ; Nardini, Viviani [2] ; Lazo Chica, Javier Emilio [1] ; Turato, Walter Miguel [4] ; Silva, Joao Santana [4] ; Zamboni, Dario Simoes [5] ; de Barros Cardoso, Cristina Ribeiro [2]
Total Authors: 10
[1] Univ Fed Triangulo Mineiro, Inst Ciencias Biol & Nat, Uberaba - Brazil
[2] Univ Sao Paulo, Dept Anal Clin Toxicol & Bromatol, Fac Ciencias Farmaceut Ribeirao Preto, Ribeirao Preto - Brazil
[3] Univ Fed Goias, Inst Patol Trop & Saude Publ, Goiania, Go - Brazil
[4] Univ Sao Paulo, Dept Bioquim & Imunol, Fac Med Ribeirao Preto, Ribeirao Preto - Brazil
[5] Univ Sao Paulo, Dept Biol Celular Mol & Bioagentes Patogen, Fac Med Ribeirao Preto, Ribeirao Preto - Brazil
Total Affiliations: 5
Document type: Journal article
Source: Immunobiology; v. 223, n. 10, p. 577-585, OCT 2018.
Web of Science Citations: 1

Mutations in NOD2 predisposes to Inflammatory Bowel Diseases. Therefore, we evaluated the role of this innate receptor in the modulation of immunity in face of host microbiota changes. NOD2(-/-) ice presented higher susceptibility to experimental colitis than WT, with increased CD4 and CD8 T lymphocytes in the spleen. NOD2(-/-) deficiency also led to reduced Th17-related cytokines in the colon, with overall augmented IFN-gamma in the gut and spleen. Nonetheless, there was increased frequency of CD4(+) IL-4(+) cells in the mesenteric lymph nodes besides elevated CTLA-4 and FoxP3 regulatory markers in the spleen of NOD2(-/-) mice, although it did not result in more efficient control of gut inflammation. Indeed, these animals also had augmented IL-1 beta and IL-5 in the peritoneum, indicating that this receptor may be important to control bacteria translocation too. Microbiota exchanging between cohoused WT and NOD2(-/-) mice led to colitis worsening in the absence of the receptor, while antibiotic therapy in WT mice abrogated this effect. Then, not only the genetic mutation confers increased susceptibility to inflammation, but it is also influenced by the microbiota harbored by the host. Finally, NOD2(-/-) mice are more prone to intestinal inflammation due to deregulated immune response and increased susceptibility to colitogenic bacteria. (AU)

FAPESP's process: 12/00984-8 - Participation of hypothalamus-pituitary-adrenal axis in experimental induced inflammatory bowel disease
Grantee:Patrícia Reis de Souza
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 10/20162-7 - The role of hypothalamus-pituitary-adrenal (HPA) axis and exogenous glucocorticoids in the modulation of immune response in inflammatory bowel disease
Grantee:Cristina Ribeiro de Barros Cardoso
Support type: Research Grants - Young Investigators Grants