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. Author manuscript; available in PMC: 2013 Aug 1.
Published in final edited form as: Biochim Biophys Acta. 2012 Mar 31;1826(1):129–169. doi: 10.1016/j.bbcan.2012.03.008

Figure 4. Mechanism of bacteriostatic action of NGAL.

Figure 4

Gram negative bacteria (like Salmonella typhimurium) trigger an immune response characterized by the activation of antigen presenting cells (macrophages and dendritic cells) upon engulfing the bacteria. These activated cells then release cytokines like IL-18 and IL-23 that in turn activate T-lymphocytes. These activated T-cell in turn release IL-17 and IL-22. These two cytokines act on the intestinal cells and stimulate the de novo synthesis of lipocalin 2 (Lcn2). The Lcn2 is secreted into the intestinal lumen and binds to bacterial iron binding proteins (siderophores) like enterochalin. Since iron is essential for the growth of bacteria, the sequesteration of bacterial siderophores by Lcn2 has a bacteriostatic effect. In some gram negative bacteria (like Salmonella typhimurium), a cluster termed as the iroBCDEiroN cluster is present which encodes for salmochelin, a gycosylated derivative of enterochelin which does not bind Lcn2. Hence, gram negative bacteria containing this cluster are resistant to the bacteriostatic effects of Lcn2. Commensals like certain species of E.coli lack the iroBCDEiroN cluster and hence are targeted by Lcn2 secreted during intestinal inflammation.