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Publication

Cytokine profile of NALT during acute stress and its possible effect on IgA secretion.

Juan Manuel Gutiérrez-Meza | Rosa Adriana Jarillo-Luna | Victor Rivera-Aguilar | Angel Miliar-García | Rafael Campos-Rodríguez

Immunology letters | 2017

Stress stimuli affect the immune system responses that occur at mucosal membranes, particularly IgA secretion. It has been suggested that acute stress increases the levels of IgA and that sympathetic innervation plays an important role in this process. We herein explore in a murine model how acute stress affects the Th1/Th2/Treg cytokine balance in NALT, and the possible role of glucocorticoids in this effect. Nine-week-old male CD1 mice were divided into three groups: unstressed (control), stressed (subjected to 4h of immobilization), and stressed after pretreatment with a single dose of the corticosterone receptor antagonist RU-486. The parameters evaluated included plasma corticosterone and epinephrine, IgA levels in nasal fluid (by ELISA), the percentage of CD19+B220+IgA+ lymphocytes and CD138+IgA+ plasma cells, and the mRNA expression of heavy α chain, J chain and pIgR. Moreover, the gene and protein expression of Th1 cytokines (TNFα, IL-2 and INF-γ), Th2 cytokines (IL-4 and IL-5) and Treg cytokines (IL-10 and TGFβ) were determined in nasal mucosa. The results show that acute stress generated a shift towards the dominance of an anti-inflammatory immune response (Th2 and Treg cytokines), evidenced by a significant rise in the amount of T cells that produce IL4, IL-5 and IL-10. This immune environment may favor IgA biosynthesis by CD138+IgA+ plasma cells, a process mediated mostly by glucocorticoids.

Pubmed ID: 28472640 RIS Download

Research resources used in this publication

IL-4 (RRID:AB_398556) (antibody)

Additional research tools detected in this publication

BD Biosciences (RRID:SCR_013311)

Antibodies used in this publication

Associated grants

None

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