Toll-interacting protein (TOLLIP) is a ubiquitin-binding protein that is involved in the signaling pathways of Interleukin-1 receptor (IL-1R) and Toll-like receptors (TLR). Previous studies have shown that single nucleotide polymorphisms in the TOLLIP gene are associated with mortality and outcomes in idiopathic pulmonary fibrosis, however, the biology of TOLLIP in lung injury and repair is unknown. While animal studies have shown that TOLLIP modulates acute inflammation, the effect of TOLLIP deficiency in the mouse model of lung injury and fibrosis is unknown. In this study, our group investigated the effect of TOLLIP deficiency in the bleomycin model of lung injury. Previously, we observed that TOLLIP deficiency attenuated acute lung injury in the lipopolysaccharide (LPS) model of lung injury. We hypothesize that TOLLIP deficiency leads to increased lung injury in bleomycin-induced lung injury. To study this, we treated wild-type (WT) and TOLLIP knockout (KO) mice with bleomycin through intratracheal instillation (IT). At 14 days post-treatment, we collected bronchial alveolar lavage fluid (BALF) and lung tissues to evaluate the degrees of lung injury and fibrosis. Throughout this study, I helped maintain the mouse colonies, genotype the mice, process the samples during the harvests, collect BALF cell differentials, and analyze the data. Preliminary analyses of weight loss, BALF total protein, and cell differentials suggest TOLLIP deficiency results in worse lung injury at 14 days post-bleomycin. This work provides insight into the role of TOLLIP deficiency as an attenuator in long-term lung injuries and how it may be used as a potential treatment for inflammatory disorders and infections.