Unc119 plays a significant role in T cell signaling by activating Lck and Fyn. Unc119 activates Fyn in fibroblasts and facilitates their differentiation into Ginsenoside-Ro myofibroblasts. As mentioned previously, Src promotes Shigella infection. For this reason we asked if Unc119 played a role in Shigella infection. To our surprise Unc119 inhibited 
Shigella infection. It did so by inhibiting Abl family kinases and their substrate Crk. On the basis of these findings we believe Unc119 represents a novel inhibitory Cinoxacin mechanism in Shigella infection. In absence of Unc119, the level of IFN-c decreases. IFN-c has been shown to be essential for innate resistance to Shigella infection in mouse lungs and in its absence the mouse become more susceptible to infection and manifest increased mortality. Mouse KC is a functional homologue of human IL8. The level of KC increases with bacterial infection, which is likely a defense mechanism and increases the recruitment of neutrophils. The increase in the level of KC in Unc119-deficient lungs could contribute to the worsening pathophysiology and increased mortality. The exact mechanism of the altered cytokine level in Unc119-deficient lungs is not known. Unc119 plays an important role in mediating intracellular signals for cytokine receptors and T cell antigen receptors. During Shigella infection the activation of some of these receptors may be impaired in the absence of Unc119, which could result in altered cytokine production. It should be pointed out that the changes in the cytokine level could be secondarily due to the increased inflammation. Unc119 is an inducible protein and Shigella infection increases the expression of Unc119 in the mouse lungs, human lung and colonic epithelial cells. Lactobacillus, a normal gut flora, also upregulates Unc119. Intestinal infection with pathogenic bacteria frequently occurs when the normal gut flora is destroyed. We speculate that the loss of Lactobacillus reduces Unc119 expression and thereby, increases susceptibility to pathogens. Butyrate is a fermentation product of the normal gut flora and provides protection against Shigella. Butyrate was shown to induce the antimicrobial peptide LL-37 in rabbit colonic epithelium. We show that butyrate upregulates Unc119. We speculate that the normal gut flora supports the expression of Unc119 in epithelial cells directly and also indirectly through the generation of butyrate.