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Background  Bacteria engage cell surface receptors and intracellular signaling molecules to enter the cell. Unc119 is an adaptor protein, which interacts with receptors and tyrosine kinases. Its role in bacterial invasion of cells is unknown.    Methodology/Principal Findings  We used biochemical, molecular and cell biology approaches to identify the binding partners of Unc119, and to study the effect of Unc119 on Abl family kinases and  Shigella  infection. We employed loss-of-function and gain-in-function approaches to study the effect of Unc119 in a mouse model of pulmonary shigellosis. Unc119 interacts with Abl family kinases and inhibits their kinase activity. As a consequence, it inhibits Crk phosphorylation, which is essential for  Shigella  infection. Unc119 co-localizes with Crk and  Shigella  in infected cells.  Shigella  infectivity increases in Unc119-deficient epithelial and macrophage cells. In a mouse model of shigellosis cell-permeable TAT-Unc119 inhibits  Shigella  infection. Conversely, Unc119 knockdown in vivo results in enhanced bacterial invasion and increased lethality. Unc119 is an inducible protein. Its expression is upregulated by probacteria and bacterial products such as lipopolysacharide and sodium butyrate. The latter inhibits  Shigella  infection in mouse lungs but is ineffective in Unc119 deficiency.    Conclusions  Unc119 inhibits signaling pathways that are used by  Shigella  to enter the cell. As a consequence it provides partial but significant protection from  Shigella  infections. Unc119 induction in vivo boosts host defense against infections.