Altered Distribution of Peripheral Blood Maturation‐Associated B‐Cell Subsets in Chronic Alcoholism

Background Although decreased counts of peripheral blood ( PB ) B cells—associated with an apparently contradictory polyclonal hypergammaglobulinemia—have been reported in chronic alcoholism, no information exists about the specific subsets of circulating B cells altered and their relationship with antibody production. Here, we analyzed for the first time the distribution of multiple maturation‐associated subpopulations of PB B cells in alcoholism and its potential relationship with the onset of liver disease. Methods PB samples from 35 male patients—20 had alcoholic hepatitis ( AH ) and 15 chronic alcoholism without liver disease ( AWLD )—were studied, in parallel to 19 male healthy donors (controls). The distribution of PB B‐cell subsets (immature/regulatory, naïve, CD 27 − and CD 27 + memory B lymphocytes, and circulating plasmablasts of distinct immunoglobulin—Ig—isotypes) was analyzed by flow cytometry. Results Patients with AH showed significantly decreased numbers of total PB B lymphocytes (vs. controls and AWLD ), at the expense of immature, memory, and, to a lesser extent, also naïve B cells. AWLD showed reduced numbers of immature and naïve B cells (vs. controls), but higher PB counts of plasmablasts (vs. the other 2 groups). Although PB memory B cells were reduced among the patients, the percentage of surface (s) IgA + cells (particularly CD 27 − / sIgA + cells) was increased in AH , whereas both sIgG + and sIgA + memory B cells were significantly overrepresented in AWLD versus healthy donors. Regarding circulating plasmablasts, patients with AH only showed significantly reduced counts of sIgG + cells versus controls. In contrast, the proportion of both sIgA + and sIgG + plasmablasts—from all plasmablasts—was reduced in AH and increased in AWLD (vs. the other 2 groups). Conclusions AH and AWLD patients display a significantly reduced PB B‐cell count, at the expense of decreased numbers of recently produced immature/regulatory B cells and naïve B cells, together with an increase in Ig‐switched memory B lymphocytes and plasmablasts, particularly of IgA + cells.