ABSTRACT
We determined whether microcrystalline cellulose (MCC), a component of pharmaceutical tablets, induces pulmonary changes. In vivo [resistive and viscoelastic pressures (DeltaP(1) and DeltaP(2)), static elastance (E(L))] and in vitro [tissue resistance (R), elastance (E), and hysteresivity (eta)] lung mechanics, histology, and bronchoalveolar lavage fluid (BALF) were analyzed 3h, 24h, and 3, 15 and 30 days after intratracheal instillation of saline (C) or MCC in BALB/c mice. DeltaP(1) increased at 3h, remaining higher than C until day 3, while E(L) and DeltaP(2) increased only at 24h. At 3 days all mechanical parameters returned to baseline. R and E increased only at 24h. MCC increased alveolar collapse and the number of neutrophils in BALF at 3h, until 3 and 15 days, respectively. At 3 days MCC migrate from the airways into the parenchyma, where they were observed until 30 days. In conclusion, microcrystalline cellulose yielded an acute and self-limited inflammation that impaired lung mechanics.
