Stress is a predisposing factor for pulmonary diseases; however, its effects on the lungs of healthy individuals have not been fully elucidated. Since bovine lactoferrin (bLf) is a powerful immunomodulator, this study aimed to evaluate whether lactoferrin can modulate the effects of chronic stress on humoral and cellular immunity in the lungs. We performed chronic restraint stress (RS) and oral administration of bLf in a BALB/c model, assessing serum corticosterone, body weight, and various lung immunity parameters, including immunoglobulin concentrations in serum and tracheobronchial lavages (TBLs), secretory IgA (S-IgA) levels in TBLs, IgA-secreting plasma cells, relative expression of pIgR, CD4⁺ lymphocyte Th1 and Th2 populations, and antigen-presenting cell (APC) populations in the lungs. Our results demonstrate that stress increases corticosterone and production of total IgA and IgG, while decreasing levels of IgM and S-IgA, promotes a Th1/Th2 profile imbalance, and decreases APC populations. Interestingly, bLf modulates serum corticosterone levels and stress-induced weight loss, and it also modulates humoral and cellular effects produced by chronic stress. These results demonstrate that bLf should be considered a new therapeutic target for further studies, focusing on prophylactic and co-therapeutic administration to treat and prevent respiratory diseases.

Stress is a predisposing factor for pulmonary diseases, but its effects on the lungs of healthy individuals have not been elucidated yet. Since bovine lactoferrin (bLf) is a powerful immunomodulator, in this study, we focused on evaluating whether lactoferrin is able to modulate the effects of chronic stress on humoral and cellular immunity of the lung. We performed a chronic restraint stress (RS) and oral administration of bLf BALB/c model and we evaluated serum corticosterone, body weight and some parameters of lung immunity, such as immunoglobulin concentrations in serum and tracheobronchial lavages (TBL), secretory IgA (S-IgA) levels in TBL, IgA-secreting plasma cells, pIgR relative expression, CD4⁺ lymphocyte Th1 and Th2 populations and Antigen Presenting Cells (APC) populations on the lung. Our results demonstrate that stress increases corticosterone, production of total IgA and IgG, while decreasing the levels of IgM and S-IgA, promotes a Th1/Th2 profile imbalance, and decreases APC populations. Interestingly, bLf modulates serum corticosterone levels and stress-induced weight loss, and it also modulates humoral and cellular effects produced by chronic stress. These results demonstrated that bLf should be considered as a new therapeutic target for further studies to focus on the prophylactic and co-therapeutic administration to treat and prevent respiratory diseases.