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Mucin5B is expressed in alveolar macrophages in long‐term smokers who have developed smoking associated lung diseases. This study investigated the expression of MUC5B by AMs in the lungs of cigarette smokers and nonsmokers. We analyzed MUC5B expression by measuring the levels of apomucin and mRNA in human BALF cells from 50 subjects (20 nonsmokers, 17 patients with CB, and 13 patients with COPD). apoMUC5B was observed in BALF mononuclear cells in 60% of all subjects, but a significantly higher frequency of apoMUC5B+cells was found in subjects with CB (95% CI, 4.5–24.9) or COPD (95% CI, 6.2–39.6) than in nonsmokers (95% CI, 0.5‐2.5). apoMUC5B+mononuclear cells showed strong expression of CD163, confirming their identity as AMs. MUC5B mRNA expression was detected by ISH in AMs of subjects investigated, and real‐time qPCR analysis confirmed MUC5B mRNA expression. In conclusion, MUC5B is expressed in a subset of lung AMs and long‐term cigarette smoking may increase the level of MUC5B produced by these cells.

We hypothesized that the allergen-induced increased number of airway eosinophils results from increased recruitment of eosinophils from bone marrow (BM) and local development of CD34+cells into eosinophils. We also assumed that the phenotype of airway eosinophils depends on whether these cells have differentiated within BM or airway. C57BL/6 mice were sensitized and subsequently exposed to ovalbumin (OVA) on 5 consecutive days. Newly produced cells were labeled with a thymidine analog. Clonogenic activity and interleukin 5 (IL-5) release from bronchoalveolar lavage fluid (BALf) CD34+cells were evaluated by using cell-culture techniques. Allergen exposure induces increase in CD135+primitive myeloid progenitors within the BM CD34+cell population, without significant changes in total number of CD34+cells or newly produced CD34+cells. CD34+/IL-5Rα+cells in the first stage of cell differentiation were found only in BM, arguing that early commitment of CD34+cells into the eosinophil lineage is restricted to the BM compartment. Allergen exposure induces a shift in differentiation of BM, blood, and BALf eosinophillineage–committed CD34+cells toward mature eosinophils and recruitment of these cells via blood into airway. We further demonstrate in vitro that ability to multiply persists in BALf CD34+cells but not CD34–cells, likely via autocrine IL-5 release and IL-5–induced up-regulation of IL-5Rα.

We hypothesized that the allergen-induced increased number of airway eosinophils results from increased recruitment of eosinophils from bone marrow (BM) and local development of CD34+ cells into eosinophils. We also assumed that the phenotype of airway eosinophils depends on whether these cells have differentiated within BM or airway. C57BL/6 mice were sensitized and subsequently exposed to ovalbumin (OVA) on 5 consecutive days. Newly produced cells were labeled with a thymidine analog. Clonogenic activity and interleukin 5 (IL-5) release from bronchoalveolar lavage fluid (BALf) CD34+ cells were evaluated by using cell-culture techniques. Allergen exposure induces increase in CD135+ primitive myeloid progenitors within the BM CD34+ cell population, without significant changes in total number of CD34+ cells or newly produced CD34+ cells. CD34+/IL-5Rα+ cells in the first stage of cell differentiation were found only in BM, arguing that early commitment of CD34+ cells into the eosinophil lineage is restricted to the BM compartment. Allergen exposure induces a shift in differentiation of BM, blood, and BALf eosinophillineage–committed CD34+ cells toward mature eosinophils and recruitment of these cells via blood into airway. We further demonstrate in vitro that ability to multiply persists in BALf CD34+ cells but not CD34– cells, likely via autocrine IL-5 release and IL-5–induced up-regulation of IL-5Rα.