The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory…

By Michael Maes, M. Kubera, J. Leunis. Neuro - endocrinology letters, 2008

594 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c3d20e46138061508306dfa09c1c2ac8852c9ac1

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Citations in the corpus

A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. (2011, background): “In depression IBS may be a clinical expression of gut-derived inflammation (Maes et al., 2008b; Maes and Leunis, 2008).”
Increased Intestinal Permeability Correlates with Sigmoid Mucosa alpha-Synuclein Staining and Endotoxin Exposure Markers in Early Parkinson's Disease (2011, unknown): “It is therefore not surprising that endotoxemia has been reported in other neurological disorders like autism, ALS, and depression [43,44] [45].”
Altered fecal microbiota composition in patients with major depressive disorder. (2015, background): “In line with these findings, human studies have demonstrated increased bacterial translocation in mood disorders such as depression (Maes et al., 2008, 2012).”
The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression (2009, background): “Indeed, the prevalence and median values for serum IgM and IgA against LPS of six different enterobacteria are significantly greater in patients with depression than in normal volunteers (Maes et al. 2008b).”
Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “Of note, relevant to depression, patients with major depression have been found to show increased peripheral blood antibody titers to LPS derived from gram negative enterobacteria as compared with normal volunteers (Maes et al, 2008).”
So depression is an inflammatory disease, but where does the inflammation come from? (2013, unknown): “Clinical depression has recently been shown to be accompanied by increased plasma levels of immunoglobulin (Ig) A and/or IgM directed against a number of gram negative bacteria, inc ludi g Hafnia Alvei, Pseudomonas Aeruginosa, Morganella Morganii, Proteus Mirabilis, Pseudom onas Putida, Citrobacter ”
Inflammation: depression fans the flames and feasts on the heat. (2015, background): “” Indeed, depressedpatients have been found to have higher antibody against gut bacteria than comparison subjects (54).”
Transferring the blues: Depression-associated gut microbiota induces neurobehavioural changes in the rat. (2016, background): “Studies have demonstrated higher IgA- and IgM-mediated immune responses directed against LPS of certain commensal gram negative gut bacteria in depression (Maes et al., 2012, 2008, 2013).”
Exposure to a Social Stressor Alters the Structure of the Intestinal Microbiota: Implications for Stressor-Induced Immunomodulation (2010, background): “through a cytokine-mediated mechanism (Maes, 2008; Maes et al., 2008).”
Breaking down the barriers: the gut microbiome, intestinal permeability and stress-related psychiatric disorders (2015, background): “Higher IgA- and IgM-mediated immune responses directed against lipopolysaccharides (LPS) of certain commensal gram negative gut bacteria have been shown in depressed patients (Maes et al., 2008, 2012).”