Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of schistosoma mansoni infection

Felipe L. Oliveira, Camila Brand, Adelzon A. Paula, Kátia D. Arcanjo, Daniel K. Hsu, Fu-Tong Liu, Christina M. Takiya, Radovan Borojevic, Roger Chammas, Márcia C. El-Cheikh

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Galectin-3 is a β-galactoside-binding protein that has been shown to regulate pathophysiological processes, including cellular activation, differentiation and apoptosis. Recently, we showed that galectin-3 acts as a potent inhibitor of B cell differentiation into plasma cells. Here, we have investigated whether galectin-3 interferes with the lymphoid organization of B cell compartments in mesenteric lymph nodes (MLNs) during chronic schistosomiasis, using WT and galectin-3-/- mice. Schistosoma mansoni synthesizes GalNAcβ1-4(Fucα1-3)GlcNAc(Lac-DiNAc) structures (N-acetylgalactosamine β1-4 N-acetylglucosamine), which are known to interact with galectin-3 and elicit an intense humoral response. Antigens derived from the eggs and adult worms are continuously drained to MLNs and induce a polyclonal B cell activation. In the present work, we observed that chronically-infected galectin-3-/- mice exhibited a significant reduced amount of macrophages and B lymphocytes followed by drastic histological changes in B lymphocyte and plasma cell niches in the MLNs. The lack of galectin-3 favored an increase in the lymphoid follicle number, but made follicular cells more susceptible to apoptotic stimuli. There were an excessive quantity of apoptotic bodies, higher number of annexin V+/PI- cells, and reduced clearance of follicular apoptotic cells in the course of schistosomiasis. Here, we observed that galectin-3 was expressed in non-lymphoid follicular cells and its absence was associated with severe damage to tissue architecture. Thus, we convey new information on the role of galectin-3 in regulation of histological events associated with B lymphocyte and plasma cell niches, apoptosis, phagocytosis and cell cycle properties in the MLNs of mice challenged with S.mansoni.

Original languageEnglish (US)
Article numbere19216
JournalPLoS One
Volume6
Issue number5
DOIs
StatePublished - 2011

Fingerprint

Galectin 3
Schistosomiasis mansoni
Schistosoma mansoni
B-lymphocytes
lymph nodes
homeostasis
niches
Homeostasis
B-Lymphocytes
Lymph Nodes
Cells
plasma cells
infection
schistosomiasis
Lymphocytes
Plasma Cells
mice
apoptosis
Schistosomiasis
cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Oliveira, F. L., Brand, C., Paula, A. A., Arcanjo, K. D., Hsu, D. K., Liu, F-T., ... El-Cheikh, M. C. (2011). Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of schistosoma mansoni infection. PLoS One, 6(5), [e19216]. https://doi.org/10.1371/journal.pone.0019216

Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of schistosoma mansoni infection. / Oliveira, Felipe L.; Brand, Camila; Paula, Adelzon A.; Arcanjo, Kátia D.; Hsu, Daniel K.; Liu, Fu-Tong; Takiya, Christina M.; Borojevic, Radovan; Chammas, Roger; El-Cheikh, Márcia C.

In: PLoS One, Vol. 6, No. 5, e19216, 2011.

Research output: Contribution to journalArticle

Oliveira, FL, Brand, C, Paula, AA, Arcanjo, KD, Hsu, DK, Liu, F-T, Takiya, CM, Borojevic, R, Chammas, R & El-Cheikh, MC 2011, 'Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of schistosoma mansoni infection', PLoS One, vol. 6, no. 5, e19216. https://doi.org/10.1371/journal.pone.0019216
Oliveira, Felipe L. ; Brand, Camila ; Paula, Adelzon A. ; Arcanjo, Kátia D. ; Hsu, Daniel K. ; Liu, Fu-Tong ; Takiya, Christina M. ; Borojevic, Radovan ; Chammas, Roger ; El-Cheikh, Márcia C. / Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of schistosoma mansoni infection. In: PLoS One. 2011 ; Vol. 6, No. 5.
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abstract = "Galectin-3 is a β-galactoside-binding protein that has been shown to regulate pathophysiological processes, including cellular activation, differentiation and apoptosis. Recently, we showed that galectin-3 acts as a potent inhibitor of B cell differentiation into plasma cells. Here, we have investigated whether galectin-3 interferes with the lymphoid organization of B cell compartments in mesenteric lymph nodes (MLNs) during chronic schistosomiasis, using WT and galectin-3-/- mice. Schistosoma mansoni synthesizes GalNAcβ1-4(Fucα1-3)GlcNAc(Lac-DiNAc) structures (N-acetylgalactosamine β1-4 N-acetylglucosamine), which are known to interact with galectin-3 and elicit an intense humoral response. Antigens derived from the eggs and adult worms are continuously drained to MLNs and induce a polyclonal B cell activation. In the present work, we observed that chronically-infected galectin-3-/- mice exhibited a significant reduced amount of macrophages and B lymphocytes followed by drastic histological changes in B lymphocyte and plasma cell niches in the MLNs. The lack of galectin-3 favored an increase in the lymphoid follicle number, but made follicular cells more susceptible to apoptotic stimuli. There were an excessive quantity of apoptotic bodies, higher number of annexin V+/PI- cells, and reduced clearance of follicular apoptotic cells in the course of schistosomiasis. Here, we observed that galectin-3 was expressed in non-lymphoid follicular cells and its absence was associated with severe damage to tissue architecture. Thus, we convey new information on the role of galectin-3 in regulation of histological events associated with B lymphocyte and plasma cell niches, apoptosis, phagocytosis and cell cycle properties in the MLNs of mice challenged with S.mansoni.",
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